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. 2021 Jul 4;11(8):363. doi: 10.1007/s13205-021-02910-9

Double emulsion-based mayonnaise encapsulated with bitter gourd extract exhibits improvement in vivo anti-diabetic action in STZ induced rats

Urmila Choudhary 1,✉, Latha Sabikhi 1, Suman Kapila 2
PMCID: PMC8260699  PMID: 34290946

Abstract

Bitter gourd contains charantin (steroidal saponins), insulin-like peptides, and alkaloids, which contribute to its hypoglycemic ability. The study aims to evaluate effects of anti-diabetic potential of bitter gourd (Momordica charantia) encapsulated double emulsion-based functional mayonnaise on the normal and streptozotocin-induced type 2 diabetes in albino male Wister rats. The rats were allocated into seven groups: a control group fed with synthetic diet (NC), two non-diabetic groups (NCM and NFM) and four diabetic-induced groups (DC, DCM, DFM, and DCMB) for 8 weeks and then analyzed for the various biochemical parameters. The results of this study revealed significant (p < 0.05) anti-diabetic potential in streptozotocin-induced diabetic male albino Wistar rats with decrease in blood glucose and HbA1c, increase in body weight, hemoglobin, and plasma insulin.

Keywords: Bitter gourd extract, Blood glucose, Diabetes, Double emulsion

Introduction

Plant extracts are used as medicines to cure diseases and have been providing relief from several medical problems since time immemorial. They also have the potential to act as preventive measures for several ailments. The role of diet in maintenance of good health is well recognized (Sofowora et al. 2013). The quality and quantity of different dietary components are determining factors for overall health. Dietary habits and lifestyle are associated with various metabolic diseases such as diabetes mellitus (Olatona et al. 2018). Diabetes is characterized by hyperglycaemia that occurs from lack in insulin secretion (type 1 diabetes mellitus) and absolute insulin insensitivity (type 2 diabetes mellitus) (Bastaki 2005; Srividya and Shailendra 2008). According to Ministry of Health data, Indian population is more prone to obesity and diabetes-related complications. Current load of diabetes in world is 463 million adults (20–79 years) and it will rise to 578 million by 2030 and 700 million by 2045. In 2019, diabetes prevalence in adults in South-East Asia Region is estimated to be 11.3% and projected to rise to 12.2% by 2030 and 12.6% by 2045. In 2019, 77 million cases of diabetes were in India and it will be 134.2 million by 2045 (IDF 2019). Bitter gourd or karela (Momordica charantia) is one such herbal vegetable plant, belonging to cucurbitaceae family and grown in tropical and subtropical countries of South Asia, South America, and Africa (Duke et al. 2002; Garau et al. 2003; Rahman et al. 2006), whose parts such as seeds, leaves, and fruit have profound uses in the field of medicine and are bitter in taste. The fruits are very cheap and available throughout the year. They are rich in nutrients, i.e., vitamin A, vitamin C, folic acid, and essential amino acids (Sekar et al. 2005; Sridhar et al. 2008). It is consumed as food in Indian cuisine and also used as a traditional medicine in Ayurveda as a remedy for diabetes (Yadav et al. 2005). Its therapeutic values as a hypoglycaemic agent are because of its active ingredients, i.e. charantins, vicine, polypeptide p, and momordin (Basch et al. 2003; Patel et al. 2006; Wu and Ng 2008; Habicht et al. 2011). They offer minimum or no side effects when used as herbal drugs. They increase insulin secretion from pancreatic β-cells and repair or promote new growth of insulin-secreting β-cells (Yibchok-Anun et al. 2006), increase blood sugar level, and suppress postprandial hyperglycemia (Uebanso et al. 2007). In vivo and in vitro studies were performed to identify the hypoglycemic constituents of Momordica charantia wild variant WB24. Triterpenes isolated from the fruit (Momordica charantia wild variant WB24) showed the activation of AMPK in an insulin-independent manner. Out of triterpenes isolated from the fruit (Momordica charantia wild variant WB24), compound, 5β,19-epoxy-25-methoxy-cucurbita-6,23-diene-3β,19-diol triterpene showed higher than that of troglitazone, a thiazolidinedione-type antidiabetic medicine (Chang et al. 2011). Effect of bitter gourd was characterized on the enterocyte cell line of IEC-18 cells and insulin resistance was induced using TNF-α. Bitter melon extract enhanced glucose consumption of the insulin-resistant cells because of the joined impact of insulin substitution and insulin-sensitizing functions of bitter melon extract. The activation of AMP-activated protein kinase was likely generated functions of insulin substitution. Then, bitter melon extract acted as a glucagon-like peptide 1 (GLP-1) secretagogue on enteroendocrine cells, which might be interceded by the activation of bitter taste receptors. Hence, bitter melon extract works as an insulin sensitizer and an insulin substitute against insulin-resistant enterocytes, and as a GLP-1 secretagogue on enteroendocrine cells (Chang et al. 2021). Ma et al. (2017) reported that Momordica charantia extracts enhance insulin resistance by regulating the expression of mRNA, protein levels of SOCS-3, and JNK in type 2 diabetes mellitus rats. They further found that the 8-week treatment of 400 mg/kg M. charantia ethanol extracts significantly lowered serum glucose, insulin, TNF-α, and IL-6 in comparison with those of the diabetic control group (p < 0.05).

Incorporation of bitter gourd extract in foods could be a helpful method to combat diabetes mellitus, while most people avoid consuming it on account of its unpleasant taste (Paul and Raychaudhuri 2010). Bitter gourd has a bitter taste because of the triterpene glycosidase compounds like K and L momordicosida, momordicin, and cucurbitacin (Donya 2007; Limtrakul et al. 2013) and alkaloids (Nagarani et al. 2014). Therefore, utilization of bitter gourd extract needs a medium by which its sensorial aspects can be made acceptable or masked as well as its bioaccessibility to be increased. Double emulsion (W/O/W) is one such technique that is used to protect and encapsulate the sensitive bioactive components, mask the unacceptable flavor and odor of plant extracts and their controlled release during eating and or digestion and also increased the bioaccessibility of the bioactive components in the gastrointestinal tract (Jiménez-Colmenero 2013; Oppermann et al. 2016; Muschiolik and Dickinson 2017). Its application in the food industry for formulation of healthier foods including nutraceutical and functional foods by reducing oil/fat (calories) content and improving healthier fatty acid profile, salt (sodium) concentrations, masking unacceptable flavors/odors through compartmentalization, and as vehicles for encapsulation and controlled release of bioactive compound, i.e. vitamins, carotenoids, ω-3 fatty acids, phytochemicals, microorganisms, lactoferrin, and minerals is gaining momentum (Muschiolik and Dickinson 2017; Raviadaran et al. 2018). Double emulsion (W/O/W) containing bitter gourd extract can function as an appropriate vehicle to incorporate the antidiabetic herbal component in functional foods, without altering their sensory properties. Mayonnaise, a semi-solid oil-in-water emulsion, is traditionally prepared from a mixture of egg yolk, vinegar, oil (70–80%, w/w), and may also include salt, sugar or sweeteners and other optional ingredients (Depree and Savage 2001). W/O/W emulsions can be replaced conventional O/W emulsions not only by reducing the oil content but also having the similar sensorial perception in mouth (Muschiolik and Dickinson 2017).

The aim of this study was to validate the anti-diabetic effects of aqueous bitter gourd extract when encapsulated in double emulsion-based mayonnaise with and without emulsification with respect to control mayonnaise and synthetic diet on streptozotocin-induced diabetic and normal rats. The parameters studied were fasting blood glucose level, body weight, oral blood glucose tolerance test, HbA1c, hemoglobin, and blood plasma insulin concentration.

Materials and methods

Plant material

Aqueous extract of bitter gourd (Momordica charantia) containing 5.95%, w/w total solids content, and 5% Charantin content (Batch No.: PEM01146) was purchased from Ambe Phytoextracts Pvt. Ltd., New Delhi.

Materials

Materials for double emulsion-based control and functional mayonnaise, animal diet preparation and kits for analysis are provided in Appendix 1.

Preparation of double emulsion based-control mayonnaise and functional mayonnaise

The double emulsion-based control mayonnaise and functional mayonnaise were prepared according to the method given in our previous work (Choudhary and Sabikhi 2020). Method for preparation of double emulsion-based-control mayonnaise and functional mayonnaise in brief is provided in Appendices 2 and 3, respectively.

Animals

Male albino rats of Wistar strain used in the experiment were obtained from Small Animal House of ICAR-National Dairy Research Institute (ICAR-NDRI), Karnal, Haryana. The animals were 6–7 weeks old and were housed in a polycarbonate cages at a temperature of 24 ± 1 °C and relative humidity of 55 ± 10%, with a 12:12 h light–dark cycle. The study was approved by the Animal Ethics Committee (Reg. No.1705/GO/ac/13/CPCSEA Dt. 3/7/2013), Livestock Research Center, Livestock Production Management, ICAR-NDRI, Karnal-132001, India.

Experimental design

The 6- to 7 week-old animals (180–200 g body weight) were acclimatized for 1 week on standard diet, while the entire experiment was run for 8 weeks. The body weight deviation of the animals in each group was ± 20 g. The animals were randomly divided into seven groups of eight rats each as per the experimental design shown in Table 1. They had access to the designated diet and water ad libitum.

Table 1.

Experimental design for hypoglycemic study

Groups Animal subjected to citrate–phosphate buffer/ STZ injection Diet plan in terms of fat source Sample collection
Day 1, 1st, 2nd, 3rd, 4th, 5th, 6th, 7th week 8th week*
(1) Normal + Synthetic Diet (NC) Citrate phosphate buffer 100% synthetic diet with rice bran oil as fat source Blood
(2) Normal + Control Mayonnaise (NCM) Citrate phosphate buffer 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise
(3) Normal + Functional Mayonnaise (NFM) Citrate phosphate buffer 70% synthetic diet with rice bran oil as fat source + 30% functional mayonnaise with fat derived from functional mayonnaise
(4) Diabetic + Synthetic Diet (DC) STZ (45 mg/kg body weight) 100% synthetic diet with rice bran oil as fat source
(5) Diabetic + Control Mayonnaise (DCM) STZ (45 mg/kg body weight) 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise
(6) Diabetic + Functional Mayonnaise (DFM) STZ (45 mg/kg body weight) 70% synthetic diet with rice bran oil as fat source + 30% functional mayonnaise with fat derived from functional mayonnaise
(7) Diabetic + Control Mayonnaise with unencapsulated Bitter gourd externally (DCMB) STZ (45 mg/kg body weight) 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise with externally added bitter gourd extract (unencapsulated form)
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*Samples were collected from sacrificed animals

Induction of type 2 diabetes

After acclimatization of the animals on standard diet for one week, diabetes was induced in rats after overnight fasting, with Streptozotocin (STZ) (Sigma, St. Louis, MO, USA; 45 mg/kg, IP) (Ayoub et al. 2014). The STZ was freshly dissolved in citrate buffer (0.1 M, pH 4.5) and maintained on ice before use. Twenty-four randomly selected rats referred as control rats were injected intraperitoneally with 10 mL of 0.1 M citrate phosphate buffer (pH 6.3) per kg body weight after 12-h fasting. Similarly, remaining rats referred as experimental rats were administered intraperitoneally with 45 mg STZ per kg body weight by single injection. Induction of diabetes was confirmed by the determination of fasting blood glucose concentration on the third day post administration of STZ. The rats having blood glucose level more than 200 mg/dL were considered to be diabetic and were taken for the experiment.

Animal diet preparation

Four diets were used in this study. Mineral mixture and vitamin mixture were prepared and mixed according to AOAC (1990). Diet for all the groups was made isocaloric (466.3 kcal/100 g of diet). Standard diet was partially replaced (30%) (Table 1).

Parameters

Body weight, food intake and food efficiency ratio

The body weight (BW) of rats was measured at weekly intervals for all the groups. Food given was kept constant, i.e. 15 ± 0.5 g/rat/day for all the groups. Total food intake of each group during the experimental period was monitored and food efficiency ratio (FER) was calculated as follows:

FER=Change in body weightg/Food intake(g)

Collection of blood

At the end of eighth week trial, overnight fasted rats were first anesthetized with diethyl ether in a glass jar and killed by cardiac puncture after dissection. The blood was collected in EDTA-coated-vaccutainers (vials) and kept in ice bath. A portion of the blood was used for hemoglobin (20 µL) and glycosylated hemoglobin (5 µL) estimation. Remaining blood after collection was transferred in Eppendorf tube and was centrifuged at 3500 rpm for 10 min at 4 °C in a refrigerated micro-centrifuge (Sigma Laborzentrifugen, Germany). After collection of plasma (top portion), buffy layer was removed and transferred to another Eppendrof tube using micropipette and stored at − 20 °C for further analysis.

Blood glucose levels

Blood glucose (BG) levels of rats were measured at weekly intervals after 12 h of fasting. Blood samples were drawn by pricking the tail, using a lancet. BG was estimated using blood monitory kit (Dr. Morepen GlucoOne).

Estimation of hemoglobin in blood

Hemoglobin was estimated using hemoglobin estimation kit (QuantiChromTm Hemoglobin Assay Kit) which uses Drabkin reagent (Drabkin 1950). Twenty µL blood was diluted with 5 mL Drabkin reagent 1. Absorbance of test sample was read at 540 nm against blank, which was Drabkin reagent 1. Also, absorbance of standard solution cyanmethemoglobin (supplied as reagent 2 in kit) was recorded. Hemoglobin was estimated (g/dL) using following equation:

Hemoglobing/dL=Optical density of test/Optical density of standard×15.06

Oral glucose tolerance test (OGTT)

The test was performed on the experimental rats under hypoglycemic study on the 8th week after 12 h of fasting. Glucose (2 g/ kg body weight; 200 g/L solution) was administered orally using gavage. Blood was drawn by puncturing the tail vein with needle gun at 0 h (before administration) and 30, 60, 90,and 120 min after glucose administration. Glucose levels were determined by taking one drop of blood sample by glucometer.

Measurement of insulin in plasma

Plasma insulin levels were measured using a standard kit [Ultra-Sensitive Rat Insulin Enzyme-Linked Immunosorbent Assay Kit (Crystal Chem Inc. Downers Grove, IL, USA)], based on sandwich ELISA method and as per manufacturer’s instructions. Standards were run in duplicate and experimental samples in triplicate.

Measurement of HbA1c levels in blood

HbA1c was measured by enzymatic ELISA method as per manufacturer’s instructions (Crystal Chem Inc. Downers Grove, IL, USA).

Statistical analysis

Animal feeding data were analyzed by one-way and two-way ANOVA with Tuckey Post Test, Duncan/Bonferroni posts-tests and Two-tailed Paired t test at 95% (P < 0.05) level of significance using SPSS software (IBM SPSS Statistics Version 21).

Results and discussion

The anti-diabetic efficacy of a double emulsion-based functional mayonnaise containing bitter gourd extract was evaluated in streptozotocin (STZ) induced diabetic rats. The different groups of animals fed on varying diets were designated as given in the Table 1. The results of the effects on body weight, blood glucose, oral glucose tolerance test, plasma insulin, and glycosylated hemoglobin in blood are presented here.

Experimental observation

The diabetic rats fed with synthetic diet (DC) showed 3P classical symptoms [polyuria, polydipsia, polyphagia] and weakness compared to normal rats fed with synthetic diet. On the other hand, diabetic rats fed with control mayonnaise (DCM), functional mayonnaise (DFM), and control mayonnaise with bitter gourd extract (DCMB) showed gradual relief of these 3P classical symptoms without weakness and death in all three diabetic groups. However, normal rats fed with synthetic diet (NC), control, and functional mayonnaise (NCM and NFM) remained healthy throughout the experimental study and they showed normal water intake, food intake, and normal urine excretion. Moreover, 33% of diabetic rats fed with synthetic diet (DC) were found dead within 3 days of STZ injection and that was expected with this model (Zhang et al. 2021). Appendix 4 describes the groups in terms of their condition, type of diet, and their effect on physiological parameters at the end (8-week) of the experimental study. These observations may indicate that the functional mayonnaise (FM), control mayonnaise + bitter gourd extract (CMB), and control mayonnaise (CM) may have effects to prevent or delay the progress of diabetic complications in rats in the following order: FM > CMB > CM. Our results were in agreement with the studies reported by Shetty et al. (2005), Ayoub et al. (2013) and Moqbel et al. (2017).

Food intake and food efficiency ratio

Consumption of different diets by animals was observed in following descending order: Control mayonnaise (CM) > control mayonnaise with bitter gourd extract (CMB) > functional mayonnaise (FM) > synthetic diet (SD). It is evident from Table 2 that the food intake significantly (p < 0.05) varied among all the groups throughout the study in the following order: DCM > NCM > NFM > DCMB > DFM > DC > NC. Moreover, there was no statistical difference (p > 0.05) between the normal group fed with control mayonnaise (NCM) and functional mayonnaise (NFM) and between diabetic group fed with synthetic diet (DC) and functional mayonnaise (DFM). The food intake did not statistically differ (p > 0.05) between normal group (NC) (−ve control group) and diabetic group (DC) (+ve control group) fed with synthetic diet. The average daily intake was approximately 7–12 g per rat per day. The food efficiency ratio was also significantly different (p < 0.05) among all the groups as shown in Table 2. The variation in intake of different diets [control mayonnaise (CM), control mayonnaise with bitter gourd extract (CMB), functional mayonnaise (FM), and synthetic diet (SD)] by animals could be due to the higher fiber (β-pectin) content in control mayonnaise (CM) and functional mayonnaise (FM), as compared to synthetic diet (SD). Our findings are in line with the findings of Klomann et al. (2010) and Mahwish et al. (2017). Mahwish et al. (2017) reported that feed intake influenced significantly the time period (weeks) of the experimental study, whereas feed intake with different parts (skin, flesh, and whole fruit powder) of bitter gourd fruit and the variations in concentration (150 and 300 mg/kg body weight) of bitter gourd in diet did not affect the food intake during the experimental period of the study.

Table 2.

Effect of double emulsion based control and functional mayonnaise on body weight gain, food intakes, and food efficiency ratio on normal and diabetic rats fed for eight weeks

Group Initial body (week 1) weight (g) Final body (8 week) weight (g) Change in body weight Total food intakes (g/period) FER
NC 163.56 ± 4.24bA 148.44 ± 7.18aB − 15.12 ± 3.99b 2836.10 ± 2.33d − 0.005 ± 1.71b
NCM 160.06 ± 2.74aA 197.31 ± 6.37bD 37.25 ± 4.08d 4482.50 ± 0.88e 0.008 ± 4.64de
NFM 161.12 ± 2.46aA 189.94 ± 8.12bC 29.82 ± 5.30 cd 4283.00 ± 1.31e 0.007 ± 4.04d
DC 160.37 ± 3.36aA 153.80 ± 4.04aB − 6.57 ± 2.22b 2971.00 ± 2.59c − 0.002 ± 0.86c
DCM 161.12 ± 3.18aA 214.75 ± 8.92bE 54.63 ± 3.06e 4999.00 ± 1.30f 0.011 ± 2.35e
DFM 160.69 ± 1.73aA 182.45 ± 3.47bC 21.76 ± 3.67c 3283.30 ± 3.61c 0.007 ± 1.02d
DCMB 161.50 ± 2.96aA 184.00 ± 9.32bC 22.50 ± 3.04c 3854.50 ± 2.65d 0.006 ± 1.15d
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Data are expressed as means ± SEM. abcdef: Values within a column with different superscripts are significantly different (p  < 0.05). ABCDE: Values within a raw to raw with different superscripts are significantly different (p  < 0.05)

Body weight

Figure 1 depicts the change in the body weight of the rats during the experimental study of 8 weeks. Though at baseline of the experiment (Week 1), the body weight was similar among the seven different groups, although, at the 2nd and 3rd weeks, normal rats fed with functional mayonnaise (NFM) exhibited a significant (p < 0.05) difference among all groups. At the week 4, diabetic rats fed with synthetic diet (DC) and functional mayonnaise (DFM) exhibited a significant (p < 0.05) difference in body weight when they were compared to all normal rats (NC, NCM, and NFM) and diabetic rats fed with control mayonnaise (DCM) and control mayonnaise with bitter gourd extract (DCMB). At week 5, there was a significant (p < 0.05) difference in body weight between normal rats fed with functional mayonnaise (NFM) and diabetic rats fed with control mayonnaise with bitter gourd extract (DCMB). Even though there was a significant (p < 0.05) difference in body weight among all normal rats (NC, NCM, and NFM) at week 5. At the 6th week, all rats, except diabetic rats fed with control mayonnaise (DCM) and normal rats fed with functional mayonnaise (NFM), had significantly different body weights. Control mayonnaise fed normal (NCM) and diabetic rats (DCM) showed a significant (p < 0.05) difference in body weight among all rats at the end of the study’s eight weeks; on the other hand, all normal rats showed a significant (p < 0.05) difference in body weight among all rats at the end of the study’s eight weeks. When compared to the other two diabetic groups (DC and DCM) and all normal rats (NC and NCM) except normal rats fed with functional mayonnaise (DFM), diabetic rats fed with functional mayonnaise (DFM) and control mayonnaise with bitter gourd extract (DCMB) showed significant differences in body weight (NFM). The normal groups fed with synthetic diet (NC) exhibited a significant (p < 0.05) decrease in body weight, while the STZ-induced diabetic group fed with synthetic diet (DC) (positive control) also exhibited a non-significant (p > 0.05) decrease in body weight at the end of the 8-week study. At the end of 8th week of the study, a significant (p < 0.05) gain in body weight was observed among all groups fed with control mayonnaise (NCM, DCM), functional mayonnaise (NFM, DFM), and control mayonnaise with bitter gourd extract (DCMB).

Fig. 1.

Fig. 1

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Effect of an 8 week treatment with synthetic diet, control mayonnaise, functional mayonnaise and control mayonnaise with bitter gourd extract diets on body weight of normal rats and STZ-induced diabetic rats. Values are expressed as mean ± SEM (n = 8). abcde: Values within a week. ABCDEFG: Values within a group. Values with different superscripts are significantly different (p < 0.05). The seven groups are identified by their respective designated diets as NC, NCM, NFM, DC, DCM, DFM, and DCMB

Our results are consistent with the study reported by Wang et al. (2011) and Mahwish et al. (2017) who found that the body weight of diabetic rats fed with bitter gourd was greater in comparison to untreated diabetic rats. A marginal increase was also found in the body weight of the diabetic group treated with bitter gourd (Shetty et al. 2005). The change in body weight among all the groups was due to the variation in food intake by animals. Due to the higher palatability of food rich in dietary fiber, high amount of food is consumed (Nandini et al. 2003; Shetty et al. 2005). Higher amount of soluble dietary fiber consumption slows the gastric-emptying rate that may allow for more complete digestion and absorption in GI tract (Schneeman 1998). It also increases the bacterial count in the large intestine that could increase energy absorption by fermenting and utilizing the short chain fatty acids (Davidson and McDonald 1998). This increases weight gain or the metabolic energy.

Blood glucose

The effect of four different diets on fasting blood glucose level of normal and STZ-induced diabetic rats is shown in Fig. 2. There was a significant difference in the mean fasting blood glucose (FBG) level between the normal and diabetic groups (p < 0.05). At the beginning of the 8-week experimental study, the three normal rats groups (NC, NCM, and NFM) showed normal FBG level (12 h) in a range of 107.00 ± 3.32 to 109.62 ± 3.19 mg/dL, whereas the FBG level (12 h) of the diabetic rats groups (DC, DCM, DFM, and DCMB) varied in a range of 264.25 ± 12.91 to 314.50 ± 6.82 mg/dL. Thus, it was evident that the intraperitoneal injection (IP) of STZ at a dose of 45 mg/kg body weight raised the FBG level approximately 2.5 to threefold compared to the normal rats groups, which caused a statistically significant diabetogenic response in the STZ-induced rats. All normal rats showed no statistical (p > 0.05) change in FBG level throughout the experimental study except those fed with control mayonnaise (NCM), which showed a significant (p < 0.05) change (108.00 ± 3.67 to 124.62 ± 3.71) in FBG level at 8th week of the study. Among diabetic rats, those fed with synthetic diet (DC) and functional mayonnaise (DFM) showed significant difference with rats fed with control mayonnaise (DCM) and control mayonnaise with bitter gourd extract (DCMB) at beginning of the experimental study. At the beginning of week 2, there was a significant difference in FBG of all diabetic rats except those fed with control mayonnaise (DCM) and control mayonnaise with bitter gourd extract (DCMB). Diabetic rats fed with synthetic diet showed significant change in FBG over week 3, while others did not show statistical difference in blood glucose till week 7 of experimental study. At the end of the 8-week experimental study, there was a significant increase in FBG levels among all normal rat groups such as NC (125.75 ± 3.46 mg/dL), NCM (124.62 ± 3.71 mg/dL), NFM (123.12 ± 3.00 mg/dL), but they kept FBG in normal range. Diabetic groups fed with control mayonnaise (DCM), functional mayonnaise (DFM), and control mayonnaise with bitter gourd extract diets (DCMB) resulted in significant (p < 0.05) decrease in mean of FBG levels as compared to diabetic control (DC) (+ ve) groups. The control mayonnaise-fed diabetic rats (DCM) had higher FBG level when compared to functional mayonnaise (p < 0.05) and control mayonnaise with bitter gourd extract-fed diabetic rats (DFM and DCMB). Among all the diabetic groups, the functional mayonnaise-fed diabetic rats (DFM) were found most effective in significantly (p < 0.05) lowering the FBG level. However, reduction was not statistically significant in the diabetic rats fed with functional mayonnaise (DFM) and control mayonnaise with bitter gourd extract (DCMB).

Fig. 2.

Fig. 2

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Effect of an 8 week treatment with synthetic diet, control mayonnaise, functional mayonnaise and control mayonnaise with bitter gourd extract diets on fasting blood glucose (mg/dL) of normal rats and STZ-induced diabetic rats. Values are expressed as mean ± SEM (n = 8). abcd: Values within a group. ABCD: Values within a week. Values with different superscripts are significantly different (p < 0.05). The seven groups are identified by their respective designated diets as NC, NCM, NFM, DC, DCM, DFM, and DCMB

Wang et al. (2007) reported the effect of dietary fiber supplementation on FBG level in mice fed on high-fat diet-fed for 12-weeks found that the FBG (4 h fasting) levels were significantly (p < 0.05) higher in cellulose- and high-fat diet fed groups than those in psyllium husk powder and sugarcane fiber-fed groups. Control mayonnaise, functional mayonnaise, and control mayonnaise with bitter gourd extract had FBG reducing effect in diabetes in the following descending order: DFM > DCMB > DCM. Our results are in line with the previous studies of Sathishsekar and Subramanian (2005); Almarzooq and Moussa (2009); Aswar and Kuchekar (2012); Mohammady et al. (2012); Perumal et al. (2015). Shetty et al. (2005) showed that supplementation with bitter gourd powder (10%) significantly (p < 0.05) decreased fasting blood glucose level by 30%. Mahwish et al. (2021) also reported that diabetic rats fed with whole fruit powder (300 mg/kg body weight) significantly (p < 0.05) lowered the blood glucose by 31.64%. In vitro study revealed that bitter gourd fed normal and STZ induced diabetic rat significantly (p < 0.05) increased glucose uptake by isolated rat diaphragms in the presence and absence of insulin (Mahmoud et al. 2017). Chang et al. (2021) reported that insulin substitution and insulin-sensitizing functions of bitter gourd extract helps in promoting the glucose utilization of insulin-resistant enterocyte cell line of IEC-8 cells.

Oral blood glucose tolerance test (OGTT)

Figure 3 shows the effect of four different diets on oral blood glucose tolerance test (OGTT) in various experimental groups. At the end (8-week) of experimental study, OGTT was conducted. The blood glucose levels at different time intervals after administration of glucose is given in Fig. 3. Blood glucose level was significantly lower in normal groups as compared to diabetic groups at zero minute. At 30 min, oral administration of glucose resulted in a significant increase in blood glucose level of all normal rats (NC, NCM, and NFM) and diabetic rats fed with functional mayonnaise (DFM), which thereafter decreased gradually with increasing time duration. The increased levels of blood glucose were restored to near-normal in the normal groups fed with all three different diets (synthetic, control mayonnaise, functional mayonnaise). A similar trend was found in STZ-induced diabetic groups. Among the diabetic groups, the maximum effect was found for the functional mayonnaise fed diabetic group (DFM) in lowering the blood glucose level at 120 min. These findings are in line with those reported by Aswar and Kuchekar (2012) and Mohammady et al. (2012), who found that the administration of aqueous extract of Momordica charantin to alloxan-induced diabetic rats was effective to decrease blood glucose levels similar to administration of glibenclamide (10 mg/kg body weight) or rosiglitazone maleate (4 mg/kg body weight) during glucose tolerance test. Wang et al. (2007) also found that the blood glucose level was significantly lower in psyllium husk powder- and sugarcane fiber-fed groups than those in cellulose- and high-fat diet-fed groups (p < 0.01 and p < 0.001).

Fig. 3.

Fig. 3

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Effect of an 8 week treatment with synthetic diet, control mayonnaise, functional mayonnaise, and control mayonnaise with bitter gourd extract diets on oral blood glucose tolerance test (mg/dL) of normal rats and STZ-induced diabetic rats. Values are expressed as mean ± SEM (n = 8). abcd: Values within a group. ABC: Values within a time interval (minute). Values with different superscripts are significantly different (p < 0.05). The seven groups are identified by their respective designated diets as NC, NCM, NFM, DC, DCM, DFM, and DCMB

Hemoglobin (Hb), blood glycosylated hemoglobin (HbA1c) and plasma insulin

Effect of different diets such as synthetic diet, control mayonnaise, functional mayonnaise, and control mayonnaise with bitter gourd extract diets on hemoglobin (Hb) concentration (g/dL), blood glycated hemoglobin (HbA1c) (%), and plasma insulin levels (ng/mL) of normal rats and STZ-induced diabetic rats was evaluated. There was a significant (p < 0.05) difference in the mean hemoglobin concentration (Hb), % HbA1c, and plasma insulin level between normal and STZ-induced diabetic groups at the end of the experimental study as presented in Fig. 4. Administration of control mayonnaise (CM) and functional mayonnaise (FM) showed significantly (p < 0.05) higher the hemoglobin concentrations (g/dL) than the synthetic diet (SD) in normal rats. Among diabetic rats, a significant difference in Hb concentration was found in all diabetic rats (DFM, DCM and DC) except DCMB rats groups, whereas diabetic rats fed with synthetic diet (DC) showed significant lowest Hb concentration (p < 0.05). DCMB rats had significantly higher average values of Hb than DC groups (p < 0.05). Among normal rats, all rats found in a normal range of HbA1c. Diabetic rats fed with functional mayonnaise (DFM) had the lowest average values of HbA1c among diabetic groups and did not show a significant difference in mean HbA1c values with the DCMB group. All diabetic groups showed significantly higher mean HbA1c values as compared to normal groups. Among normal rats, rats fed with control and functional mayonnaise (NCM and NFM) showed significantly higher insulin values than rats fed with synthetic diet (NC). Diabetic rats fed with synthetic diet (DC) showed significantly (p < 0.05) lowest mean plasma insulin values among diabetic groups. All diabetic groups exhibited a significant (p < 0.05) difference in average plasma insulin values in comparison to normal rats fed with control mayonnaise (NCM) and functional mayonnaise (NFM). Diabetic rats fed with synthetic diet (DC) had significantly lowest mean insulin values among all normal and diabetic groups.

Fig. 4.

Fig. 4

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Effect of four different diets on a hemoglobin (g/dL), b percent glycosylated hemoglobin (% HbA1c), and c plasma insulin (ng/mL) in normal rats and STZ-induced diabetic rats. Values are expressed as mean ± SEM (n = 8). abcd: Values within a group. Values with different superscripts are significantly different (p < 0.05). The seven groups are identified by their respective designated diets as NC, NCM, NFM, DC, DCM, DFM, and DCMB

Our findings are in line with the results obtained by Ayoub et al. (2013) and Moqbel et al. (2017), who found that the hemoglobin (Hb) concentration significantly (p ≤ 0.001; p < 0.05) decreased in diabetic control group while a significant (p ≤ 0.001; p < 0.05) improvement was observed in Hb concentration of diabetic groups treated with different dose of M. charantia during the experimental (45 days; 12 weeks) study.

Our results are in agreement with the studies reported by Almarzooq and Moussa (2009), Fernandes et al. (2007) and Mohammady et al. (2012), who reported the influence of the bitter gourd juice/ bitter gourd extract on alloxan-induced diabetic animals and found a significant decrease in percent glycosylated hemoglobin (% HbA1c) level of the diabetic animals treated with bitter gourd as compared with diabetic control animals. The insulin results were in parallel with the studies reported by Shih et al. (2008, 2009), Hafizur et al. (2011) and Mohammady et al. (2012), who found that bitter melon improved the insulin levels (p < 0.05; p < 0.001) and β-cell function (p < 0.01) over different periods of experimental studies. Furthermore, the islet size, total β-cell area, and the number of β-cells increased twofold in the diabetic rats with bitter melon fruit pulp treatment. The increased diabetic β-cells were abundant with insulin granules as compared to control islets. This may have been possible by decreasing blood glucose and enhancing insulin resistance through the regulation of PPARγ-mediated pathway and improving lipid metabolism through the regulation of PPARα -mediated pathway. Mahwish et al. (2021) also reported that whole fruit powder (300 mg/kg body weight) significantly (p < 0.05) increased insulin by 27.35% in diabetic rats. Ma et al. (2017) reported that Momordica charantia extracts improve insulin resistance by regulating the expression of mRNA, protein levels of SOCS-3 and JNK in type 2 diabetic rats. In vitro study revealed that bitter gourd extract bitter works as an insulin sensitizer and an insulin substitute (generated due to the activation of AMP-activated protein kinase.) against insulin-resistant enterocytes, and as a GLP-1 secretagogue on the enteroendocrine cell line of IEC-18 cells (Chang et al. 2021).

Conclusion

The anti-diabetic effect of the double emulsion-based functional mayonnaise containing bitter gourd extract was studied and validated in normal and Streptozotocin (STZ)-induced diabetic and normal rats. The seven different groups were formed by feeding four different diets such as synthetic diet (SD), control mayonnaise (without bitter gourd extract) (CM), functional mayonnaise (FM), and control mayonnaise with unencapsulated bitter gourd extract (CMB). Functional mayonnaise (FM) and control mayonnaise with unencapsulated bitter gourd extract (CMB) showed better anti-diabetic potential as compared to synthetic diet (SD) and control mayonnaise (CM), as they improved the body weight, decreased the fasting blood glucose, and HbA1C levels and also increased hemoglobin and plasma insulin level. The study resulted in a functional double emulsion-containing bitter gourd extract as a potential delivery vehicle, to incorporate the antidiabetic herbal component in functional foods, without altering their sensory properties.

Acknowledgements

The first author thanks the ICAR-National Dairy Research Institute, Karnal (Haryana), India, for the grant of Institute Fellowship for conducting this research. The authors also acknowledge M/s. DuPont India Pvt. Ltd. and M/s. CP Kelco, Huber India Company (Mumbai, India) for the supply of free samples of PGPR, β-pectin (GENU® β-pectin).

Appendix 1

Materials for double emulsion-based control and functional mayonnaise, animal diet preparation, and kits for analysis

No. Item Features Procured from
1 Whey protein concentrate-80 79.86% protein, 8.09% lactose Mahaan Proteins Ltd., New Delhi
2 Sodium caseinate (Protonate 8868) 88% protein
3 β-Pectin Degree of acetylation of about 18%, Degree of esterification (DE) > 50% CPKelco, Huber India Company, Mumbai, Maharashtra
4 Gum Arabic (Fibre gum B) – KP Manish Global Ingredients Pvt. Ltd., Chennai
5 Polyglycerol polyricinoleate (PGPR) GRINSTED® PGPR 90 GRINSTED® PGPR 90 DuPont Danisco India Private Limited, Gurgaon, Haryana
6 Sodium chloride – Local market, Karnal, Haryana
7 Refined rice bran oil (Fortune)
8 Vinegar (4% acetic acid)
9 Reverse osmosis (RO) water – –
10 Bitter gourd extract 5.95%, w/w total solids content and 5% charantin content Ambe Phytoextracts Pvt. Ltd., New Delhi
11 Cellulose – Hi-Media Labs Pvt. Ltd., Maharashtra
12 Vitamin mixture –
13 Mineral mixture –
14 Streptozotocin CMS 1758–1 G
15 Corn starch – Roquette India Pvt. Ltd., Maharashtra
16 Acid casein – Modern Dairy Pvt. Ltd., Karnal
17 QuantiChromTm Hemoglobin Assay Kit Cat. No.- DIHB-250 (Size-250 T) Genxbio Health Sciences Pvt. Ltd., Delhi, India
18 Rat Hemoglobin A1c (HbA1c) Assay Kit Cat. No.- 80,300 (Size-96 T)
19 Ultra-Sensitive Rat Insulin ELISA kit Cat. No.- 90,060 (Size-96 T
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Appendix 2

Method for preparation of double emulsion based control mayonnaise.

Briefly, inner aqueous phase (W1) was prepared with NaCl (3.0%, w/w) in RO water. Middle oil phase (O) consisted of rice bran oil containing PGPR as hydrophobic emulsifier (4%, w/w) and outer aqueous phase (W2) consisted of 4.5% sodium caseinate-pectin). Both W1 and O were pasteurized at 72 °C for 15 s, while outer aqueous phase heated at 85 °C for 20 min to prepare biopolymer particles because of thermal denaturation and aggregation of the proteins followed by cooling to 4–7 °C in ice water bath. A primary water-in-oil (W1/O) emulsion was premixed by mixing the inner aqueous phase (W1) (30%, w/w) with the oil phase (O) (70%, w/w) at room temperature, using a magnetic stirrer at moderate speed for 5 min. The mixture was then homogenized using an Ultra-Turrax [IKA Ultra-Turrax T25 (IKA®) India Pvt. Ltd., Bangalore, India] operating at 22,000 rpm for 5 min to form primary W1/O emulsion. The primary (W1/O) emulsion (30%, w/w) was gradually added to the outer aqueous phase (W2) (70%, w/w) and mixed with magnetic stirring at moderate speed for 5 min. The pre-mix was finally homogenized using Ultra-Turrax at 15,000 rpm for 5 min to produce final double emulsion (W1/O/W2) (9:21:70::W1/O/W2).

Appendix 3

Method for preparation of double emulsion based functional mayonnaise.

Briefly, inner aqueous phase (W1) was prepared with an aqueous soluble bitter gourd extract, (55.2%, w/w) and NaCl (3.0%, w/w) in RO water. Middle oil phase (O) consisted of rice bran oil containing PGPR as hydrophobic emulsifier (4%, w/w) while outer aqueous phase (W2) consisted of 4.5% sodium caseinate-pectin. Both W1 and O were pasteurized at 72 °C for 15 s, while outer aqueous phase heated at 85 °C for 20 min to prepare biopolymer particles because of thermal denaturation and aggregation of the proteins followed by cooling to 4–7 °C in ice water bath.

A primary water-in-oil (W1/O) emulsion was premixed by mixing the inner aqueous phase (W1) (30%, w/w) with the oil phase (O) (70%, w/w) at room temperature, using a magnetic stirrer at moderate speed for 5 min. The mixture was then homogenized using an Ultra-Turrax [IKA Ultra-Turrax T25 (IKA®) India Pvt. Ltd., Bangalore, India] operating at 22,000 rpm for 5 min to form primary W1/O emulsion. The primary (W1/O) emulsion (30%, w/w) was gradually added to the outer aqueous phase (W2) (70%, w/w) and mixed with magnetic stirring at moderate speed for 5 min. The pre-mix was finally homogenized using Ultra-Turrax at 15,000 rpm for 5 min to produce final double emulsion (W1/O/W2) (9:21:70::W1/O/W2).

Appendix 4

Description of groups in terms of their condition, type of diet and their effect on physiological parameters

Group Diet Effect on physiological parameter after 8 weeks of experiment
Normal rats fed with synthetic diet (NC) 100% synthetic diet with rice bran oil as fat source Body weight Decreased (p < 0.05)
Blood glucose Increased (p < 0.05)
OGTT Increased (p > 0.05) at 120 min
Hb Found in normal range
HbA1c Found in normal range
Plasma insulin 0.22 ng/mL
Normal rats fed with control mayonnaise (NCM) 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise Body weight Increased (p < 0.05)
Blood glucose Increased (p < 0.05)
OGTT Increased (p > 0.05)
Hb Found in normal range
HbA1c Found in normal range
Plasma insulin 0.45 ng/mL
Normal rats fed with functional mayonnaise (NFM) 70% synthetic diet with rice bran oil as fat source + 30% functional mayonnaise with fat derived from functional mayonnaise Body weight Increased (p < 0.05)
Blood glucose Increased (p < 0.05)
OGTT Increased (p > 0.05) at 120 min
Hb Found in normal range
HbA1c Found in normal range
Plasma insulin 0.49 ng/mL
Diabetic rats fed with synthetic diet (DC) 100% synthetic diet with rice bran oil as fat source Body weight Decreased (p < 0.05)
Blood glucose Increased (p < 0.05)
OGTT Increased (p > 0.05)
Hb Found in low range
HbA1c Found in high range
Plasma insulin 0.12 ng/mL
Diabetic rats fed with control mayonnaise (DCM) 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise Body weight Increased (p < 0.05)
Blood glucose Increased (p > 0.05)
OGTT Decreased (p > 0.05)
Hb Found in normal range
HbA1c Found in high range
Plasma insulin 0.30 ng/mL
Diabetic rats fed with functional mayonnaise (DFM) 70% synthetic diet with rice bran oil as fat source + 30% functional mayonnaise with fat derived from functional mayonnaise Body weight Increased (p < 0.05)
Blood glucose Decreased (p < 0.05)
OGTT Decreased (p > 0.05)
Hb Found in normal range
HbA1c Found in high range
Plasma insulin 0.34 ng/mL
Diabetic rats fed with control mayonnaise with bitter gourd extract (DCMB) 70% synthetic diet with rice bran oil as fat source + 30% control mayonnaise with fat derived from control mayonnaise with externally added bitter gourd extract (unencapsulated form) Body weight Increased (p < 0.05)
Blood glucose Decreased (p > 0.05)
OGTT Decreased (p > 0.05)
Hb Found in normal range
HbA1c Found in high range
Plasma insulin 0.32 ng/mL
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Author contributions

UC and LS designed the research and managed the dissertation. LS guided the first author during the whole dissertation work and editing of manuscript. SK guided the first author in conducting animal study. UC conducted the research, analyzed data, reviewed, wrote and edited the manuscript. All authors have read and agreed to the publication version of the manuscript.

Declarations

Conflict of interest

The authors of this paper declare that they have no conflict of interest in the publication.

Contributor Information

Urmila Choudhary, Email: chaudharyurmila89@gmail.com.

Latha Sabikhi, Email: lsabikhindri@gmail.com.

Suman Kapila, Email: skapila69@gmail.com.

References

  1. Almarzooq MA, Moussa EA. Hypoglycemic effect of Momordicacharantia (Karela) on normal and alloxan diabetic albino mice. Egypt J Exp Biol. 2009;5:487–493. [Google Scholar]
  2. AOAC (1990) Official methods of analysis. In: 16th Edn. Association of Official Agricultural Chemists Washington, DC
  3. Aswar PB, Kuchekar BS. Phytochemical, microscopic, antidiabetic, biochemical and histopathological evaluation of Momordica charantia fruits. Int J Pharm Phar Sci. 2012;4(1):325–331. [Google Scholar]
  4. Ayoub SM, Rao S, Byregowda SM, Satyanarayana ML, Bhat N, Shridhar NB, Shridhar PB. Evaluation of Hypoglycemic effect of Momordicacharantia extract in distilled water in streptozotocin-diabetic rats. Brazilian J Vet Pathol. 2013;6(2):56–64. [Google Scholar]
  5. Ayoub SM, Rao S, Byregowda SM, Satyanarayana ML. Immunohistochemical evaluation of antidiabetic effect of Momordicacharantia extract in cow urine in streptozotocin-induced diabetic rat model. Indian J Vet Pathol. 2014;38(4):239–243. doi: 10.5958/0973-970X.2014.01184.5. [DOI] [Google Scholar]
  6. Basch E, Gabardi S, Ulbricht C. Bitter melon (Mormordicacharantia): a review of efficacy and safety. Am J Health-Syst Pharm. 2003;60:356–359. doi: 10.1093/ajhp/60.4.356. [DOI] [PubMed] [Google Scholar]
  7. Bastaki S. Review Diabetes mellitus and its treatment. Int J Diabetes Metab. 2005;13(3):111–134. doi: 10.1159/000497580. [DOI] [Google Scholar]
  8. Chang C-I, Tseng H-I, Liao Y-W, Yen C-H, Chen T-M, Lin C-C, Cheng H-L. In vivo and In vitro studies to identify the hypoglycaemic constituents of Momordicacharantia wild variant WB24. Food Chem. 2011;125:521–528. doi: 10.1016/j.foodchem.2010.09.043. [DOI] [Google Scholar]
  9. Chang C-I, Cheng S-Y, Nurlatifah AO, Sung W-W, Tu J-H, Lee L-L, Cheng H-L. Bitter melon extract yields multiple effects on intestinal epithelial cells and likely contributes to anti-diabetic functions. Int J Med Sci. 2021;18(8):1848–1856. doi: 10.7150/ijms.55866. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Choudhary U, Sabikhi L. Selection of stabilizers and processing aids to encapsulate bitter gourd extract in a stable double emulsion. Indian J Dairy Sci. 2020;73(5):1–7. doi: 10.33785/IJDS.2020.v73i05.004. [DOI] [Google Scholar]
  11. Davidson MH, McDonald A. Fiber forms and functions. Nutr Res. 1998;18:617–624. doi: 10.1016/S0271-5317(98)00048-7. [DOI] [Google Scholar]
  12. Depree JA, Savage GP. Physical and flavor stability of mayonnaise. Trends Food Sci Technol. 2001;12:157–163. doi: 10.1016/S0924-2244(01)00079-6. [DOI] [Google Scholar]
  13. Donya AB (2007) The Effects of Various Processing Methods on the Momordicosides K and L Contents, and the Sensory Characteristics of Bitter Melon Vegetable (Momordica charantia L.). University of Arkansas, United States
  14. Drabkin DL. Spectrophotometric studies. XV. Hydration of macro sized crystals of human hemoglobin and osmotic concentrations in red cells. J Biol Chem. 1950;185:231–245. doi: 10.1016/S0021-9258(18)56411-5. [DOI] [PubMed] [Google Scholar]
  15. Duke JA, Bogenschutz-Godwin MJ, DuCellier J, Duke PK. Handbook of medicinal herbs. 2. London, UK: CRC Press; 2002. [Google Scholar]
  16. Fernandes NPC, Lagishetty CV, Panda VS, Naik SR. An experimental evaluation of the antidiabetic and antilipidemic properties of a standardized Momordicacharantia fruit extract. BMC Complement Altern Med. 2007;7(1):29. doi: 10.1186/1472-6882-7-29. [DOI] [PMC free article] [PubMed] [Google Scholar]
  17. Garau C, Cummings E, Phoenix DA, Singh J. Beneficial effect and mechanism of action of Momordica charantia in the treatment of diabetes mellitus: a mini review. Int J Diabetes Metab. 2003;11:46–55. [Google Scholar]
  18. Habicht SD, Kind V, Rudloff S, Borsch C, Mueller AS, Pallauf J, Yang R, Krawinkel MB. Quantification of antidiabetic extracts and compounds in bitter gourd varieties. Food Chem. 2011;126:172–176. doi: 10.1016/j.foodchem.2010.10.094. [DOI] [Google Scholar]
  19. Hafizur RM, Kabir N, Chishti S. Modulation of pancreatic beta-cells in neonatally streptozotocin-induced type 2 diabetic rats by the ethanolic extract of Momordicacharantia fruit pulp. Nat Prod Res. 2011;25:353–367. doi: 10.1080/14786411003766904. [DOI] [PubMed] [Google Scholar]
  20. IDF (2019) International Diabetes Federation. IDF Diabetes Atlas, 9th edn
  21. Jiménez-Colmenero F. Potential applications of multiple emulsions in the development of healthy and functional foods. Food Res Int. 2013;52:64–74. doi: 10.1016/j.foodres.2013.02.040. [DOI] [Google Scholar]
  22. Klomann SD, Mueller AS, Pallauf J, Krawinkel MB. Antidiabetic effects of bitter gourd extracts in insulin-resistant db/db mice. Br J Nutr. 2010;104:1613. doi: 10.1017/S0007114510002680. [DOI] [PubMed] [Google Scholar]
  23. Limtrakul P, Pitchakarn P, Suzuki S, Kuguacin J. A triterpenoid from Momordicacharantia Linn: a comprehensive review of anticarcinogenic properties. Open Sci. 2013;13:276–296. [Google Scholar]
  24. Ma C, Yu H, Xiao Y, Wang H. Momordicacharantia extracts ameliorate insulin resistance by regulating the expression of SOCS-3 and JNK in type 2 diabetes mellitus rats. Pharm Biol. 2017;55(1):2170–2177. doi: 10.1080/13880209.2017.1396350. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Mahmoud MF, El Ashry FEZZ, El Maraghy NN, Fahmy A. Studies on the antidiabetic activities of Momordicacharantia fruit juice in streptozotocin-induced diabetic rats. Pharm Biol. 2017;55(1):758–765. doi: 10.1080/13880209.2016.1275026. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Mahwish, Saeed F, Arshad MS, un Nisa M, Nadeem MT, Arshad MU (2017) Hypoglycemic and hypolipidemic effects of different parts and formulations of bitter gourd (Momordica Charantia). Lipids Health Dis 16:211. 10.1186/s12944-017-0602-7 [DOI] [PMC free article] [PubMed]
  27. Mahwish, Saeed F, Sultan MT, Riaz A, Ahmed S, Bigiu N, Amarowicz R, Manea R (2021) Bitter Melon (Momordica charantia L.) Fruit Bioactives Charantin and Vicine Potential for Diabetes Prophylaxis and Treatment. Plants 10:730. 10.3390/plants10040730 [DOI] [PMC free article] [PubMed]
  28. Mohammady I, Elattar S, Mohammed S, Ewais M. An evaluation of anti-diabetic and anti-lipidemic properties of Momordicacharantia (Bitter Melon) fruit extract in experimentally induced diabetes. Life Sci J. 2012;9(2):363–374. [Google Scholar]
  29. Moqbel MS, Al-Hizab FA, Barakat M. Clinicopathological study on the effects of Momordicacharantia on Streptozotocin-induced diabetic wistar rats. Open J Vet Med. 2017;7:49–62. doi: 10.4236/ojvm.2017.75006. [DOI] [Google Scholar]
  30. Muschiolik G, Dickinson E. Double emulsions relevant to food systems: preparation, stability and applications. Compr Rev Food Sci Food Saf. 2017;16:532–555. doi: 10.1111/1541-4337.12261. [DOI] [PubMed] [Google Scholar]
  31. Nagarani G, Abirami A, Siddhuraju P. Food prospects and nutraceutical attributes of Momordica species: a potential tropical bioresources—a review. Food Sci Hum Wellness. 2014;3(3–4):117–126. doi: 10.1016/j.fshw.2014.07.001. [DOI] [Google Scholar]
  32. Nandini CD, Sambaiah K, Salimath PV. Dietary fibers ameliorate decreased synthesis of heparan sulphate in streptozotocin induced diabetic rats. J Nutr Biochem. 2003;14:203–210. doi: 10.1016/S0955-2863(03)00007-X. [DOI] [PubMed] [Google Scholar]
  33. Olatona FA, Onabanjo OO, Ugbaja RN, Nnoaham KE, Adelekan DA. Dietary habits and metabolic risk factors for non-communicable diseases in a university undergraduate population. J Health Popul Nutr. 2018;37(1):21. doi: 10.1186/s41043-018-0152-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Oppermann AKL, Piqueras-Fiszman B, de Graaf C, Scholten E, Stieger M. Descriptive sensory profiling of double emulsions with gelled and non-gelled inner water phase. Food Res Int. 2016;85:215–223. doi: 10.1016/j.foodres.2016.04.030. [DOI] [PubMed] [Google Scholar]
  35. Patel PM, Patel KN, Patel NM, Goyal RK. Development of HPTLC method for estimation of charantin in herbal formulations. Pharmacogn Mag. 2006;2(8):224–226. [Google Scholar]
  36. Paul A, Raychaudhuri SS. Medicinal uses and molecular identification of two Momordica charantia varieties—a review. Electron J Biol. 2010;6(2):43–51. [Google Scholar]
  37. Perumal V, Khoo WC, Abdul-Hamid A, Ismail A, Saari K, Murugesu S, Abas F, Ismail IS, Lajis NH, Mushtaq MY, Khatib A. Evaluation of antidiabetic properties of Momordicacharantia in streptozotocin induced diabetic rats using metabolomics approach. Int Food Res J. 2015;22(3):1298–1306. [Google Scholar]
  38. Rahman M, Anisuzzaman M, Alam MZ, Islam AKMR. Taxonomic studies of the cucurbits grown in the northern parts of Bangladesh. Res J Agric Biol Sci. 2006;2(6):299–302. [Google Scholar]
  39. Raviadaran R, Ng MH, Muthoosamy K. Manickam S (2018) Simple and multiple emulsions emphasizing on industrial applications and stability assessment. In: Mohan CO, Carvajal-Millan E, Ravishankar CN, Haghi AK, editors. Food process engineering and quality assurance. New York: Apple Academic Press Inc.; 2018. pp. 179–230. [Google Scholar]
  40. Sathishsekar D, Subramanian S. Beneficial effects of Momordicacharantia seeds in the treatment of STZ-induced diabetes in experimental rats. Biol Pharm Bull. 2005;28(6):978–983. doi: 10.1248/bpb.28.978. [DOI] [PubMed] [Google Scholar]
  41. Schneeman BO. Dietary fiber and gastrointestinal function. Nutr Res. 1998;18:625–632. doi: 10.1016/S0271-5317(98)00049-9. [DOI] [PubMed] [Google Scholar]
  42. Sekar DS, Sivagnanam K, Subramanian S. Antidiabetic activity of Momordicacharantia seeds on streptozotocin induced diabetic rats. Pharmazie. 2005;60:383–387. [PubMed] [Google Scholar]
  43. Shetty AK, Kumar GS, Sambaiah K, Salimath PV. Effect of bitter gourd (Momordicacharantia) on glycaemic status in streptozotocin induced diabetic rats. Plant Foods Hum Nutr. 2005;60(3):109–112. doi: 10.1007/s11130-005-6837-x. [DOI] [PubMed] [Google Scholar]
  44. Shih CC, Lin CH, Lin WL. Effects of Momordicacharantia on insulin resistance and visceral obesity in mice on high-fat diet. Diabetes Res Clin Pract. 2008;81:134–143. doi: 10.1016/j.diabres.2008.04.023. [DOI] [PubMed] [Google Scholar]
  45. Shih CC, Lin CH, Lin WL, Wu JB. Momordicacharantia extract on insulin resistance and skeletal muscle GLUT4 protein in fructose-fed rats. J Ethnopharmacol. 2009;123:82–90. doi: 10.1016/j.jep.2009.02.039. [DOI] [PubMed] [Google Scholar]
  46. Sofowora A, Ogunbodede E, Onayade A. The role and place of medicinal plants in the strategies for disease prevention. Afr J Tradit Complement Altern Med. 2013;10(5):210–229. doi: 10.4314/ajtcam.v10i5.2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  47. Sridhar MG, Vinayagamoorthi R, Suyambunathan AV, Bobby Z, Selvaraj N. Bitter gourd (Momordicacharantia) improves insulin sensitivity by increasing skeletal muscle insulin-stimulated IRS-1 tyrosine phosphorylation in high-fat-fed rats. Br J Nutr. 2008;99:806–812. doi: 10.1017/S000711450783176X. [DOI] [PubMed] [Google Scholar]
  48. Srividya K, Shailendra B. Diabetes mellitus: considerations for dentistry. J Am Dent Assoc. 2008;139:8S–18S. doi: 10.14219/jada.archive.2008.0364. [DOI] [PubMed] [Google Scholar]
  49. Uebanso T, Arai H, Taketani Y, Fukaya M, Yamamoto H, Mizuno A, Hada T, Takeda E. Extracts of Momordicacharantia suppress postprandial hyperglycemia in rats. J Nutr Sci Vitaminol. 2007;53(6):482–488. doi: 10.3177/jnsv.53.482. [DOI] [PubMed] [Google Scholar]
  50. Wang ZQ, Zuberi AR, Zhang XH, Macgowan J, Qin J, Ye X, Son L, Wu Q, Lian K, Cefalu WT. Effects of dietary fibers on weight gain, carbohydrate metabolism, and gastric ghrelin gene expression in mice fed a high-fat diet. Metab Clin Exp. 2007;56:1635–1642. doi: 10.1016/j.metabol.2007.07.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  51. Wang ZQ, Zhang XH, Yu Y, Poulev A, Ribnicky D, Floyd ZE, Cefalu WT. Bioactives from bitter melon enhance insulin signaling and modulate acyl carnitine content in skeletal muscle in high-fat diet-fed mice. J Nutr Biochem. 2011;22:1064–1073. doi: 10.1016/j.jnutbio.2010.09.004. [DOI] [PMC free article] [PubMed] [Google Scholar]
  52. Wu S, Ng L. Antioxidant and free radical scavenging activities of wild bitter melon (Momordicacharantia Linn. var. abbreviata Ser.) in Taiwan. LWT. 2008;41(2):323–330. doi: 10.1016/j.lwt.2007.03.003. [DOI] [Google Scholar]
  53. Yadav UC, Moorthy K, Baquer NZ. Combined treatment of sodium orthovanadate and Momordicacharantia fruit extract prevents alterations in lipid profile and lipogenic enzymes in alloxan diabetic rats. Mol Cell Biochem. 2005;26:111–120. doi: 10.1007/s11010-005-3703-y. [DOI] [PubMed] [Google Scholar]
  54. Yibchok-Anun S, Adisakwattana S, Yao CY. Slow acting protein extract from fruit pulp of Momordicacharantia with insulin secretagogue and insulinomimetic activities. Biol Pharm Bull. 2006;29:1126–1131. doi: 10.1248/bpb.29.1126. [DOI] [PubMed] [Google Scholar]
  55. Zhang Y, Zhang J, Hong M, Huang J, Wang R, Tan B, Huang P, Cao H. Study on the optimization and stability of single-dose streptozotocin-induced diabetic modelling in rats. Res Square. 2021 doi: 10.21203/rs.3.rs-310098/v1. [DOI] [Google Scholar]

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