Correlation Between Serum 25(OH)D and Abdominal Visceral Fat Area in Patients with Type 2 Diabetes Mellitus in the Context of different Bone Mass

Abstract

Objective

To investigate the correlation between serum levels of 25-hydroxy vitamin D [25(OH)D] and the visceral fat area of patients with type 2 diabetes mellitus (T2DM) in the context of different bone mass.

Materials and Methods

A total of 180 patients with T2DM were randomly selected for bone mineral density (BMD) examination. According to the results, they were divided into three groups: T2DM normal bone group (group A); T2DM bone mass reduction group (group B); T2DM osteoporosis group (group C).

Result

Serum 25(OH)D levels in NC group, A group, B group and C group decreased in turn, and Visceral fat area (VFA) in group B and group C were significantly higher than those in group A and NC [(29.41±4.87) vs. (22.76±4.23) vs. (17.78±3.61) vs. (9.70±3.01), P<0.05], [(117.76±38.79), (125.08±37.90) vs. (89.79±26.51), (97.53±28.61), P<0.05]. Pearson correlation analysis showed that L1-L4 lumbar vertebrae bone density was positively correlated with 25(OH)D and VFA; left femoral neck bone density was positively correlated with 25(OH)D, and negatively correlated with VFA.

Conclusion

Serum 25(OH)D and VFA may be associated with the development of T2DM combined with OP.

Introduction

Osteoporosis (OP) is a systemic disease characterized by reduced bone mass, fine structural changes in bone tissue, increased bone fragility and susceptibility to fracture. OP is closely related to type 2 diabetes(T2DM) and they often exist in the same body (1, 2). T2DM and OP have a common pathogenesis, and glucose and lipid metabolism disorders can affect bone metabolism in various ways (3). Epidemiological investigations have found that the incidence of OP in T2DM population is significantly higher than that of normal healthy people with gender and age matching (4). On the other hand, obesity is closely related to T2DM. In 2016, China’s consensus on the comprehensive management of type 2 diabetes and obesity (3) showed that the prevalence of diabetes in overweight and obese people in China was 12.8% and 18.5%, respectively; in the diabetes (DM) patients, the proportion of overweight was 41%, and the proportion of obesity was 24.3%, of which abdominal obesity was up to 45.4%. Abdominal obesity caused by deposition of abdominal visceral fat is closely related to insulin resistance (IR) and disorders of glucose and lipid metabolism, which is related to the occurrence of T2DM (5, 6). At the same time, the study confirmed that the difference in fat distribution is closely related to OP. Abnormal accumulation of abdominal visceral fat leads to abnormal secretion of adipokines, which can affect bone metabolism and reduce bone mineral density (BMD) through multiple pathways, which is closely related to the occurrence of OP (7). Studies have shown that abdominal obesity is an independent risk factor for OP (8. 9). Sugar metabolism, lipid metabolism and bone metabolism interact, and are closely related to each other. 1,25 hydroxy vitamin D (1,25(OH)D), as a representative of vitamin D (VitD), not only regulates calcium and phosphorus metabolism, but also regulates immunity, cell proliferation, differentiation, apoptosis and IR in T2DM patients. It is closely related to the onset of T2DM and blood glucose control (10, 11). Serum 25-hydroxy Vitamin D (25(OH)D) is regarded as a representative indicator of VitD levels in the body due to its long half-life and relatively stable nature (12). However, there are few reports on the correlation between serum 25(OH)D and visceral fat area (VFA) in patients with T2DM under different bone mass. Therefore, by observing the levels of serum 25(OH)D and VFA in patients with T2DM in the context of different bone mass levels, the relationship between them was preliminarily analyzed and discussed, which may provide a new target for early combined prevention and treatment of T2DM and OP.

Material and Methods

Study subjects

Subjects

One hundred eighty patients with type 2 diabetes diagnosed in our hospital between February 2017 and March 2018 were recruited. Each patient’s BMD was assessed by Dual energy X-ray absorptiometry (DXA); and referring to the Diagnosis and Treatment Criteria of Primary Osteoporosis issued in 2017 by the Osteoporosis and Bone Mineral Disease Branch of Chinese Medical Association, the patients were allocated into one of three groups according to BMD. The normal bone mass group (group A, n=58, age 62.82±7.33 years old, 28 males and 30 females); the osteopenia group (group B, n=59, age 63.71±7.95 years old, 30 males and 29 females), and the osteoporosis group (group C, n=63, age 65.32±8.74 years old, 32 males and 31 females). Sixty healthy age and sex matched subjects were recruited from the Physical Examination Center and served as the normal control group (NC, age 60.06±6.96 years old, 30 males and 30 females). All subjects discontinued all drugs on the day of the trial, and were subjected to abdominal quantitative spiral CT plain scan and dual-energy X-ray absorptiometry for bone mineral density determination. All subjects signed an informed consent form and were approved by the hospital ethics committee.

Inclusion criteria

1. Selection criteria for T2DM patients: 1) the newly diagnosed T2DM patients in line with the WHO diagnostic criteria in 1999 (13). 2) No abnormal liver and kidney function, no other serious organic diseases and acute diabetic complications. 3) All subjects have not received any diabetes treatment measures including diet and exercise therapy. 2. All subjects were postmenopausal women (menopausal age longer than 1 years) or men aged 60 or above; 3. Long term residence in local; 4. No smoking history or long history of heavy drinking.

Exclusion criteria

1. Patients with rheumatoid arthritis, thyroid, bone tumors, pituitary gland, parathyroid gland, adrenal gland, gonad and other diseases affecting bone metabolism; 2. Before examination (within half a year), use of drugs affecting bone metabolism, such as high doses of calcium, estrogen, androgen, diphosphate, glucocorticoid, etc; 3. Hormone replacement therapy was used in the past 3 months; 4. Patients who took or injected vitamin D preparations within six months; 5. Malignant tumor patients and fracture patients; 6. T1DM, T2DM combined with acute and chronic complications, liver and kidney dysfunction, special types of DM and other endocrine diseases; 7. A history of chronic diseases such as hypertension, cardiovascular and cerebrovascular diseases, and a history of clear infection 2 weeks before the examination;

Diagnostic criteria for osteoporosis

The diagnostic criteria for osteoporosis as outlined in the Diagnosis and Treatment criteria of Primary Osteoporosis (2017) (14). BMD measurements by DXA is the current general diagnostic indicator of osteoporosis: a BMD within 1 standard deviation (sd) of the peak BMD in healthy adults of the same sex and ethnicity is defined as normal; BMD reduced by 1 to 2.5 sd is defined as low bone mass; whereas BMD reduced by more than 2.5 sd is defined as osteoporosis; the degree of BMD reduction meeting the diagnostic criteria for osteoporosis, together with one or more brittle fractures, is defined as severe osteoporosis. The BMD is usually expressed as a T-Score, which is equal to (actual value – peak BMD in healthy adults of the same sex and ethnicity) / (sd of the peak BMD in healthy adults of the same sex and ethnicity). The diagnostic criterion for osteoporosis based on DXA-measured axial bone density (L1-4, femoral neck, or total hip), or distal 1/3 radial bone, is T-score ≤-2.5.

Methods

General information

Gender, age, course of disease were recorded, height, weight, waist circumference, hip circumference were measured, and waist-hip ratio (WHR), body mass index (BMI) = body weight (kg) / height² (m²) were calculated. All data were entered in the database.

General information

All the subjects were fasted for 10 hours. On the next morning, 5 mL of venous blood was collected from the anterior elbow, centrifuged at 3000 rpm for 10 minutes in a centrifuge, and the upper serum was taken for measurement within 4 hours. At the same time, 1.5 mL of serum was extracted and dispensed into the EP tube and stored in a refrigerator at -80°C. The blood of the elbow vein was collected after fasting with the following indexes examined: 25(OH)D, fasting plasma glucose (FPG), fasting plasma insulin (FINS), glycosylated hemoglobin (HbA1c), Total cholesterol (TC), Triglyceride (TG), High density lipoprotein cholesterol (HDL-C), Low density lipoprotein cholesterol (LDL-C), Alkaline phosphatase (ALP), blood calcium, blood phosphorus,Parathyroid hormone (PTH), Procollagen I N-Terminal Propeptide (PINP), Beta-Crosslaps (β-CTX). Blood lipids, ALP, blood calcium, and blood phosphorus were detected by Olympus (AU2700) automatic analyzer, FPG using hexokinase method, FINS, PTH by chemiluminescence method (the above reagents were purchased from Beckman Coulter Experimental System Co., Ltd.). HbA1c was prepared by high pressure liquid chromatography (reagent purchased from Bio-Rad Life Medicine Co., Ltd.), serum 25 (OH)D, PINP, and β-CTX were determined by electrochemiluminescence (reagent purchased from Roche, Germany); the HOMA-IR = FPG × FINS/22.5; the QUICKI = 1/Log (I0) + Log (G0) [I0: fasting insulin content (μU/mL); G0: fasting blood glucose concentration (mg/dL)].

Measurement of BMD

Operated by the imaging department and recorded, measured lumbar spine bone mineral density (LS-BMD) and hip bone mineral density, including femoral neck bone mineral density (FN-BMD), Ward’s triangle bone mineral density (WT-BMD), total hip bone mineral density (TH-BMD), and T value were recorded. The results were analyzed by the corresponding software configured by MEDILINK, France.

Assessing abdominal fat distribution

Abdominal fat distribution was determined by spiral CT. Model: SIEMENS SOMATOM Definition AS+. Related parameters: Scanning conditions are voltage 120 kV, current 120 mA, scanning time 1.25s, scanning layer thickness 1 mm, layer spacing1mm. The reconstruction layer has a thickness of 0.625 mm and a reconstruction layer spacing of 0.625 mm. Measurement parameters: fat density (g/cm3): 0.923 Fat CT value: -89.9. The CT value of adipose tissue ranges from (-250) to (-50)Hu. The patient was placed in the supine position and scanned in the lumbar vertebrae 2, 3 plane and the umbilical horizontal plane in a breath holding state. The data results of the umbilical level measurement are selected, and the relevant measurement data is transmitted to the QCT GE workstation, and the supporting software automatically colors the section layer image, automatically identifies the target image and its boundary from the image, and measures the area and perimeter of the extracted target image. The region of interest (ROI) is automatically drawn according to the watershed effect of the abdominal wall muscle CT value higher than the fat CT value, and can be manually fine-tuned to accurately conform to the abdominal wall morphology, and the intra-abdominal fat area (VFA) is calculated in the box. The abdominal subcutaneous fat area (SFA) and waist circumference were calculated. All measurements are performed by a professionally designated radiologist.

Statistical analysis

All the research data were analyzed by software using SPSS 19.0 software. Before the data analysis, the variance and normality test were performed. The continuous variable data that conformed to the normal distribution were described as mean ± standard deviation (x̅±s), and the non-normal distribution data were used with median (interquartile range), [M(Q25-Q75)] formal description; comparison between groups was firstly carried out by one-way analysis of variance (ANOVA), and LSD method was used for comparison between indicators; normal distribution of continuous variables using Pearson correlation analysis; application of logistic regression analysis, the factor of T2DM merge OP. The bilateral alpha value was 0.05, and p < 0.05 indicates that the difference was statistically significant.

Results

Comparison of clinical data and laboratory indexes

1. There were no significant differences in gender structure, age, duration of disease, hip circumference, BMI, FINS, TG, Ca and P between the four groups (p>0.05). 2. Compared with NC group, the levels of HbA1c, FPG, HOMA-IR and LDL-C in group A, group B and group C were significantly increased, and the levels of HDL-C and QUICK were significantly decreased, the difference was statistically significant (p<0.05); Compared with the NC group, the levels of WHR and PTH in group B and group C were significantly higher, and the difference was statistically significant (p<0.05). Compared with NC group, the level of TC in group C was significantly higher, and the difference was statistically significant (p<0.05). 3. Compared with group A, the levels of WHR, HbA1c, HOMA-IR and PTH in group B and group C were significantly increased, and the levels of QUICK and HDL-C were significantly lower (p<0.05). Compared with group A, the levels of TC and LDL-C in group C were significantly increased, and the difference was statistically significant (p<0.05). 4. Compared with group B, the levels of HbA1c, HOMA-IR, TC and LDL-C in group C were significantly increased, and the level of QUICK was significantly lower, the difference was statistically significant (p<0.05) (Table 1).

Table 1.

Comparison of clinical data and laboratory indexes in each group [x̅±s, M(Q25, Q75)] vs. NC group, *P<0.05; vs. A group, #P <0.05; vs. B group, ^ΔP <0.05.

Group	(n)	(M/F)	Age(y)	Disease duration (y)	BMI(kg/m2)	WHR	HbA1c(%)	FPG (mmol/L)	FIns (uIU/mL)
NC	60	30/30	62.54±8.70	-	23.73±2.66	0.80±0.05	4.12±0.57	5.32±1.01	19.79±8.93
A	58	28/30	62.82±7.33	8.46±6.96	24.09±2.71	0.82±0.06	7.53±1.05*	10.82±1.92*	18.73±9.07
B	59	30/29	63.71±7.95	8.95±7.38	24.25±2.93	0.91±0.10*#	9.22±1.92*#	11.98±2.02*	20.84±9.86
C	63	32/31	64.32±8.74	8.12±8.53	25.06±2.69	0.90±0.12*#	11.35±2.11*#Δ	12.31±2.21*	21.87±10.78

Group	HOMA-IR	QUICK	TG (mmol/L)	TC (mmol/L)	HDL-C (mmol/L)	LDL-C (mmol/L)	PTH (pg/mL)	Ca (mmol/L)	P (mmol/L)
NC	1.84(0.07,2.85)	0.65(0.43,0.81)	2.01±0.27	3.93±1.53	1.63±0.78	1.99±0.42	42.63±13.68	2.21±0.18	0.92±0.19
A	2.32(1.13,3.39) *	0.41(0.35,0.63)*	2.13±0.29	4.04±1.60	1.27±0.43*	2.83±0.68*	41.33±13.50	2.18±0.14	0.88±0.17
B	2.89(1.58,4.24) *#	0.34(0.19,0.49)*#	2.25±0.31	3.89±1.57	0.98±0.27*#	2.68±0.72*	53.67±17.64*#	2.20±0.20	0.90±0.20
C	3.58(2.01,5.47) *#Δ	0.20(0.08,0.32) *#Δ	2.55±0.51	4.86±2.01*#Δ	0.93±0.27*#	3.23±1.01*#Δ	54.19±18.27*#	2.20±0.17	0.89±0.18

Correlation between biochemical indexes and bone mineral density

1. Compared with NC group, serum 25(OH)D levels in group A, group B and group C were significantly lower, the difference was statistically significant [(29.41±4.87) vs. (22.76±4.23), (17.78±3.61), (9.70±3.01) p<0.05)]; Compared with NC group, group B and group C VFA, the level of VFA/SFA was significantly increased, and the bone mineral density of SFA and the four sites was significantly decreased. The difference was statistically significant (p<0.05). There was no significant change in the bone mineral density of VFA, SFA, VFA/SFA and the four sites in the A group. The difference was not statistically significant (p>0.05); 2. Compared with group A, the levels of VFA and VFA/SFA in group B and group C were significantly increased, and the levels of bone mineral density in serum 25(OH)D, SFA and four sites were significantly lower (p<0.05); 3. Compared with group B, group C serum 25(OH)D, the level of BMD of L1-L4 and the level of BMD of left femoral neck was significantly lower, the difference was statistically significant (p<0.05), and there was no significant change in the levels of VFA, SFA, VFA/SFA, the level of BMD of Ward’s trigone, and the level of BMD of total hip. The difference was not statistically significant (p>0.05) (Table 2).

Table 2.

Comparison of biochemical indexes and bone mineral density in each group [x̅±s,M vs. NC group, *P <0.05; vs. A group, #P < 0.05; vs. B group, ^ΔP <0.05.

Group	25(OH)D (ng/mL)	VFA (cm2)	SFA (cm2)	VFA/SFA	BMD of L1-L4 (g/cm2)	BMD of left femoral neck (g/cm2)	BMD of Ward’s trigone (g/cm2)	BMD of total hip (g/cm2)
NC	29.41±4.87	89.74±26.51	246.80±52.92	0.38(0.27,0.52)	1.09±0.15	0.89±0.20	0.83±0.21	1.14±0.14
A	22.76±4.23*	97.53±28.61	221.38±55.74	0.42(0.34,0.58)	1.13±0.13	0.91±0.23	0.81±0.19	1.09±0.12
B	17.78±3.61*#	117.76±38.79*#	186.58±40.93*#	0.78(0.45,1.05)*#	0.85±0.09*#	0.76±0.08*#	0.68±0.10*#	0.79±0.05*#
C	9.70±3.01*#Δ	125.08±37.90*#	174.65±38.75*#	0.81(0.50,1.12)*#	0.64±0.02*#Δ	0.54±0.05*#Δ	0.65±0.09*#	0.78±0.07*#

Correlation analysis of bone mineral density and indexes

After adjusting for gender, body weight, BMI and other indicators, L1-L4 lumbar vertebrae bone density was positively correlated with 25(OH)D, VFA, HDL-C (r =0.258, P=0.028; r=0.223, P=0.032; r=0.294, P=0.009), and negatively correlated with HOMA-IR (r=-0.281, P=0.025); The left femoral neck bone density was positively correlated with 25(OH)D and HDL-C (r=0.574, P=0.000; r=0.478, P=0.000), and negative with VFA correlation (r=-0.455, P=0.000); total hip bone density was positively correlated with 25(OH)D (r=0.375, P=0.001), and negatively correlated with HOMA-IR (r=-0.231, P=0.030) (Table 3).

Table 3.

Correlation analysis of T2DM bone density with each index (r)

Related factors	L1-L4		Left femoral neck		Ward’s trigone		Total hip
	r	P	r	P	r	P	r	P
Age(y)	-0.123	0.179	-0.097	0.201	-0.087	0.199	-0.135	0.286
HOMA-IR	-0.281	0.025*	-0.146	0.187	-0.097	0.563	-0.231	0.030*
25(OH)D(ng/mL)	0.258	0.028*	0.574	0.000*	0.204	0.050	0.375	0.001*
VFA(cm2)	0.223	0.032*	-0.455	0.000*	0.201	0.057	0.164	0.173
HDL-C(mmol/L)	0.294	0.009*	0.478	0.000*	0.209	0.050	0.163	0.175

HOMA-IR; *p<0.05.

Logistic regression analysis of risk factors for T2DM combined with OP

The mean bone mineral density of left proximal femoral neck was used as dependent variable in group C. The course of disease, age, HbA1c, HOMA-IR, FBG, VFA, SFA, VFA/SFA, 25(OH)D, TG, TC, LDL, HDL were used as independent variables in multivariate stepwise regression analysis. The results showed that HDL-C, HbA1c, VFA, VFA/SFA were independent factors affecting the mean bone mineral density of left neck (Table 4).

Table 4.

T2DM patients with multiple factor regression analysis of bone mineral density

Variable	β	Waldc2	P	OR(95%CI)
HbA1c	1.360	11.093	0.001	3.902(1.750~8.628)
25(OH)D(ng/mL)	-1.010	4.381	0.037	0.364(0.142~0.398)
VFA(cm2)	0.043	4.923	0.027	1.044(1.005~1.084)
VFA/SFA	2.021	8.681	0.003	7.548(1.967~28.962)
HDL-C(mmol/L)	-1.785	4.423	0.034	0.198(0.075~0.895)

Discussion

T2DM, dyslipidemia and OP are common systemic metabolic diseases, and they often coexist in the same patient (15). Patients with T2DM are prone to OP because of increased IR, advanced glycation end products (AGEs), long-term hyperglycemia and bone mineral loss caused by various complications. Abdominal obesity due to abnormal accumulation of visceral fat plays an important role in the disorder of glucose and lipid metabolism and the pathogenesis of T2DM (16). Studies have confirmed that visceral fat is more active than subcutaneous fat decomposition, excessive visceral fat accumulation will produce a large number of free fatty acids (FFA), more likely to induce DM, metabolic syndrome and other related disorders of glycolipid metabolism disease (17). Campos et al. showed that visceral fat was one of the strongest predictors of bone mineral density in obese women, and it was closely related to bone mineral density, suggesting that VFA might be involved in OP (18). As a classical calcium and phosphorus regulator, VitD deficiency cannot only inhibit bone ossification by decreasing the absorption of Ca and P, but also reduce BMD. Low levels of 25(OH)D can induce or aggravate IR, resulting in the elevation of AGEs in vivo, which accelerates bone resorption, inhibits bone formation, and eventually leads to OP (19, 20). Therefore, we found that the decrease of serum 25(OH)D level and the increase of VFA are related to the metabolism of sugar, lipid and bone in T2DM patients, which may be closely related to the development of T2DM and OP.

The results of this study show that as the level of BMD decreases, the level of 25(OH)D gradually decreases. Correlation analysis suggests that serum 25(OH)D and lumbar spine bone density, left femoral neck bone density and total hip bone density are positive. Multiple linear regression analysis suggested that serum 25(OH)D was an independent protective factor for left Neck bone density. Cangussu et al. (21) divided 163 diabetic patients into OP group and non-OP group. Comparing the serum levels of 25(OH)D between the two groups, it was found that 25(OH)D levels in OP group were significantly lower than those in non-OP group, suggesting that 25(OH)D might be involved in the process of T2DM with OP as a protective factor (21). The results of this study are consistent with those of Cangussu et al. (21). Decreased VitD levels will disrupt bone turnover balance, resulting in bone resorption greater than bone formation. On the other hand, the lack of VitD will accelerate the proliferation of osteoclasts, causing an increase in serum parathyroid hormone levels, resulting in secondary parathyroidism. Hyperthyroidism accelerates bone resorption, leads to a decrease in bone density, triggering OP (22, 23).

The results of this study also showed that VFA increased with the decrease of BMD in different bone mass. Multiple linear regression analysis suggested that VFA was a risk factor for BMD. Abdominal obesity T2DM patients characterized by abdominal visceral fat accumulation are more likely to develop OP (24). In previous studies, BMI was found to be an independent protective factor for BMD, and obesity has a protective effect on OP (25). The increase of VFA can reduce BMD and accelerate the occurrence of OP (26). The mechanism may be as follows: firstly, visceral adipose tissue overexpresses adiponectin, which activates RANK-RANKL signal transduction pathway through adiponectin receptor, thereby activating osteoclasts and inhibiting the high expression of osteoprotegerin, weakening the inhibitory effect of osteoprotegerin on osteoclasts and activating osteoclasts (27). Secondly, studies have found that adipocytes and osteoblasts are derived from the same bone marrow derived mesenchymal stem-cells (BMSC), and their differentiation process is regulated by PPAR-γ. PPAR-γ can induce BMSCs to differentiate into adipocytes. The high expression of such cytokines in visceral adipose tissue leads to excessive adipose tissue formation and too little bone formation, which easily induces OP (28). The last, visceral adipose tissue can secrete a variety of inflammatory cytokines acting on osteoblasts, promote the production of prostaglandin E2 and then activate adenylatecyclase activity in osteoblasts, increase the concentration of intracellular cyclic adenosine phosphate, and finally activate RANK on the surface of osteoclast precursor cells, stimulate the production of a large number of osteoclasts, and ultimately accelerate bone absorption (29-31). Cheng et al. by examining the contents of visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) in 1882 non-diabetic subjects, 25(OH)D was found to be independently and negatively correlated with VAT and SAT, respectively. Further stratification revealed that VAT levels in BMI<25 kg/m² were negatively correlated with 25(OH)D, whereas SAT levels were negatively correlated with 25(OH)D. The correlation disappeared, indicating that excessive deposition of visceral fat was significantly associated with 25(OH)D (32). It is speculated that the decrease of VitD level may result in the decrease of the inhibition of the differentiation of preadipocytes into adipocytes and the increase of adipogenesis on the one hand (33). On the other hand, it may also produce secondary hyperthyroidism, which leads to increased activity of lipid synthesis-related enzymes, thereby promoting fat synthesis (34). The results of this study showed that compared with T2DM normal bone group, T2DM bone mass reduction group and T2DM osteoporosis group parathyroid hormone were significantly increased, the difference was statistically significant, which is consistent with the above conclusions. The relationship between serum 25(OH)D and VFA has not been specifically analyzed in this study, and further detailed stratification design and larger sample size are needed for further research.

In conclusion, 25(OH)D in serum of T2DM patients decreased with the decrease of BMD in different bone mass states (NC group > A group > B group > C group), while the VFA of patients with T2DM and OP is significantly higher than that of patients with T2DM alone. It is speculated that the decrease of serum 25(OH)D level will lead to the disorder of lipid metabolism and the excessive deposition of visceral fat, which will lead to the increase of VFA. The increase of VFA will further aggravate the disorder of lipid metabolism and IR, resulting in the further decrease of serum 25(OH)D level. Both of them interact with each other to form a vicious circle and eventually accelerate the process of T2DM with OP. It is speculated that active supplementation of VitD and reduction of excessive deposition of abdominal visceral fat may play a positive role in the prevention and treatment of T2DM and OP, but the specific mechanism remains to be further explored.

Conflict of interest

The authors declare that they have no conflict of interest.

Acknowledgement

This work is funded by National Natural Science Foundation of China (project number: 81460168); Task plan of Zunyi science and technology plan[Science and technology project of Zunyi Science and Technology Bureau 2018(63)]; Special Post-subsidy Fund for Academic New Seedling Training and Innovation Exploration of Zunyi Medical College (Qiankehe Platform Talents [2017] 5733-043). National Natural Science Foundation of China (project number: 82060159);The Natural Science Foundation of Guizhou Provincial Department of Science and Technology(Qiankehe Foundation[2020]1Y314).