Table 1.

A summary of all articles included in the review *.

Study	Results	Conclusion
[15]	Cases were from Kingdom of Saudi Arabia (55 cases) and Turkey (43 patients) (Total 78.2%) and they were consanguineous marriage. Positive responds when using fructose-based formula. SLC5A1 gene mutations were found in 73 cases (68.2%) after gene testing.	Two major mechanisms in detecting and diagnosing CGGM is fasting and gene testing. The use of fructose-based formulas is the best management for CGGM cases.
[7]	GLUT5 is regulated by LXRα in both mice and humans.	The treatment of metabolic disease and cancer as well LXRα might provide novel pharmacologic strategies for the selective modulation of GLUT5 activity.
[10]	Reduce the intake of SBBS several strategies and policies are needed.	Increased risk of CVD, weight gain, and NIDDM (type 2 diabetes mellitus) with the consumption of SBBS.
[4]	Non-immune- mediated food intolerance has a cumulative prevalence of 30% to 40%, while true (immune-mediated) food allergies affect only 2% to 5% of the German population.	Eliminate the intake of the responsible carbohydrate substance or reduce it to a fair amount might improve the malabsorption.
[13]	Mutant protein is inserted into the plasma. In a duodenal biopsy from a GGM patient, the mutant protein is in the brush border membrane of enterocytes.	Autosomal recessive mode of inheritance was confirmed by the studies of this isolated pedigree of GGM patients, and this provides unique insights into the molecular mechanism of glucose transport by SGLT-1.
[16]	Absorption rate of glucose and galactose is 13% and 22%, respectively. The control group was 85% for glucose and galactose.	There was no difference in the rate absorption of fructose in the control group (healthy individuals) and the study group (three CGGM patients). the rate was 66%.
[45]	The role of excessive intake of fructose and SSBS in developing cardiometabolic diseases was supported by epidemiological data and mechanistic data.	Holistic approaches to bear on present metabolic epidemics to better understand the underlying pathways through which sugar and fructose can cause disease.
[12]	Five patients reported one or more symptoms of bloating (n = 3), diarrhea (n = 3) and abdominal pain (n = 1) during follow up. All had normal development, and none had neurological complications secondary to dehydration.	Early detection and management are crucial might prevent the consequences of dehydration and death resulting from this condition.
[8]	Describes how dietary fructose can affect the expression and activity of fructolytic enzymes and transporters by affecting the cellular response to fructose in the gut.	Dietary fructose may have a potential relation to the gastrointestinal and gut microbe.
[56]	Children, with their preference for sweet foods and drinks, are prone to excessive sugar consumption. Toddlers under age two are especially vulnerable.	The effects that have been observed with the consumption of large amounts of fructose cannot be reliably distinguished from the effects of a generally excessive caloric intake.
[55]	Logistic regression analysis demonstrated that a higher level of Hs-CRP, fructose consumption, and smoking were independently associated with SCF.	The SCF group demonstrated a higher level of fructose consumption. Excessive fructose consumption may play a role in SCF pathophysiology.
[58]	An energy-matched (isocaloric) exchange of dietary carbohydrates by fructose promoted hepatic insulin resistance but had no effect on fasting plasma insulin concentrations. Hypercaloric fructose raised fasting plasma insulin concentrations.	Short-term fructose consumption, in isocaloric exchange or in hypercaloric supplementation, promotes the development of hepatic insulin resistance in nondiabetic adults without affecting peripheral or muscle insulin sensitivity.
[14]	In 22 out of the 23 missense mutations tested in the oocyte expression system, the proteins were translated and were stable in the cell but did not reach the plasma membrane. In four of these mutants, an alanine residue was replaced by a valine, and in two, the trafficking defect was rescued by changing the valine to cysteine. One mutant protein (Q457R) did reach the plasma membrane, but it was unable to transport the sugar across the cell membrane.	Mutations in the SGLT-1 gene are the cause of glucose-galactose malabsorption, and sugar transport is impaired mainly because the mutant proteins are either truncated or are not targeted properly to the cell membrane.

* Abbreviations: SLC5A1, solute carrier family 5 member 1; GLUT5, glucose transport protein 5; SBBS, sugar sweetened beverages; CGGM, congenital glucose-galactose malabsorption; LXRα, liver X receptor alpha; CVD, cardiovascular disease; NIDDM, Non-insulin-dependent diabetes mellitus; GGM, glucose galactose malabsorption; SGLT-1, is sodium-dependent glucose transporter-1; Hs-CRP, high-sensitivity C-reactive protein; SCF, slow coronary flow; Q457R, gln457Arg.