Glucose transporters in the small intestine in health and disease.
Level 5 - mechanism / opinion, no new human data
Narrative review describing physiological mechanisms and disease states without systematic synthesis or primary human clinical data.
PubMed 32829466 · doi:10.1007/s00424-020-02439-5
What was done
This is a narrative review synthesizing physiological, molecular, and pathophysiological mechanisms governing small intestinal monosaccharide transport. The authors describe the localization, regulation, and functional roles of Na+-D-glucose cotransporter SGLT1, GLUT2, and GLUT5 across varying luminal carbohydrate concentrations, diurnal cycles, and enterohormone secretion pathways. The review also surveys transporter-related genetic disorders such as glucose-galactose malabsorption, Fanconi syndrome, and fructose intolerance, alterations occurring in conditions such as diabetes and intestinal inflammation or following bariatric surgery, and pharmacological or dietary inhibitors targeting SGLT1.
What was found
The abstract provides a mechanistic overview and reports no quantitative effect sizes or primary experimental numbers. Mechanistically, at low luminal D-glucose concentrations, absorption is mediated primarily by SGLT1 at the brush border membrane and GLUT2 at the basolateral membrane. At high luminal glucose concentrations, brush border SGLT1 abundance increases and GLUT2 is also localized to the brush border membrane to facilitate high-capacity absorption. GLUT5 mediates D-fructose absorption across the brush border membrane.
Why it matters
Understanding the dynamic regulation and membrane trafficking of enterocyte glucose transporters clarifies the pathophysiology of carbohydrate malabsorption syndromes and highlights therapeutic targets, such as SGLT1 inhibitors, for metabolic disease.
Limits
This is a narrative review lacking a systematic search protocol, meta-analytic data pooling, or quality assessment of included studies. No quantitative experimental metrics, effect estimates, or sample sizes are reported in the abstract, and claims rely on preclinical models and mechanistic theory.
Cited by
- supports The glucose transporter in the intestinal tract is sodium-mediated, allowing glucose with salt to be absorbed faster than glucose alone.