Glucose absorption in small intestinal diseases

Abstract

Recent developments in the field of diabetes and obesity management have established the central role of the gut in glucose homeostasis; not only is the gut the primary absorptive site, but it also triggers neurohumoral feedback responses that regulate the pre- and post-absorptive phases of glucose metabolism. Structural and/or functional disorders of the intestine have the capacity to enhance (eg: diabetes) or inhibit (eg: short-gut syndrome, critical illness) glucose absorption, with potentially detrimental outcomes. In this review, we first describe the normal physiology of glucose absorption and outline the methods by which it can be quantified. Then we focus on the structural and functional changes in the small intestine associated with obesity, critical illness, short gut syndrome and other malabsorptive states, and particularly Type 2 diabetes, which can impact upon carbohydrate absorption and overall glucose homeostasis.

Keywords::

• bariatric surgery
• critical illness induced hyperglyaemia
• gastric emptying
• GLP-1
• GLUT2
• SGLT1
• short gut syndrome
• sweet-taste receptor

Financial & competing interests disclosure

The authors' research in this area has been supported by grants awarded by the National Health and Medical Research Council of Australia. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Key issues

• The central role of gut in glucose homeostasis is being increasingly recognized with the ongoing developments in the areas of diabetes and obesity management; gut is not only the site of nutrient absorption, but also a regulator of pre- and postabsorptive phases of glucose metabolism via neurohumoral feedback responses.

• Small intestinal glucose absorption is influenced by the rate of gastric emptying, motility of the small intestine, flow of luminal contents, digestive capacity of the gut and the efficacy of glucose transporters.

• Disorders of one or more of these interrelated factors could potentially stimulate, or attenuate, glucose absorption; interventions to modulate these elements could, therefore, be therapeutically important.

• Recent insights into the role of sweet taste receptor signaling in the regulation of intestinal glucose transporters and release of neurohumoral mediators, such as incretin and satiety hormones, have deepened our understanding of nutrient–gut and gut–brain interactions, especially in conditions such as diabetes, obesity and critical illness. However, further human studies are necessary before pharmacological modulation of sweet taste receptors can be considered as a therapeutic option.

Notes