Accelerated Intestinal Glucose Absorption in Morbidly Obese Humans: Relationship to Glucose Transporters, Incretin Hormones, and Glycemia

Abstract

In morbid obesity, proximal intestine glucose absorption is accelerated and related to increased SGLT-1 expression, leading to an incretin-glucagon profile promoting hyperinsulinemia and hyperglycemia. These findings are consistent with the concept that accelerated glucose absorption in the proximal gut underlies the foregut theory of obesity and type 2 diabetes.

Roles of the Gut in Glucose Homeostasis

“…Inconsistency exists between studies about whether incretin secretion is altered in obesity or type 2 diabetes compared with health, and although decreases in GLP-1 secretion usually can be demonstrated (63), no substantial differences, particularly in the early postprandial phase, have been found (64). However, individuals with morbid obesity manifest accelerated glucose absorption from the proximal small intestine, with a corresponding shift toward greater secretion of GIP and less of GLP-1 than seen in lean individuals (65).…”

Immunologic impact of the intestine in metabolic disease

“…In the context of obesity, nutrients enter circulation at an increased rate, as is evident by the enhanced secretion of chylomicrons in obesity. While the mechanisms remain to be fully explored, the expression and/or activity of protein transporters that influence nutrient absorption, such as SGLT1 and CD36, are altered on a HFD and in obesity (105,106). This suggests that decreased levels of preabsorptive nutrient accumulation resulting from increased apical transport may contribute to a failure in the induction of nutrient-sensing mechanisms that regulate energy homeostasis.…”

Physiologic changes in obesity and patient preparation for bariatric surgery

“…[36][37][38][39][40][41] Animal experiments have shown that intestinal glucose absorption is dependent on the presence of luminal glucose or sweet nutrients via activation of intestinal sweet taste receptors (STRs), which are heterodimers of G-protein-coupled receptors. [36,37] When activated, the capacity of these receptors increase the availability of intestinal sodium-dependent glucose cotransporter-1 (SGLT-1) and glucose transporter-2 (GLUT2).…”

“…[39,40] Nguyen et al have shown that obese individuals have rapid proximal intestinal glucose absorption which is linked to increased SGLT-1 expression which results in hyperinsulinemia and hyperglycemia. [41] …”