Accelerated intestinal glucose absorption in morbidly obese humans: relationship to glucose transporters, incretin hormones, and glycemia.

摘要: CONTEXT: Intestinal glucose absorption is mediated by sodium-dependent transporter 1 (SGLT-1) and 2 (GLUT2), which are linked to sweet taste receptor (STR) signaling incretin responses. OBJECTIVE: This study aimed examine intestinal in morbidly obese humans its relationship the expression of STR transporters, glycemia, DESIGN/SETTING/PARTICIPANTS: Seventeen nondiabetic, subjects (body mass index [BMI], 48 ± 4 kg/m(2)) 11 lean controls (BMI, 25 underwent endoscopic duodenal biopsies before after a 30-minute intraduodenal infusion (30 g 3 3-O-methylglucose [3-OMG]). MAIN OUTCOME MEASURES: Blood plasma concentrations 3-OMG, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide (GLP-1), insulin, glucagon were measured over 270 minutes. Expression SGLT-1, GLUT2, (T1R2) was quantified PCR. RESULTS: The increase 3-OMG (P < .001) blood .0001) greater than subjects. Plasma correlated directly with (r = 0.78, P .01). In response glucose, GIP .001), insulin higher, but GLP-1 less compared lean. SGLT-1 .035), not GLUT2 or T1R2, higher obese, related peak 0.60, .01), 0.67, .003), 0.58, .02). CONCLUSIONS: morbid obesity, proximal intestine accelerated increased expression, leading an incretin-glucagon profile promoting hyperinsulinemia hyperglycemia. These findings consistent concept that gut underlies foregut theory obesity type diabetes.