Literature DB >> 22238398

Comparative effects of variations in duodenal glucose load on glycemic, insulinemic, and incretin responses in healthy young and older subjects.

Laurence G Trahair1, Michael Horowitz, Christopher K Rayner, Diana Gentilcore, Kylie Lange, Judith M Wishart, Karen L Jones.   

Abstract

CONTEXT: Aging is associated with deteriorating glucose tolerance. Studies assessing glucose tolerance and subsequent insulin and incretin hormone release often fail to take into account the rate of gastric emptying when evaluating these responses.
OBJECTIVE: Our objective was to determine the comparative effects of variations in the small intestinal glucose load on the glycemic, insulinemic, and incretin responses in healthy young and older subjects.
MATERIALS AND METHODS: Twelve healthy young (six males, six females; age 22.2±2.3 yr) and 12 older (six males, six females; age 68.7±1.0 yr) subjects had measurements of blood glucose, serum insulin and plasma incretin hormones [glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)] and calculations of insulin resistance (homeostatic model assessment) and β-cell function corrected for insulin sensitivity, before and during intraduodenal infusions of glucose at 1, 2, or 3 kcal/min or saline for 60 minutes. The study was double-blinded and randomized, and performed in the Discipline of Medicine at the Royal Adelaide Hospital.
RESULTS: At baseline, blood glucose and serum insulin were slightly higher in the older subjects (P<0.001), whereas GLP-1 and GIP were comparable between groups. In both groups, the glycemic, insulinemic, and GLP-1 responses were dependent on the duodenal glucose load in a nonlinear fashion (P<0.001). The glycemic response was greater (P<0.001) in the older subjects, whereas GLP-1 and GIP responses were comparable between groups. The older subjects were more insulin resistant (P<0.001) and had impaired β-cell function, particularly at higher glucose loads (P<0.05).
CONCLUSION: When glucose is infused into the small intestine at equal rates in healthy young and older subjects, GLP-1 and GIP responses are comparable, indicating that impaired incretin secretion does not account for age-related glucose intolerance.

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Year:  2012        PMID: 22238398     DOI: 10.1210/jc.2011-2583

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  19 in total

1.  Alterations of Gastric Emptying Features Following Laparoscopic Sleeve Gastrectomy in Chinese Patients with Obesity: a Self-Controlled Observational Study.

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2.  Effects of exogenous glucagon-like peptide-1 on blood pressure, heart rate, gastric emptying, mesenteric blood flow and glycaemic responses to oral glucose in older individuals with normal glucose tolerance or type 2 diabetes.

Authors:  Laurence G Trahair; Michael Horowitz; Julie E Stevens; Christine Feinle-Bisset; Scott Standfield; Diana Piscitelli; Christopher K Rayner; Adam M Deane; Karen L Jones
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Review 3.  Ghrelin, CCK, GLP-1, and PYY(3-36): Secretory Controls and Physiological Roles in Eating and Glycemia in Health, Obesity, and After RYGB.

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4.  Effects of small intestinal glucose on glycaemia, insulinaemia and incretin hormone release are load-dependent in obese subjects.

Authors:  L G Trahair; C S Marathe; S Standfield; C K Rayner; C Feinle-Bisset; M Horowitz; K L Jones
Journal:  Int J Obes (Lond)       Date:  2016-12-06       Impact factor: 5.095

Review 5.  Gastric emptying and glycaemia in health and diabetes mellitus.

Authors:  Liza K Phillips; Adam M Deane; Karen L Jones; Chris K Rayner; Michael Horowitz
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6.  Mild diabetes: long-term effects on gastric motility evaluated in rats.

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7.  Ethnic disparities in insulin and glucose-dependent insulinotropic peptide (GIP) responses to intraduodenal glucose in health.

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Review 9.  Relationships between gastric emptying, postprandial glycemia, and incretin hormones.

Authors:  Chinmay S Marathe; Christopher K Rayner; Karen L Jones; Michael Horowitz
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10.  Disordered control of intestinal sweet taste receptor expression and glucose absorption in type 2 diabetes.

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