Physiology and pathophysiology of GIP: A review

Scandinavian Journal of Gastroenterology

1996

237

140

Section: Resultsmentioning

confidence: 98%

Secretion of the Incretin Hormones Glucagon-Like Peptide-1 and Gastric Inhibitory Polypeptide Correlates with Insulin Secretion in Normal Man Throughout the Day

Ørskov

Wettergren

Scandinavian Journal of Gastroenterology

1996

237

140

“…Research has placed GLPs and GIP in glucose metabolism as some of the main incretin factors, at least in healthy individuals (Krarup & Groop, 1991). The incremental GIP response to oral glucose or a mixed meal has been linked to the pathogenesis of hyperinsulinaemic states such as type 2 diabetes and obesity (Tedde et al ., 1995).…”

Section: Discussionmentioning

confidence: 99%

Comparisons of leptin, incretins and body composition in obese and lean patients with hypopituitarism and healthy individuals

Mersebach

Svendsen

et al. 2003

Clinical Endocrinology

Fasting levels of GIP were elevated in obese substituted hypopituitary patients, while fasting concentrations of GLPs were similar. Obese hypopituitary patients had the same degree of hyperinsulinaemia, affected glucose tolerance, dyslipoproteinaemia and central obesity as obese healthy controls. Further studies are required to identify the possible biochemical reasons for obesity in patients with apparently well-substituted hypopituitarism.

“…Studies addressing the role(s) of GIP and GLP-1 in the pathophysiology of the defective insulin secretion in NIDDM have not been conclusive (4,5,8,11).…”

mentioning

confidence: 98%

“…The incretin effect is supposed to be mediated through release of one or more insulinotropic hormones from the gut after oral glucose ingestion (2,3). Two gut incretin hormones have been identified: gastric inhibitory polypeptide (GIP) (4,5) and glucagon-like peptide 1 (GLP-1) (6)(7)(8). Gastric inhibitory polypeptide is secreted in the proximal part and GLP-1 in the distal part of the small intestine in response to mixed meals, oral glucose and fat ingestion (4,8).…”

mentioning

confidence: 99%

Gut incretin hormones in identical twins discordant for non-insulin-dependent diabetes mellitus (NIDDM)—evidence for decreased glucagon-like peptide 1 secretion during oral glucose ingestion in NIDDM twins

Vaag

European Journal of Endocrinology

Vølund

et al. 1996

146

103

The incremental glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP) responses (areas under curves; AUCs) were determined during a standard 180-min 75-g oral glucose tolerance test in a group of 12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) and 13 matched controls without family history of diabetes using highly sensitive and specific radioimmunoassay hormone assays. Data were analysed using multifactor analysis of variance (ANOVA) to identify and correct for possible covariates and to correct for multiple comparisons. Fasting plasma GLP-1 and GIP concentrations were similar in all groups. The twins with frank NIDDM had a decreased incremental GLP-1 response during oral glucose ingestion compared with controls without family history of diabetes (AUC +/- SEM: 0.55 +/- 0.14 vs 1.17 +/- 0.25 (mmol/l) x min, p < 0.05). The incremental GLP-1 secretion in the non-diabetic twins was not significantly different from neither their NIDDM co-twins nor the controls without family history of diabetes. The incremental GIP responses were similar in all study groups. Gender was identified as the major independent covariate for incremental glucose, insulin, GIP and GLP-1 responses, with higher values of all parameters in females. Waist-to-hip ratio and body mass index (BMI) were identified as independent but oppositely directed covariates for the incremental GLP-1 responses (waist-to-hip ratio: r = 0.43, p < 0.02; BMI: r = -0.34, p = 0.06). Incremental GLP-1 responses correlated with incremental insulin responses in the combined study population (N = 37; R = 0.42, p = 0.01). In conclusion, a decreased intestinal GLP-1 secretion may contribute to the abnormal insulin secretion during oral glucose ingestion in NIDDM twins. However, decreased secretion of gut incretin hormones (GLP-1 or GIP) does not explain all of the defects of pancreatic insulin secretion in NIDDM patients/twins or in non-diabetic individuals (identical twins) with a genetic predisposition to NIDDM.