Identification and Actions of Gastric Inhibitory Polypeptide

Brown, John C.; Dryburgh, Jill R.; Ross, Stephanie; Dupré, J.

doi:10.1016/b978-0-12-571131-9.50017-7

Cited by 204 publications

(210 citation statements)

References 40 publications

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“…Since it has been demonstrated that GIP as a component of the entero-insular axis modulates insulin secretion from the endocrine pancreas [1,2], an indirect insulin-mediated contribution to the regulation of hepatic glucose metabolism is well established. In contrast, direct metabolic effects of GIP on the liver have received little attention; moreover, results of in vitro and in vivo studies yielded contradictory data [8][9][10].…”

Section: Discussionmentioning

confidence: 99%

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Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver

1986

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Summary. The effect of porcine gastric inhibitory polypeptide on hepatic glycogen metabolism was investigated in the isolated in situ perfused rat liver. Glycogenolysis was stimulated by infusion of glucagon into the portal vein (half maximal effective portal vein concentration -30 pmol/1). When glucagon was infused at a final portal vein concentration of 0.5 nmol/1, simultaneous addition of insulin inhibited the glucagon-dependent glycogenolysis in a dose-dependent way (half maximal effective concentration for insulin about 2 nmol/1). Gastric inhibitory polypeptide alone at a concentration of 1 nmol/1 reduced glucagon-dependent glycogenolysis only slightly. However, when infused simultaneously at low insulin concentrations (0.1 nmol/1), gastric inhibitory polypeptide suppressed hepatic glucose production dose-dependently up to 70%. The data suggest that gastric inhibitory polypeptide exerts direct metabolic effects on hepatic glycogen metabolism predominantly in a situation where insulin is simultaneously present, e.g. following ingestion of glucose.

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Section: Discussionmentioning

confidence: 99%

“…The role of gastric inhibitory polypeptide (GIP) -a gastrointestinal hormone released upon oral ingestion of glucose and fat -in modulating pancreatic insulin secretion has been well established [1,2]. GIP is regarded as a component of the entero-insular axis [3].…”

mentioning

confidence: 99%

Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver

1986

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“…The intestinal hormone gastric inhibitory polypeptide (GIP) is a potent stimulator of glucose-induced insulin secretion [2] and is currently thought to be one of the major endocrine components of the entero-insular axis. GIP is released after ingestion of glucose [2,3] amino acids [4] or fat [2,5], the latter being especially potent.…”

Section: Discussionmentioning

confidence: 99%

“…GIP is released after ingestion of glucose [2,3] amino acids [4] or fat [2,5], the latter being especially potent. Exogenous insulin [2,6] and C-peptide [7] have been shown to inhibit fat-induced GIP release and may play a physiological role in the regulation of GIP secretion.…”

Section: Discussionmentioning

confidence: 99%

“…Various workers [2,6,18,19] have demonstrated that intravenous infusions of either insulin or glucose reduce the rise in plasma GIP provoked by fat ingestion and have suggested the existance of a negative feedback control of insulin upon GIP release. In the present study the control group of rats on a low fat diet showed inhibition of fat-induced GIP release by insulin but the fat-pretreated ones did not.…”

Section: Discussionmentioning

confidence: 99%

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Effect of pretreatment with a high fat diet on the gastric inhibitory polypeptide and insulin responses to oral triolein and glucose in rats

1983

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Summary.Male Wistar rats were pretreated with 3 ml triolein orally for 4 days in addition to their normal diet. A similar control group were allowed free access to normal laboratory food. When given an oral fat load (1 ml triolein) plasma gastric inhibitory polypeptide (GIP) and triglyceride levels were significantly higher in the fat pretreated group. Inhibition of fat-stimulated GIP release by exogenous insulin was demonstrated in the untreated control group (plasma GIP: 663 +49 versus 853 + 92 ng/1, mean_+ SEM p < 0.025), but pretreatment with an oral fat load abolished this effect (plasma GIP: 1008+95 versus 1116+100ng/1, p NS). Plasma glucose levels were significantly higher in fat pretreated rats given oral fat and intraperitoneal insulin compared with untreated controls (plasma glucose nadir 2.6+0.48 versus 1.6+0.15 mmol/1, p< 0.05). Fat-pretreated rats showed significantly higher insulin and glucose levels compared with the untreated rats when given oral glucose (plasma insulin: 6.2 + 1.2 versus 2.5+0.59p~g/1, p<0.01; plasma glucose: 10.2+0.39 versus 8.9 _+ 0.41 mmol/1, p < 0.025). Pretreatment of rats on a high fat diet causes (1) increased GIP secretion in response to an oral fat load, (2) abolition of the feed-back inhibition of exogenous insulin on fat-stimulated GIP release, and (3) some degree of insulin resistance.

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Gastric inhibitory polypeptide (GIP) in anorexia nervosa

Dixon

O'Dorisio

Zipf

et al. 1985

Int. J. Eat. Disord.

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Simultaneous glucose, insulin, and gastric inhibitory polypeptide (GIP) responses to meal stimulation were measured in five anorexia nervosa patients, eight bulimia patients with a past history of anorexia nervosa, and twenty‐two healthy subjects. Although basal levels of GIP were similar, anorexia nervosa patients had an early and significantly higher (p <.05) mean peak GIP response than controls or bulimics with past anorexia nervosa. Mean peak insulin levels in anorexia nervosa patients did not differ significantly from those of control or bulimia/past anorexia nervosa patients, although anorexia nervosa patients had a nonsignificantly prolonged elevation of serum insulin. Glucose responses were not significantly different among the various groups. The exaggerated CIP response to meal stimulation with no significant difference in insulin levels suggests that the usual association between insulin and GIP is altered in anorexia nervosa. This is apparently a state‐dependent abnormality since GIP responses in bulimia patients with a history of anorexia nervosa do not differ from healthy subjects. Altered GIP responses may contribute to the gastric hypomotility and acid secretion changes previously reported in low‐weight anorexia nervosa patients.

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Identification and Actions of Gastric Inhibitory Polypeptide

Cited by 204 publications

References 40 publications

Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver

Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver

Effect of pretreatment with a high fat diet on the gastric inhibitory polypeptide and insulin responses to oral triolein and glucose in rats

Gastric inhibitory polypeptide (GIP) in anorexia nervosa

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