Physiological role of cholecystokinin on postprandial insulin secretion and gastric meal emptying in man. Studies with the cholecystokinin receptor antagonist loxiglumide

Fried, Michael; Schwizer, Werner; Beglinger, Christoph; Keller, Ulrich; Jansen, J. B. M. J.; Lamers, C. B. H. W.

doi:10.1007/bf00401517

Cited by 42 publications

(17 citation statements)

References 41 publications

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“…Carbohydrate and glucose appear to be weak stimulants for CCK release. 17,28,33 Several studies have shown a modest increase in plasma CCK levels after oral glucose ingestion 16,34–36 ( Fig. 1).…”

Section: Cholecystokinin Releasementioning

confidence: 99%

Pathophysiological role of cholecystokinin in humans

Ōtsuki

2000

J of Gastro and Hepatol

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Cholecystokinin (CCK) is a major gastrointestinal hormone that plays an important role in stimulation of pancreatic secretion and gall-bladder contraction, regulation of gastrointestinal motility and induction of satiety. Ingestion of fat and protein induces significant increases in plasma CCK. Intraluminal mediators of CCK secretion, luminal CCK releasing factor and diazepam-binding inhibitor, were purified from rat intestinal secretion. These CCK-releasing factors (RF) are secreted tonically by the small intestine and stimulate CCK release. Another kind of CCK-RF named 'monitor peptide' was purified from the rat pancreatic juice that stimulates CCK secretion when introduced into rat intestine. Bile exclusion from the duodenum causes an increase in basal CCK and enhances stimulated plasma CCK release, and bile salt replacement reverses these effects. Thus, the CCK-RF are spontaneously secreted into the intestinal lumen in humans, while the CCK-producing cells are under constant suppression by intraduodenal bile acids. In acute pancreatitis, plasma CCK levels are high in patients with gallstone pancreatitis, but not in patients with pancreatitis from other causes, such as alcoholic and idiopathic pancreatitis. A transient disturbance of bile flow into the duodenum by stones or oedema of the pancreas together with impairment of pancreatic exocrine function might cause the increase in plasma CCK release in gallstone pancreatitis. Patients with chronic pancreatitis with mild to moderate impairment of exocrine function and abdominal pain, had significantly higher plasma CCK concentrations, whereas patients with pancreatic insufficiency had a significantly lower plasma CCK response to a test meal than the healthy subjects. The increased CCK may further aggravate pancreatitis and worsen the prognosis of pancreatitis by stimulating the injured pancreas, resulting in the vicious circle via endogenous CCK release. The CCK-A receptor antagonist might be therapeutically useful in acute pancreatitis by stopping the vicious circle.

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Section: Cholecystokinin Releasementioning

confidence: 99%

Pathophysiological role of cholecystokinin in humans

Ōtsuki

2000

J of Gastro and Hepatol

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“…GLP-1 and CCK are intestinal incretins; that is, proteins that stimulate pancreatic insulin secretion 52–54. GPR120 activation can induce GLP-1 and CCK secretion, which may further regulate pancreatic islet function and β-cell proliferation and survival.…”

Section: Role Of Gpr120 In Regulating Cell and Tissue Functionsmentioning

confidence: 99%

Potential roles of GPR120 and its agonists in the management of diabetes

Zhang¹,

Leung²

2014

DDDT

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Free fatty acids (FFAs) serve not only as nutrients that provide energy but also as extracellular signaling molecules that manipulate intracellular physiological events through FFA receptors (FFARs) such as FFAR4. FFAR4 is also known as G-protein coupled receptor 120 (GPR120). The main role of GPR120 is to elicit FFA regulation on metabolism homeostasis. GPR120 agonism correlates with prevention of the occurrence and development of metabolic disorders such as obesity and diabetes. GPR120 activation directly or indirectly inhibits inflammation, modulates hormone secretion from the gastrointestinal tract and pancreas, and regulates lipid and/or glucose metabolism in adipose, liver, and muscle tissues, which may help prevent obesity and diabetes. This review summarizes recent advances in physiological roles of GPR120 in preventing insulin resistance and protecting pancreatic islet function, and examines how resident GPR120 in the pancreas may be involved in modulating pancreatic islet function.

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“…This hypothesis has not been explored. In normoinsulinemic (NI) individuals, appetite and food intake are inversely related to blood concentrations of glucose, [15][16][17] insulin, 8 leptin 18 and gastrointestinal hormones including cholecystokinin (CCK) 19 immediately following carbohydrate consumption.…”

Section: Introductionmentioning

confidence: 99%

Enhanced food intake regulatory responses after a glucose drink in hyperinsulinemic men

2007

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Objective: To determine the effect of hyperinsulinemia on food intake and plasma concentrations of glucose and food intake regulatory hormones in men after a glucose drink. Design: Cross-sectional clinical intervention study of the effect of a glucose drink on food intake regulation. Subjects: Thirty-three normoinsulinemic (NI) (body mass index (BMI) ¼ 25.370.6; age ¼ 41.472.4) and 32 hyperinsulinemic (HI) men (BMI ¼ 29.570.6; age ¼ 43.472.6). Measurements: Food intake was measured from a pizza meal 1 h after subjects consumed either a noncaloric sweetened drink or a glucose-containing drink (75g/300 ml) in random order on two occasions. On another occasion, blood samples were taken every 30 min for 2 h after the glucose drink. Results: Fasting insulin in the HI and NI men was 6573 (mean7s.e.m.) and 2671.5 pmol/l, respectively. Food intake at the pizza meal was reduced by the glucose drink (Po0.01), but more so in HI (À9.774.1 %) than NI men (À5.473.4 %) (P ¼ 0.06). The increase in plasma insulin and cholecystokinin (CCK) after the glucose drink was greater and the plasma concentrations of leptin were higher, and ghrelin and adiponectin were lower in HI men than in NI men (Po0.05). Conclusion: These results support epidemiological data suggesting that hyperinsulinemia, at least in the early stages, may provide resistance to weight gain, possibly through physiological mechanisms of food intake control.

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Physiological role of cholecystokinin on postprandial insulin secretion and gastric meal emptying in man. Studies with the cholecystokinin receptor antagonist loxiglumide

Cited by 42 publications

References 41 publications

Pathophysiological role of cholecystokinin in humans

Pathophysiological role of cholecystokinin in humans

Potential roles of GPR120 and its agonists in the management of diabetes

Enhanced food intake regulatory responses after a glucose drink in hyperinsulinemic men

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