Pathology of Gastric Inhibitory Polypeptide

2015 ◽  
pp. 145-154 ◽  
Author(s):  
S. Cataland ◽  
T. M. O�Dorisio
Keyword(s):  
Gastric Inhibitory Polypeptide

Synthetic gastric inhibitory polypeptide. Stimulatory effect on insulin and glucagon secretion in the rat

Diabetes ◽  
1977 ◽  
Vol 26 (5) ◽  
pp. 480-484 ◽  
Author(s):  
T. Taminato ◽  
Y. Seino ◽  
Y. Goto ◽  
Y. Inoue ◽  
S. Kadowaki
Keyword(s):  
Glucagon Secretion ◽  
Gastric Inhibitory Polypeptide ◽  
Insulin And Glucagon Secretion

scholarly journals Gastric inhibitory polypeptide (GIP) decreases bone resorptive activity of human osteoclasts in vitro

Bone Reports ◽  
2021 ◽  
Vol 14 ◽  
pp. 100872
Author(s):  
Morten Steen Svarer Hansen ◽  
Kent Søe ◽  
Caroline Gorvin ◽  
Morten Frost
Keyword(s):  
Gastric Inhibitory Polypeptide ◽  
Human Osteoclasts ◽  
Resorptive Activity

Gastric Inhibitory Polypeptide Release after Oral Glucose: Relationship to Glucose Intolerance, Diabetes Mellitus, and Obesity

1982 ◽  
Vol 55 (2) ◽  
pp. 329-336 ◽  
Author(s):  
MARCELLO SALERA ◽  
PIERLUIGI GIACOMONI ◽  
LORIS PIRONI ◽  
GIANLUCA CORNIA ◽  
MAURIZIO CAPELLI ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Glucose Intolerance ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose

Interactions between cholinergic agonists and enteric factors in the regulation of insulin secretion from isolated perifused rat islets

1989 ◽  
Vol 120 (6) ◽  
pp. 702-707 ◽  
Author(s):  
Walter S. Zawalich ◽  
Kathleen C. Zawalich ◽  
Howard Rasmussen
Keyword(s):  
Insulin Secretion ◽  
Gastric Inhibitory Polypeptide ◽  
Moderate Increase ◽  
Rat Islets ◽  
Insulin Requirements ◽  
Isolated Rat Islets ◽  
First Phase Insulin Secretion ◽  
Sensitizing Effect ◽  
Stimulation Of

Abstract. The ability of the cholinergic agonist carbachol to sensitize islets to the action of combined glucose, cholecystokinin and gastric inhibitory polypeptide was determined in isolated rat islets. In response to this combination, peak first phase insulin secretion from control islets averages 85 ± 5 pg · islet−1 · min−1 (mean ± sem) and the insulin secretory rates measured 35–40 min after the onset of stimulation averages 127 ± 34 pg · islet−1 · min−1. A prior 20 min exposure to 1 mmol/l carbachol potentiates the modest insulin stimulatory response to this combination of stimulants: peak first phase release is 354 ± 61 pg · islet−1 · min−1, and release measured 35–40 min after the onset of stimulation is 179 ± 34 pg · islet−1 · min−1. This sensitizing effect of carbachol lasts for at least 40 min and can be duplicated by the natural in vivo agonist acetylcholine. These results demonstrate that cholinergic stimulation of isolated islets primes them to the subsequent stimulatory effect of a moderate increase in the circulating glucose level and to several postulated incretin factors. If operative in vivo, this communications network between cephalic and enteric factors represents a remarkable control system to ensure the release of insulin in amounts commensurate to meet the anticipated and actual insulin requirements for insulin-mediated fuel disposition.

scholarly journals Gastric Inhibitory Polypeptide as an Endogenous Factor Promoting New Bone Formation after Food Ingestion

2006 ◽  
Vol 20 (7) ◽  
pp. 1644-1651 ◽  
Author(s):  
Katsushi Tsukiyama ◽  
Yuichiro Yamada ◽  
Chizumi Yamada ◽  
Norio Harada ◽  
Yukiko Kawasaki ◽  
...  
Keyword(s):  
Bone Formation ◽  
Intracellular Signaling ◽  
Gastric Inhibitory Polypeptide ◽  
Calcium Deposition ◽  
High Turnover ◽  
Blood Calcium ◽  
Gut Hormone ◽  
High Turnover Osteoporosis ◽  
Meal Ingestion

Abstract Calcium plays a fundamental role as second messenger in intracellular signaling and bone serves as the body’s calcium reserve to tightly maintain blood calcium levels. Calcium in ingested meal is the main supply and inadequate calcium intake causes osteoporosis and bone fracture. Here, we describe a novel mechanism of how ingested calcium is deposited on bone. Meal ingestion elicits secretion of the gut hormone gastric inhibitory polypeptide (GIP) from endocrine K cells in the duodenum. Bone histomorphometrical analyses revealed that bone formation parameters in the mice lacking GIP receptor (GIPR−/−) were significantly lower than those of wild-type (GIPR+/+) mice, and that the number of osteoclasts, especially multinuclear osteoclasts, was significantly increased in GIPR−/− mice, indicating that GIPR−/− mice have high-turnover osteoporosis. In vitro examination showed the percentage of osteoblastic cells undergoing apoptosis to be significantly decreased in the presence of GIP. Because GIPR−/− mice exhibited an increased plasma calcium concentration after meal ingestion, GIP directly links calcium contained in meal to calcium deposition on bone.

The Entero-Insular Axis in Polycystic Ovarian Syndrome

1996 ◽  
Vol 33 (3) ◽  
pp. 190-195 ◽  
Author(s):  
R Garaa ◽  
F Norris ◽  
J Wright ◽  
L Morgan ◽  
S Hampton ◽  
...  
Keyword(s):  
Polycystic Ovarian Syndrome ◽  
Gastric Inhibitory Polypeptide ◽  
Tolerance Test ◽  
Normal Weight ◽  
Immunoreactive Insulin ◽  
Oral Glucose ◽  
Hepatic Extraction ◽  
C Peptide ◽  
Molar Ratios ◽  
Ovarian Syndrome

We investigated the contributions made by the entero-insular axis, proinsulin and the fractional hepatic extraction of insulin to the hyperinsulinaemia characteristic of polycystic ovarian syndrome (PCOS). We measured plasma glucose, gastric inhibitory polypeptide (GIP), glucagon-like peptide-1 (7–36 amide) (GLP-17–36 amide), immunoreactive insulin (IRI), intact proinsulin (IPI), and C-peptide concentrations during a 75 g oral glucose tolerance test in seven normal weight women with PCOS and eight healthy women. Women with PCOS had higher fasting ( P = 0·05) and integrated ( P < 0·01) IRI concentrations than controls. Fasting C-peptide levels were similar in both groups but integrated C-peptide ( P < 0·05) concentrations were greater in PCOS subjects than controls. Fasting and integrated concentrations of glucose, GIP and GLP-17–36 amide were similar in subjects with PCOS and controls. Although fasting IPI concentrations were similar in both groups, integrated IPI concentrations were higher ( P = 0·05) in patients with PCOS. Women with PCOS had similar fasting but higher ( P <0·05) integrated IRI: C-peptide molar ratios than controls. Fasting and integrated IPI: IRI molar ratios were similar in both groups. These results confirm that lean women with PCOS have peripheral hyperinsulinaemia. The mild fasting hyperinsulinaemia is due to increased pancreatic secretion, whereas the stimulated hyperinsulinaemia is due to both pancreatic hypersecretion and reduced fractional hepatic extraction of insulin. Hyperproinsulinaemia is modest and appropriate in PCOS. GIP and GLP-17–36 amide do not contribute to the stimulated hyperinsulinaemia in PCOS.

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