Serum Gastric Inhibitory Polypeptide (GIP) in Duodenal Ulcer Disease: Relationship to Glucose Tolerance, Insulin, and Gastrin Release

Arnold, R.; Creutzfeldt, W.; Ebert, R.; Becker, H. D.; Börger, H. W.; Schafmayer, A.

doi:10.3109/00365527809179804

Cited by 41 publications

(16 citation statements)

References 31 publications

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“…GIP appears to contribute to the regulation of pancreatic insulin release under physiological conditions; however, the precise contribution of this peptide to pathological states is unclear, as no definite and consistent abnormalities in GIP release in patients with diabetes mellitus have been found. Enhanced GIP release into the circulation has been reported in patients with obesity (43), chronic pancreatitis (44,45), and duodenal ulcer (46). In this last group of patients, increased fasting and foodstimulated serum GIP concentrations were found primarily in a subgroup ofpatients with an exaggerated early rise in serum glucose (46), further supporting its physiological role as a mediator of the enteroinsular axis.…”

Section: Resultsmentioning

confidence: 59%

“…Enhanced GIP release into the circulation has been reported in patients with obesity (43), chronic pancreatitis (44,45), and duodenal ulcer (46). In this last group of patients, increased fasting and foodstimulated serum GIP concentrations were found primarily in a subgroup ofpatients with an exaggerated early rise in serum glucose (46), further supporting its physiological role as a mediator of the enteroinsular axis.…”

Section: Resultsmentioning

confidence: 59%

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Glucose-dependent insulinotropic peptide: structure of the precursor and tissue-specific expression in rat.

Tseng

Jarboe

Landau

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Glucose-dependent insulinotropic peptide (GIP) is a 42-amino acid gastrointestinal regulatory peptide that stimulates insulin secretion from pancreatic beta cells in the presence of glucose. Approximately 7.8 x 105 recombinant dones of a neonatal rat intestinal cDNA library were screened by using plaque hybridization, and three dones were identified and sequenced with the dideoxynucleotide chain-termination method. The translated amino acid sequence deduced from the nucleotide sequence of the cDNA indicated that rat GIP was derived by proteolytic processing of a 144-amino acid precursor polypeptide. The mature peptide is flanked by a 43-amino acid NH2-terminal peptide that contains a 21-amino add signal peptide and by a 59-amino acid COOH-terminal peptide. Analysis of the nucleotide and amino acid sequence of rat GIP revealed only two substitutions from the known human GIP peptide. The use of high-stringency RNA blot-hybridization analysis of total RNA extracted from various organs demonstrated expression of the GIP gene in the duodenum and jejunum and, to a lesser extent, in the ileum. In addition, expression of the GIP gene was observed in the submandibular salivary gland both by RNA analysis and RIA. In response to duodenal perfusion of a 20% Lipomul meal for 60 min, duodenal mucosal GIP mRNA concentrations increased by 42.8% and 48.2% at 30 and 60 min, respectively.Glucose-dependent insulinotropic peptide (GIP) was first isolated from porcine small intestine in 1969 and was originally named "gastric inhibitory peptide" on the basis of its ability to inhibit acid secretion in dogs (1). Its primary structure was initially described in 1971 (2) and revised in 1981 (3), and its amino acid sequence placed it in the secretin family of gastrointestinal regulatory peptides. GIP has been demonstrated in the cytoplasmic granules ofenteroendocrine K-cells in mucosa throughout the small intestine (4). After intestinal glucose perfusion, the primary site of endogenous GIP release appears to be the duodenum and proximal jejunum (5). Although several studies have supported the role of GIP as an inhibitor of acid secretion (6-10), some have challenged the notion that GIP inhibits acid output under physiological conditions (11,12). In addition to its inhibitory effects in the stomach, further investigation of the physiological properties of GIP demonstrated that in the presence of glucose, GIP enhanced insulin release by pancreatic beta islet cells when administered in physiological doses (13)(14)(15). It was, therefore, suggested that GIP may function as an "incretin," a proposed enteric factor that stimulates the release of pancreatic insulin and that may play a physiological role in maintaining glucose homeostasis (16,17). Accordingly, the hormone is now often referred to as "glucose-dependent insulinotropic peptide," thereby maintaining the original acronym (18).Numerous past studies have characterized GIP release into the circulation; however, few have examined the biosynthesis of this peptide. The rat serves as...

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Section: Resultsmentioning

confidence: 59%

Section: Resultsmentioning

confidence: 59%

Glucose-dependent insulinotropic peptide: structure of the precursor and tissue-specific expression in rat.

Tseng

Jarboe

Landau

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…In this study, we investigated the interrelationship between acid output and GIP release, and found that there was a positive correlation between maximum acid output in response to tetragastrin and integrated incremental response of GIP after oral glucose loading. As mentioned above, Arnold et al (1978) reported that both fasting and food-stimulated IR-GIP levels were significantly higher in duodenal ulcer patients. Moreover, in most patients with duodenal ulcer, the hyperacidity is related to vagus-dependency.…”

Section: Commentsmentioning

confidence: 72%

“…Through many investigations (Maxwell et al 1980; Yamagishi and Debas 1980; Simmons et al 1981), however, a lot of questions have been brought out as to the enterogastrone action of GIP. Arnold et al (1978) reported high levels of GIP both at fasting and after test meal loading in patients with peptic ulcer, and ruled out the hyposecretion of GIP as a cause of gastric acid hypersecretion in duodenal ulcer patients. Recently, it has become a popular belief that GIP is important for its insulinotropic effect (Anderson et al 1978).…”

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confidence: 96%

Influence of vagotomy upon GIP release in patients with peptic ulcer.

Imamura

Kameyama

Naitö

et al. 1984

Tohoku J. Exp. Med.

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Twenty-two vagotomized peptic ulcer patients were studied on the influence of vagotomy on the release of GIP. Moreover, the relationship between acid output and GIP release was analyzed. These patients underwent one of the three types of operation ; truncal vagotomy with pyloroplasty (TV +P) selective vagotomy with pyloroplasty (SV+P) and selective vagotomy with antrectomy (SV+A). Before and after surgery, a gastric juice study and an oral glucose tolerance test were performed on separate days. Maximum acid output in response to tetragastrin correlated significantly with integrated GIP response after oral glucose loading. In the SV+P group, the response of GIP was slightly greater after surgery. In the SV+A group, the integrated GIP response diminished postoperatively, although, after surgery, GIP reached its peak sooner. The integrated GIP response was greater in the SV + P group than in the TV + P group. The response of GIP was less in the SV + A group than in the SV+P group. These changes were insignificant. In conclusion, it is presumed that GIP release is affected by gastric acid, gastric emptying time, intestinal transit time and vagal nerve action.vagotomy ; gastric acid secretion ; gastric inhibitory polypeptide (GIP) ; insulin

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“…In our experiments we studied healthy volunteers only and the experimental conditions (diet, smoking, time of the test) were strictly controlled: in these conditions we never observed deterioration of glucose handling after oral glucose. It is possible, however, that cimetidine therapy in peptic ulcer patients could change the altered gut hormone profile [1] and then modify the insulin response to oral glucose.…”

Section: Discussionmentioning

confidence: 99%

Effect of Acute and Chronic Cimetidine Administration on Glucose Tolerance and Insulin Secretion in Man

Scarpignato¹,

Tirelli²,

Starcich³

et al. 1981

Horm Res

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The effect of acute and chronic cimetidine administration on glucose tolerance and insulin secretion was studied in healthy male volunteers. Cimetidine was administered intravenously (4 mg · kg^-1 followed by 0.7 mg · kg^-1 · h^-1) in acute studies and by oral route (1 g/die for 4 weeks) in long-term studies. Oral (100 g) or intravenous (0.5 g · kg^-1) glucose was used as a stimulus for insulin secretion in both studies. Neither acute nor chronic cimetidine administration modified insulin secretion and glucose tolerance. These data are consistent with the idea that H₂-receptors are not involved in the insulinogenic effect of glucose.

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Serum Gastric Inhibitory Polypeptide (GIP) in Duodenal Ulcer Disease: Relationship to Glucose Tolerance, Insulin, and Gastrin Release

Cited by 41 publications

References 31 publications

Glucose-dependent insulinotropic peptide: structure of the precursor and tissue-specific expression in rat.

Glucose-dependent insulinotropic peptide: structure of the precursor and tissue-specific expression in rat.

Influence of vagotomy upon GIP release in patients with peptic ulcer.

Effect of Acute and Chronic Cimetidine Administration on Glucose Tolerance and Insulin Secretion in Man

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