Food-Dependent Cushing's Syndrome: Characterization and Functional Role of Gastric Inhibitory Polypeptide Receptor in the Adrenals of Three Patients
Marie-Christine LebrethonO. AvalletYves ReznikF. ArchambeaudJ. CombesTed B. UsdinG NarboniJ MahoudeauJ.M. Saez
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Gastric inhibitory polypeptide
Characterization
Gastric inhibitory polypeptide, originally isolated from porcine intestine, is a gastrointestinal hormone belonging to the vasoactive intestinal peptide (VIP)/glucagon/secretin family. GIP consists of 42 amino acid residues which is derived by proteolytic processing of a GIP precursor. In vivo and in vitro experiments have indicated that GIP auguments glucose-stimulated insulin secretion, suggesting that GIP plays an important role in the regulation of insulin secretion as an incretin. Thus, GIP now is generally referred to as glucose-dependent insulinotropic polypeptide. It is also suggested that GIP may be involved in the pathogenesis of non insulin-dependent diabetes mellitus (NIDDM). GIP exerts its biological actions by binding to its specific receptors, which appear to be coupled to G proteins. We have isolated a cDNA encoding a GIP receptor from a hamster insulinoma(HIT-T15) cDNA library. The hamster GIP receptor is a 462 amino acid protein having seven transmembrane segments. Expression of recombinant of hamster GIP receptors in Chinese hamster ovary (CHO) cells shows that it binds specifically to GIP with high affinity (IC50 = 9.6 nM) and is positively coupled to adenylate cyclase. RNA blot analysis reveals that a 3.8-kb GIP receptor mRNA is expressed at high levels in rat pancreatic islets as well as in HIT-T15 cells.
Gastric inhibitory polypeptide
Incretin
Secretin family
Secretin
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A radioimmunoassay for the measurement of gastric inhibitory polypeptide (GIP) in unextracted plasma in man has been developed using a rabbit antiserum raised against porcine GIP. Porcine GIP was employed also as standard and to produce a 125I-labelled tracer. The assay was able to distinguish 110 pg/ml GIP from zero in plasma samples. Negligible cross-reactivity was demonstrated with cholecystokinin, insulin, pancreatic polypeptide, glucagon, secretin, and vasoactive intestinal polypeptide. The mean overnight fasting plasma GIP level in 28 normal subjects was 203 pg/ml (range: undetectable--420 pg/ml). Plasma GIP levels rose, within 45 minutes of eating a mixed meal, to a mean level of 1573 pg/ml.
Gastric inhibitory polypeptide
Secretin
Pancreatic polypeptide
Pepsin
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Abstract This article provides a general introduction of materials characterization and describes the principles and applications of a limited number of techniques that are most commonly used to characterize the composition and structure of metals used in engineering systems. It briefly describes the classification of materials characterization methods including, bulk elemental characterization, bulk structural characterization, microstructural characterization, and surface characterization. Further, the article reviews the selection of materials characterization methods most commonly used with metals.
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Glucose-dependent insulinotropic polypeptide (GIP) is an incretin secreted from enteroendocine K cells after nutrient ingestion. Fat strongly induces GIP secretion, and GIP hypersecretion is involved in high-fat diet-induced obesity and insulin resistance. Aging also induces GIP hypersecretion, but its effect on body weight gain and insulin sensitivity remains unclear. In the present study, we investigated the effect of GIP on age-related body weight gain and insulin resistance using GIP-knockout homozygous (GIP −/ − ) and heterozygous (GIP +/ − ) mice, which have entirely absent and 50% reduced GIP secretion compared to wild-type (WT) mice, respectively. Under 12% fat-containing normal diet feeding condition, body weight was significantly lower in GIP −/ − mice compared to that in WT and GIP +/ − mice from 38 weeks of age, while there was no significant difference between WT and GIP +/ − mice. Visceral and s.c. fat mass were also significantly lower in GIP −/ − mice compared to those in WT and GIP +/ − mice. During oral glucose tolerance test, blood glucose levels did not differ among the three groups. Insulin levels were significantly lower in GIP −/ − mice than those in WT and GIP +/ − mice. During insulin tolerance test, GIP −/ − mice showed higher insulin sensitivity than that of WT and GIP +/ − mice. Adiponectin mRNA levels were increased and leptin mRNA levels tended to be decreased in adipose tissue of GIP −/ − mice. These results demonstrate that GIP is involved in age-related obesity and insulin resistance and that inhibition of GIP secretion alleviates age-related fat mass gain and insulin resistance under carbohydrate-based diet feeding condition.
Gastric inhibitory polypeptide
Incretin
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Characterization
Zeta potential
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Materials characterization is a crucial issue in the development and application of new materials. Materials characterization aims to mine and acquire characteristic information and their evolution in the materials. It mainly includes three important topics which are microstructural characterization, properties characterization, and environmental degradation. In this paper, characterization techniques about these topics were discussed for C/SiC composites and a characterization system was preliminarily established. All these characterization research and their results further the better understanding of the relationship between microstructure and properties and of the failure mechanisms in the C/SiC composites.
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The involvement of the gut hormone GIP (gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide) in the hyperinsulinemia of the adult obese Zucker rat was investigated. Glucose, insulin, and GIP responses to oral glucose were compared in lean and obese rats. The sensitivity of the isolated, perfused pancreas to glucose and GIP was studied in basal and hyperglycemie conditions in lean and obese rats. Immunocytochemical studies of the gut and pancreas were also carried out. The glucose and GIP responses to oral glucose were similar in lean and obese rats, but obese animals were hyperinsulinemic compared with lean controls under fasting conditions and after oral glucose. The isolated, perfused pancreas of obese Zucker rats had an elevated insulin response to 300 mg/dl glucose. GIP increased the insulin response to 300 mg/dl glucose threefold in both lean and obese rats. At basal glucose levels (80 mg/dl), GIP augmented insulin release in obese but not in lean rats. Immunocytochemical studies demonstrated the presence of enlarged islets in obese rats due to an increase in the B-cell mass. A-, D-, and PP-cells appeared normal. Obese and lean rats had similar numbers of GIP-containing cells in the gut. This study suggests that GIP may contribute to the fasting hyperinsulinemia characteristic of adult obese Zucker rats. GIP infusion to achieve levels equivalent to those seen in the basal state are capable of stimulating insulin release in the absence of hyperglycemia in the obese rat, which suggests an impairment of the regulatory mechanisms controlling the glucose-dependent insulinotropic action of GIP in these animals.
Gastric inhibitory polypeptide
Hyperinsulinemia
Basal (medicine)
Pancreatic polypeptide
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Hyperinsulinemia
Gastric inhibitory polypeptide
Pancreatic Islets
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We previously reported that the short-form gastric inhibitory polypeptide (GIP) 1-30 is released from islet alpha cells and promotes insulin secretion in a paracrine manner in vitro. However, the role played by GIP 1-30 in glucose metabolism in vivo remains unclear. We developed an enzyme-linked immunosorbent assay (ELISA) specific for GIP 1-30 and measured GIP 1-30 secretion in nondiabetic subjects (ND, n = 8) and patients with type 2 diabetes (T2D, n = 9). We developed a sandwich ELISA by combining a novel antibody to the GIP C-terminus with the N-terminal anti-GIP 1-42 antibody that is already available. We explored cross-reactivities with incretins and glucagon-related peptides. We next subjected ND and T2D subjects to the cookie meal test (CMT: carbohydrates 75 g, lipids 28.5 g, proteins 8.5 g) and measured GIP 1-30 blood levels. Absorbance increased in a dose-dependent manner on addition of the GIP 1-30 amide but not GIP 1-42, GLP-1, or glucagon. Post-CMT loading, GIP 1-30 concentrations increased in both ND and T2D subjects; however, in ND subjects, the increases were much lower than those of GIP 1-42 (GIP 1-30, before loading: 1.4 ± 0.5 pmol/L, after: 1.9 ± 0.6 pmol/L; GIP 1-42, before: 8.2 ± 0.1 pmol/L, after: 204.0 ± 35.2 pmol/L, P<0.05). In T2D patients, the GIP 1-30 levels, as assessed by the areas under the curves, tended to be lower than those in ND patients. The DPP-4 inhibitor significantly increased both GIP 1-30 and GIP 1-42 secretion in T2D patients. In conclusion, we developed a novel ELISA that is highly specific for GIP 1-30, the secretion of which was promoted by a mixed meal to a blood level lower than that of GIP 1-42. As is also true of the incretins, GIP 1-30 levels increased upon administration of DPP-4 inhibitor; GIP 1-30 secretion may differ between ND and T2D subjects. Disclosure Y. Takeda: None. Y. Fujita: None. T. Yanagimachi: None. N. Maruyama: Employee; Self; Immuno-Biological Laboratoties Co.,Ltd. R. Bessho: None. H. Sakagami: None. M. Haneda: None. T. Ota: None. Funding Japan Society for the Promotion of Science
Gastric inhibitory polypeptide
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