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Glucose-dependent insulinotropic polypeptide

A recent investigation has demonstrated lipolytic action of glucose-dependent insulinotropic polypeptide (GIP) on 3T3-L1 adipocytes [384]. The effect appeared to be cAMP-mediated and could be blocked by insuhn in a wortmannin-sensitive [Pg.283]

Of the various factors suggested to play a part in impaired adipocyte function in insuhn resistance and NIDDM, increased TNF-a expression and production have attracted interest. TNF-a is produced and secreted from adipose tissue in obesity and thus acts in an autocrine fashion to alter adipocyte function during obesity-hnked insuhn resistance [385-387]. Long-term exposure ( 6h) to TNF-a has been shown to stimulate hpolysis in adipocytes [368, 388], despite inducing reduced HSL expression [389, 390]. An early study showed a down-regulation of HSL gene expression upon TNF-a treatment of 3T3-L1 cells, as measured by Northern blot analysis and enzyme activity measurements [391]. A similar effect, although much more moderate, was seen more recenfly at the protein level [264]. In a study wifh primary rat adipocytes, however, no alteration of the levels of HSL protein occurred upon treatment wifh TNF-a [392]. [Pg.283]

Studies using human adipose tissue have now shown that TNF-a inhibits LPL activity by down-regulating its protein expression [388]. Increased TNF-a mRNA levels are correlated wifh decreased LPL activity in human subcutaneous adipose tissue [393]. In addition, TNF-a reduces the expression of FA transporters in adi- [Pg.283]

Antidiabetic Drugs other than Insulin. Table 3 Actions of the incretin hormones GIP (glucose-dependent insulinotropic polypeptide, gastric inhibitory peptide) and GLP-1 (glucagon-like peptide-1)... [Pg.122]

R. P. Pauly, F. Rosche, M. Wermann, C. H. McIntosh, R. A. Pederson, and H. U. Demuth. Investigation of Glucose-Dependent Insulinotropic Polypeptide-(l-42) and Glucagon-like Peptide-1-(7-36) Degradation In Vitro by Dipeptidyl Peptidase IV Using Matrix-Assisted... [Pg.81]

Salhanick AI, Clairmont KB, Buckholz TM, Pellegrino CM, Ha S, Lumb KJ (2005) Contribution of site-specific PEGylation to the dipeptidyl peptidase IV stability of glucose-dependent insulinotropic polypeptide. Bioorg Med Chem Lett 15 4114-4117 Sanderink G-J, Artur Y, Siest G (1988) Human aminopeptidase a review of the literature. J Clin Chem Clin Biochem 26 795-807... [Pg.84]

The approval of sitagliptin (1) by the U.S. FDA in 2006 established dipeptidyl peptidase IV (DPP-4) inhibitors as an important new therapy for the treatment of type 2 diabetes.4 7 DPP-4 inhibitors stimulate insulin secretion indirectly by enhancing the action of the incretin hormones glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (G1P). GLP-1 and G1P stimulate insulin secretion in a... [Pg.125]

GIP, gastric inhibitory peptide, glucose-dependent insulinotropic. polypeptide Glc, (3-D-gluc.ose... [Pg.842]

Glucose-dependent insulinotropic polypeptide (GIP) GIP receptor 42-residue peptide Inhibit gastric acid and stimulate insulin secretion Solution-phase chemistry... [Pg.2181]

Glucose-dependent insulinotropic polypeptide is originally known as gastric inhibitory polypeptide (GIP), which is a 42-residue peptide first isolated by Brown and Dryburgh (14). It is secreted from the duodenum and proximal jejunum in response to food. Two major physiological effects of GIP are inhibition of gastric acid secretion and stimulation of insulin release. [Pg.2187]

Human-glucose-dependent insulinotropic polypeptide (human GIP) was synthesized by the route shown in Scheme Trimethylsilyl trifluoromethanesulfonate (TMSOTf) has also... [Pg.622]

Musso G, Gambino R, Pacini G, De Michieli F, Cassader M. Prolonged saturated fat-induced, glucose-dependent insulinotropic polypeptide elevation is associated with adipokine imbalance and liver injury in nonalcoholic steatohepati-tis Dysregulated enteroadipocyte axis as a novel feature of fatty liver. Am J Clin Nutr. 2009 89(2) 55 8-567. [Pg.72]

Postprandial glucose-dependent insulinotropic polypeptide (GIP) levels were lowered in a guar-gum-supplemented meal (Morgan et al., 1990) and may contribute to lower insulin levels. Guar delays intestinal calcium absorption in humans (Gulliford et al., 1988b). The decrease in pancreatic amylase release may simply be a result of diminished insular-exocrine axis. [Pg.152]

GIP Glucose-dependent-insulinotropic polypeptide = Gastric inhibitory peptide... [Pg.253]

Glucose-Dependent Insulinotropic Polypeptide (GIP) Analogs (Incretin Hormone Analog o-Ala2GIP)... [Pg.442]

Gastric inhibitory polypeptide, glucose-dependent insulinotropic polypeptide. [Pg.139]

Fig. 1. Peptide structures of the two main incretin hormones, glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, GIP), and glucagon-like peptide 1 (GLP-1). Amino acids shared between both peptides are shown in dark blue, and amino acids unique to GIP and GLP-1 are shown in light and dark green, respectively. The red arrow indicates the position of cleavage by dipeptidyl peptidase-4 (DPP-4), the alanine residue in position 2, which is recognized by DPP-4, is highlighted by a red margin. Fig. 1. Peptide structures of the two main incretin hormones, glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, GIP), and glucagon-like peptide 1 (GLP-1). Amino acids shared between both peptides are shown in dark blue, and amino acids unique to GIP and GLP-1 are shown in light and dark green, respectively. The red arrow indicates the position of cleavage by dipeptidyl peptidase-4 (DPP-4), the alanine residue in position 2, which is recognized by DPP-4, is highlighted by a red margin.
Jones IR, Owens DR, Luzio S, Williams S, Hayes TM. The glucose dependent insulinotropic polypeptide response to oral glucose and mixed meals is increased in patients with type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia 1989 32 668-677. [Pg.134]

Jones IR, Owens DR, Moody AJ, Lnzio SD, Morris T, Hayes TM. The effects of glucose-dependent insulinotropic polypeptide infused at physiological concentrations in normal snbjects and Type 2 (non-insulin-dependent) diabetic patients on glncose tolerance and B-cell secretion. Diabetologia 1987 30 707-712. [Pg.134]

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