Literature DB >> 9439558

Metabolic abnormalities in impaired glucose tolerance.

J E Gerich1.   

Abstract

Impaired glucose tolerance (IGT) is a state in which there is postprandial hyperglycemia (> 7.8 mmol/L, or 140 mg/dL) with minimal elevations of fasting plasma glucose (> 5.5 < 7.8 mmol/L, > 100 < 140 mg/dL). This condition generally precedes the development of diabetes mellitus (DM) by several years. However, in IGT many of the metabolic abnormalities of DM are already present and provide insight into the pathogenesis of DM. Impaired early insulin release is the most consistent defect almost universally observed. Insulin resistance, attributable mainly to obesity, decreased physical fitness, or glucose toxicity, is also often present. The main reason that postprandial hyperglycemia occurs in IGT is impaired suppression of endogenous (hepatic and renal) glucose release; this can be largely explained by impaired early insulin release and impaired suppression of glucagon release. Postprandial glucose disposal is normal or increased, the result of hyperglycemia and delayed hyperinsulinemia. Postabsorptive (fasting) rates of glucose release and disposal and circulating levels of free fatty acids, glycerol, ketone bodies, lactate, and alanine are generally normal.

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Year:  1997        PMID: 9439558     DOI: 10.1016/s0026-0495(97)90316-4

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


  8 in total

1.  Glucagon secretion in relation to insulin sensitivity in healthy subjects.

Authors:  B Ahrén
Journal:  Diabetologia       Date:  2005-12-17       Impact factor: 10.122

Review 2.  Central nervous system regulation of eating: Insights from human brain imaging.

Authors:  Olivia M Farr; Chiang-Shan R Li; Christos S Mantzoros
Journal:  Metabolism       Date:  2016-02-06       Impact factor: 8.694

Review 3.  Regulation of Glucose Production in the Pathogenesis of Type 2 Diabetes.

Authors:  Ashot Sargsyan; Mark A Herman
Journal:  Curr Diab Rep       Date:  2019-08-03       Impact factor: 4.810

4.  Plasma levels of marine n-3 fatty acids and cardiovascular risk markers in renal transplant recipients.

Authors:  I A Eide; D O Dahle; M Svensson; A Hartmann; A Åsberg; K S Bjerve; J H Christensen; E B Schmidt; M E Lauritsen; K Lund; T Jenssen
Journal:  Eur J Clin Nutr       Date:  2016-03-02       Impact factor: 4.016

5.  Changing metabolic signatures of amino acids and lipids during the prediabetic period in a pig model with impaired incretin function and reduced β-cell mass.

Authors:  Simone Renner; Werner Römisch-Margl; Cornelia Prehn; Stefan Krebs; Jerzy Adamski; Burkhard Göke; Helmut Blum; Karsten Suhre; Adelbert A Roscher; Eckhard Wolf
Journal:  Diabetes       Date:  2012-04-09       Impact factor: 9.461

6.  Novel murine model of congenital diabetes: The insulin hyposecretion mouse.

Authors:  Kenta Nakano; Rieko Yanobu-Takanashi; Yuki Takahashi; Hayato Sasaki; Yukiko Shimizu; Tadashi Okamura; Nobuya Sasaki
Journal:  J Diabetes Investig       Date:  2018-08-17       Impact factor: 4.232

7.  Discriminatory ability of simple OGTT-based beta cell function indices for prediction of prediabetes and type 2 diabetes: the CODAM study.

Authors:  Louise J C J den Biggelaar; Simone J S Sep; Simone J P M Eussen; Andrea Mari; Ele Ferrannini; Marleen M J van Greevenbroek; Carla J H van der Kallen; Casper G Schalkwijk; Coen D A Stehouwer; Pieter C Dagnelie
Journal:  Diabetologia       Date:  2016-12-08       Impact factor: 10.122

8.  Low doses of bisphenol A and diethylstilbestrol impair Ca2+ signals in pancreatic alpha-cells through a nonclassical membrane estrogen receptor within intact islets of Langerhans.

Authors:  Paloma Alonso-Magdalena; Ouahiba Laribi; Ana B Ropero; Esther Fuentes; Cristina Ripoll; Bernat Soria; Angel Nadal
Journal:  Environ Health Perspect       Date:  2005-08       Impact factor: 9.031

  8 in total

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