Cargando…
Studies of insulin resistance in adipocytes induced by macrophage mediator
An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability...
Formato: | Texto |
---|---|
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
1983
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186991/ https://www.ncbi.nlm.nih.gov/pubmed/6833952 |
_version_ | 1782146070616211456 |
---|---|
collection | PubMed |
description | An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability of insulin to stimulate the uptake of glucose. The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. These studies offer a new in vitro model for investigating the molecular basis of insulin resistance. |
format | Text |
id | pubmed-2186991 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1983 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21869912008-04-17 Studies of insulin resistance in adipocytes induced by macrophage mediator J Exp Med Articles An apparent insulin resistance is noted in 3T3-L1 adipocytes after the addition of an endotoxin-induced mediator from macrophages. Examination at the level of the insulin receptor has revealed that the mediator does not effect either the functional ability of the cells to bind insulin or the ability of insulin to stimulate the uptake of glucose. The resistance appears to reflect a post-receptor interference with the insulin-induced biosynthesis of the anabolic enzymes, acetyl Co-A carboxylase and fatty acid synthetase, which are required for the conversion of glucose into storage lipid. These studies offer a new in vitro model for investigating the molecular basis of insulin resistance. The Rockefeller University Press 1983-04-01 /pmc/articles/PMC2186991/ /pubmed/6833952 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Studies of insulin resistance in adipocytes induced by macrophage mediator |
title | Studies of insulin resistance in adipocytes induced by macrophage mediator |
title_full | Studies of insulin resistance in adipocytes induced by macrophage mediator |
title_fullStr | Studies of insulin resistance in adipocytes induced by macrophage mediator |
title_full_unstemmed | Studies of insulin resistance in adipocytes induced by macrophage mediator |
title_short | Studies of insulin resistance in adipocytes induced by macrophage mediator |
title_sort | studies of insulin resistance in adipocytes induced by macrophage mediator |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2186991/ https://www.ncbi.nlm.nih.gov/pubmed/6833952 |