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Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice

Ahrén, Bo LU and Pacini, G (2002) In American Journal of Physiology: Endocrinology and Metabolism 283(4). p.738-744
Abstract
This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (S-G) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast,... (More)
This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (S-G) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast, early (10 min) insulin secretion was not sufficiently increased; DI10 min was reduced after 1, 3, and 10 mo. SG was reduced after 1 wk; the reduction persisted throughout the study period. Thus glucose intolerance induced by high-fat diet is, in early phases, solely explained by reduced glucose effectiveness, whereas insufficient early insulin secretion is of importance after long-term feeding. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
glucose intolerance, insulin secretion, glucose tolerance, high-fat diet
in
American Journal of Physiology: Endocrinology and Metabolism
volume
283
issue
4
pages
738 - 744
publisher
American Physiological Society
external identifiers
  • pmid:12217891
  • wos:000177873200014
  • scopus:0036785664
ISSN
1522-1555
DOI
10.1152/ajpendo.00199.2002
language
English
LU publication?
yes
id
13fd0bf7-ed1f-4e6d-8f66-9865c5443c0f (old id 329916)
date added to LUP
2007-08-06 13:47:15
date last changed
2017-12-10 04:34:52
@article{13fd0bf7-ed1f-4e6d-8f66-9865c5443c0f,
  abstract     = {This study evaluated the relative contribution of insulin-dependent mechanisms vs. mechanisms independent on dynamic insulin for glucose intolerance induced by high-fat diet. C57BL/6J mice underwent a frequently sampled intravenous glucose tolerance test (1 g/kg glucose) at 1 wk and 1, 3, and 10 mo after initiation of a high-fat diet (58% fat; control diet 11% fat) to measure glucose effectiveness (S-G) and disposition index (DI), i.e., insulin sensitivity (SI) times early or total insulin secretion. Glucose disappearance (KG) and SI were reduced in high-fat-fed mice at all time points. Total (50 min) insulin secretion was sufficiently increased at all time points to compensate for the reduced SI, as judged by normal DI50 min. In contrast, early (10 min) insulin secretion was not sufficiently increased; DI10 min was reduced after 1, 3, and 10 mo. SG was reduced after 1 wk; the reduction persisted throughout the study period. Thus glucose intolerance induced by high-fat diet is, in early phases, solely explained by reduced glucose effectiveness, whereas insufficient early insulin secretion is of importance after long-term feeding.},
  author       = {Ahrén, Bo and Pacini, G},
  issn         = {1522-1555},
  keyword      = {glucose intolerance,insulin secretion,glucose tolerance,high-fat diet},
  language     = {eng},
  number       = {4},
  pages        = {738--744},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Endocrinology and Metabolism},
  title        = {Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice},
  url          = {http://dx.doi.org/10.1152/ajpendo.00199.2002},
  volume       = {283},
  year         = {2002},
}