Insufficient islet compensation to insulin resistance vs. reduced glucose effectiveness in glucose-intolerant mice
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/329916
- author
- Ahrén, Bo LU and Pacini, G
- organization
- publishing date
- 2002
- 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
- 2016-04-01 16:36:35
- date last changed
- 2024-01-11 11:17:24
@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}},
keywords = {{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}},
doi = {{10.1152/ajpendo.00199.2002}},
volume = {{283}},
year = {{2002}},
}