AJCN Cancer Health Disparities Conference
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Grimditch, G. K.
Right arrow Articles by Weitzman, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grimditch, G. K.
Right arrow Articles by Weitzman, D.
Agricola
Right arrow Articles by Grimditch, G. K.
Right arrow Articles by Weitzman, D.

American Journal of Clinical Nutrition, Vol 48, 38-43, Copyright © 1988 by The American Society for Clinical Nutrition, Inc

ORIGINAL RESEARCH COMMUNICATIONS

Peripheral insulin sensitivity as modified by diet and exercise training

GK Grimditch, RJ Barnard, L Hendricks and D Weitzman
Kinesiology Department, University of California, Los Angeles 90024.

To determine which component of a high-fat sucrose diet (HFS) caused insulin resistance and whether exercise training or fiber could prevent it, six dietary treatments were tested in rats: low-fat complex carbohydrate (LFCC); high-fat complex carbohydrate (HFCC); low-fat sucrose (LFS); high-fat sucrose (HFS); HFS plus fiber (HFS + F); and HFS plus exercise training (HFS + EX). After 10 wk rats were subjected to an intravenous glucose-tolerance test. The HFS and HFS + F groups developed glucose intolerance, as indicated by significantly greater areas under their glucose curves compared with the LFCC group's areas. The LFS, HFS, HFS + F, and HFS + EX groups developed insulin resistance, as indicated by significantly greater areas under their insulin curves compared with the LFCC and HFCC groups' areas. Either the presence of sucrose or the absence of complex carbohydrates, not high fat, was responsible for the insulin resistance and it was not improved by adding fiber to the diet or by exercise training.


This article has been cited by other articles:


Home page
 J. Dent. Res.Home page
E. Pekkala, L. Valikangas, M. Puukka, L. Tjaderhane, and M. Larmas
The Effect of a High-sucrose Diet on Dentin Formation and Dental Caries in Hyperinsulinemic Rats
J. Dent. Res., August 1, 2002; 81(8): 536 - 540.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. F. Youngren, J. Paik, and R. J. Barnard
Impaired insulin-receptor autophosphorylation is an early defect in fat-fed, insulin-resistant rats
J Appl Physiol, November 1, 2001; 91(5): 2240 - 2247.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
C. K. Roberts, N. D. Vaziri, K. H. Liang, and R. J. Barnard
Reversibility of Chronic Experimental Syndrome X by Diet Modification
Hypertension, May 1, 2001; 37(5): 1323 - 1328.
[Abstract] [Full Text] [PDF]

Home page
 J. Nutr.Home page
L. Tjäderhane and M. Larmas
A High Sucrose Diet Decreases the Mechanical Strength of Bones in Growing Rats
J. Nutr., October 1, 1998; 128(10): 1807 - 1810.
[Abstract] [Full Text]

Home page
 J. Appl. Physiol.Home page
R. J. Barnard, C. K. Roberts, S. M. Varon, and J. J. Berger
Diet-induced insulin resistance precedes other aspects of the metabolic syndrome
J Appl Physiol, April 1, 1998; 84(4): 1311 - 1315.
[Abstract] [Full Text] [PDF]

Home page
 J. Nutr.Home page
S. Huumonen, L. Tjäderhane, and M. Larmas
Greater Concentration of Dietary Sucrose Decreases Dentin Formation and Increases the Area of Dentinal Caries in Growing Rats
J. Nutr., November 1, 1997; 127(11): 2226 - 2230.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1988 by The American Society for Nutrition