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Table of Contents
Vol. 50, No. 6, 2006
Issue release date: February 2007
Section title: Original Paper
Ann Nutr Metab 2006;50:499–505
(DOI:10.1159/000098141)

High-Fat- and Lipid-Induced Insulin Resistance in Rats: The Comparison of Glucose Metabolism, Plasma Resistin and Adiponectin Levels

Li L.a · Yang G.b · Li Q.a · Tang Y.b · Li K.b
aDepartment of Clinical Biochemistry and Key Laboratory of Laboratory Medical Diagnostics, Ministry of Education, and bDepartment of Endocrinology, Second Affiliated Hospital, Chongqing University of Medical Sciences, Chongqing, China

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 09, 2006
Accepted: August 08, 2006
Published online: February 07, 2007
Issue release date: February 2007

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 2

ISSN: 0250-6807 (Print)
eISSN: 1421-9697 (Online)

For additional information: http://www.karger.com/ANM

Abstract

Aims: In animal models, both an acute elevation in plasma free fatty acid (FFA) via intravenous infusion of a lipid emulsion and a chronic elevation in plasma FFA via high-fat feeding have been shown to induce skeletal muscle and liver insulin resistance. However, there have been very few studies comparing the effects of high-fat- and lipid-induced insulin resistance on glucose metabolism and adipocytokines. Methods: In the current study, we used lipid infusion and a high-fat feed in combination with the hyperinsulinemic-euglycemic clamp technique to assess the impact of acute and chronically elevated FFA levels on overall glucose metabolism and insulin action; two adipocytokines, resistin and adiponectin, were used. Results: At baseline, plasma FFA levels were significantly increased in the high-fat diet (HF) group compared to the control group (p < 0.05). During clamp steady-state, the FFA levels were reduced by ∼25% in the control and ∼48% in the HF groups. In contrast, there was a significant increase in the plasma FFA level in the lipid-infused group (from 0.82 ± 0.03 to 2.87 ± 0.18 mmol/l). The glucose infusion rates (GIRs) in the HF and lipid groups were obviously lower than in the control group (p < 0.01). Moreover, GIR was lower in the lipid group compared with the HF group (p < 0.05). The rate of glucose disappearance (GRd) was significantly lower in the lipid group compared with the control group. Hepatic glucose production in the control group was suppressed by ∼15% compared with the HF and lipid groups where it was suppressed by only ∼72 and ∼91%, respectively. The resistin level of muscle tissues in the lipid group was significantly higher compared with the control and HF groups (both p < 0.05). After the insulin clamp, the circulating adiponectin level was significantly decreased in the lipid group compared with the control and HF groups (p < 0.05). Conclusions: Lipid infusion, which was more effective than a high-fat diet, can induce peripheral and hepatic insulin resistance in rats. Insulin-induced resistance might be associated with elevated resistin and decreased adiponectin.

© 2006 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: January 09, 2006
Accepted: August 08, 2006
Published online: February 07, 2007
Issue release date: February 2007

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 2

ISSN: 0250-6807 (Print)
eISSN: 1421-9697 (Online)

For additional information: http://www.karger.com/ANM


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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