Cited by 443Adipokines, Inflammation, and Metabolic DiseasesMetabolism, Diabetes, and CancerAdipose Tissue and Metabolism

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Mechanism of Insulin Resistance in A-ZIP/F-1 Fatless Mice

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Kim, Jason K., Gavrilova, Oksana, Chen, Yan, Reitman, Marc L., Shulman, Gerald I.·2000·Journal of Biological Chemistry

DOI 10.1074/jbc.275.12.8456

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Abstract

Insulin resistance is a major factor in the pathogenesis of type 2 diabetes and may be related to alterations in fat metabolism. Fatless mice have been created using dominant-negative protein (A-ZIP/F-1) targeted gene expression in the adipocyte and shown to develop diabetes. To understand the mechanism responsible for the insulin resistance in these mice, we conducted hyperinsulinemic-euglycemic clamps in awake fatless and wild type littermates before the development of diabetes and examined insulin action and signaling in muscle and liver. We found the fatless mice to be severely insulin-resistant, which could be attributed to defects in insulin action in muscle and liver. Both of these abnormalities were associated with defects in insulin activation of insulin receptor substrate-1 and -2-associated phosphatidylinositol 3-kinase activity and a 2-fold increase in muscle and liver triglyceride content. We also show that upon transplantation of fat tissue into these mice, triglyceride content in muscle and liver returned to normal as does insulin signaling and action. In conclusion, these results suggest that the development of insulin resistance in type 2 diabetes may be due to alterations in the partitioning of fat between the adipocyte and muscle/liver leading to accumulation of triglyceride in the latter tissues with subsequent impairment of insulin signaling and action.

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Authors: Kim, J. K., Gavrilova, O., Chen, Y., Reitman, M. L., & Shulman, G. I.
Affiliations: Howard Hughes Medical Institute (US)
National Institutes of Health (US)
Corresponding author: Shulman, Gerald I.
ORCID: Kim, Jason K.
Gavrilova, Oksana
Reitman, Marc L.
Shulman, Gerald I.
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 2000-03
Volume: 275
Issue: 12
Pages: 8456-8460
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1074/jbc.275.12.8456
OpenAlex: W2111445543
Cited by: 443
References: 30
Citations by year: 2026: 3 · 2025: 3 · 2024: 7 · 2023: 4 · 2022: 8 · 2021: 13 · 2020: 12 · 2019: 15 · 2018: 10 · 2017: 19 · 2016: 18 · 2015: 18 · 2014: 14 · 2013: 19 · 2012: 17
FWCI: 25.12
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 7526 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: Eli Lilly and Company
National Institute of Diabetes and Digestive and Kidney Diseases (P30DK45735, R01-DK40936, R01DK040936, P30DK045735)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
Keywords: insulin resistance, type 2 diabetes, IRS-1, insulin receptor substrate 2, phosphatidylinositol 3-kinase, insulin signaling, liver triglyceride accumulation, fat partitioning, fat transplantation, hyperinsulinemic-euglycemic clamp
MeSH terms: Adipose Tissue, Animals, Body Composition, Insulin, Insulin Resistance, Liver, Mice, Mutant Strains, Mice, Transgenic, Muscles, Phosphoproteins, Transcription Factors, Glucose Clamp Technique, Phosphatidylinositol 3-Kinases, Intracellular Signaling Peptides and Proteins, Mice, Insulin Receptor Substrate Proteins

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Mechanism of Insulin Resistance in A-ZIP/F-1 Fatless Mice

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