Cited by 129Peroxisome Proliferator-Activated ReceptorsAdipose Tissue and MetabolismMetabolism, Diabetes, and Cancer

Thiazolidinediones upregulate fatty acid uptake and oxidation in adipose tissue of diabetic patients.

Boden, Guenther, Homko, Carol, Mozzoli, Maria, Showe, Louise C., Nichols, Calen, Cheung, Peter·2005·Diabetes

Abstract

Thiazolidinediones (TZDs) are a new class of insulin-sensitizing drugs. To explore how and in which tissues they improve insulin action, we obtained fat and muscle biopsies from eight patients with type 2 diabetes before and 2 months after treatment with rosiglitazone (n = 5) or troglitazone (n = 3). TZD treatment was associated with a coordinated upregulation in the expression of genes and synthesis of proteins involved in fatty acid uptake, binding, beta-oxidation and electron transport, and oxidative phosphorylation in subcutaneous fat but not in skeletal muscle. These changes were accompanied by a 13% increase in total body fat oxidation, a 20% decrease in plasma free fatty acid levels, and a 46% increase in insulin-stimulated glucose uptake. We conclude that TZDs induced a coordinated stimulation of fatty acid uptake, oxidation, and oxidative phosphorylation in fat of diabetic patients and thus may have corrected, at least partially, a recently recognized defect in patients with type 2 diabetes consisting of reduced expression of genes related to oxidative metabolism and mitochondrial function.

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Crossref · 10.2337/diabetes.54.3.880

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  • Administration of thiazolidinediones induces changes in mitochondrial content and remodeling in white adipocytes concomitantly with an improvement in insulin sensitivity.

    “Administration of thiazolidinediones induces changes in mitochondrial content and remodeling in white adipocytes concomitantly with an improvement in insulin sensitivity (170, 173, 177, 190, 194 -198).”

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Authors
Boden, G., Homko, C., Mozzoli, M., Showe, L. C., Nichols, C., & Cheung, P.
Affiliations
  • Temple University (US)
  • The Wistar Institute (US)
Venue
Diabetes
Published
2005-03-01
Volume
54
Issue
3
Pages
880-885
ISSN
  • 0012-1797 (ISSN-L)
  • 1939-327X
OpenAlex
W2031020280
Cited by
129
References
44
Citations by year
2026: 2 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 6 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 5 · 2016: 5 · 2015: 6 · 2014: 4 · 2013: 8 · 2012: 6
FWCI
5.79
Type
journal article
Language
en
Open access
closed
Locations
  • Diabetes (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • American Diabetes Association
  • National Institutes of Health
  • National Institute on Aging (R01 AG 15353)
  • National Heart, Lung, and Blood Institute (R01-HL-0733267)
  • National Institute on Drug Abuse (P30-DA13429, P30DA013429)
  • National Cancer Institute (P30CA010815)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK58895, R01DK066003, R01DK058895)
  • NIH Clinical Center
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords
thiazolidinediones, rosiglitazone, troglitazone, type 2 diabetes, insulin sensitizers, fatty acid uptake, fatty acid oxidation, adipose tissue, skeletal muscle, fatty acid beta-oxidation, oxidative phosphorylation, mitochondrial function, plasma free fatty acids, insulin-stimulated glucose uptake, gene expression
MeSH terms
Rosiglitazone, Troglitazone, Adipose Tissue, Biological Transport, Chromans, Diabetes Mellitus, Type 2, Fatty Acids, Female, Humans, Hypoglycemic Agents, Male, Middle Aged, Oxidation-Reduction, Oxidative Phosphorylation, Up-Regulation, Gene Expression, Thiazolidinediones

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