The Effects of Rosiglitazone on Insulin Sensitivity, Lipolysis, and Hepatic and Skeletal Muscle Triglyceride Content in Patients With Type 2 Diabetes
Open accessAbstract
We examined the effect of three months of rosiglitazone treatment (4 mg b.i.d.) on whole-body insulin sensitivity and in vivo peripheral adipocyte insulin sensitivity as assessed by glycerol release in microdialysis from subcutaneous fat during a two-step (20 and 120 mU · m−2 · min−1) hyperinsulinemic-euglycemic clamp in nine type 2 diabetic subjects. In addition, the effects of rosiglitazone on liver and muscle triglyceride content were assessed by 1H-nuclear magnetic resonance spectroscopy. Rosiglitazone treatment resulted in a 68% (P < 0.002) and a 20% (P < 0.016) improvement in insulin-stimulated glucose metabolism during the low- and high- dosage−insulin clamps, respectively, which was associated with ∼40% reductions in plasma fatty acid concentration (P < 0.05) and hepatic triglyceride content (P < 0.05). These changes were associated with a 39% increase in extramyocellular lipid content (P < 0.05) and a 52% increase in the sensitivity of peripheral adipocytes to the inhibitory effects of insulin on lipolysis (P = 0.04). In conclusion, these results support the hypothesis that thiazolidinediones enhance insulin sensitivity in patients with type 2 diabetes by promoting increased insulin sensitivity in peripheral adipocytes, which results in lower plasma fatty acid concentrations and a redistribution of intracellular lipid from insulin responsive organs into peripheral adipocytes.
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Previous studies by our group and others have demonstrated a strong relationship between triglyceride content in liver and muscle and insulin resistance in these tissues.
“Previous studies by our group (9, 17-20) and others (7, 21, 22) have demonstrated a strong relationship between triglyceride content in liver and muscle and insulin resistance in these tissues.”
From Leptin reverses insulin resistance and hepatic steatosis in patients with severe lipodystrophy (2002) · cites this paper as [9]
Treatment for 3 months with rosiglitazone in patients with type 2 diabetes mellitus was associated with roughly 40% increase in extramyocellular triglyceride concentration.
“Treatment for 3 months with rosiglitazone was associated with an almost 40% reduction in hepatic triglyceride content, and roughly 40% increase in extramyocellular triglyceride concentration, and improved suppression of adipocyte lipolysis.133”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
Treatment for 3 months with rosiglitazone in patients with type 2 diabetes mellitus was associated with an almost 40% reduction in hepatic triglyceride content.
“Treatment for 3 months with rosiglitazone was associated with an almost 40% reduction in hepatic triglyceride content, and roughly 40% increase in extramyocellular triglyceride concentration, and improved suppression of adipocyte lipolysis.133”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
No reductions in the concentration of intramyocellular triglyceride were noted with rosiglitazone in this study.
“Though no reductions in the concentration of intramyocellular triglyceride were noted in this study, rosiglitazone improved insulin-mediated whole-body glucose disposal, consistent with improvements in muscle insulin sensitivity.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
Treatment for 3 months with rosiglitazone in patients with type 2 diabetes mellitus was associated with improved suppression of adipocyte lipolysis.
“Treatment for 3 months with rosiglitazone was associated with an almost 40% reduction in hepatic triglyceride content, and roughly 40% increase in extramyocellular triglyceride concentration, and improved suppression of adipocyte lipolysis.133”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
Thiazolidinediones, which are potent PPARγ agonists, can effectively reduce hepatic steatosis.
“Thiazolidinediones, which are potent PPARγ agonists, can effectively reduce hepatic steatosis.133”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
Reductions in intracellular diacylglycerol content account for the improvements in insulin sensitivity after weight loss and therapy with thiazolidinediones.
“Moreover, reductions in intracellular diacylglycerol content account for the improvements in insulin sensitivity after weight loss81 and therapy with thiazolidinediones.133”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
Rosiglitazone improved insulin-mediated whole-body glucose disposal, consistent with improvements in muscle insulin sensitivity.
“Though no reductions in the concentration of intramyocellular triglyceride were noted in this study, rosiglitazone improved insulin-mediated whole-body glucose disposal, consistent with improvements in muscle insulin sensitivity.”
From Lipid-induced insulin resistance: unravelling the mechanism (2010) · cites this paper as [133]
The TZDs improve insulin resistance by increasing glucose disposal in muscle and decreasing hepatic glucose output.
“The TZDs improve insulin resistance by increasing glucose disposal in muscle and decreasing hepatic glucose output.26”
From A pilot study of pioglitazone treatment for nonalcoholic steatohepatitis (2004) · cites this paper as [26]
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- Authors
- Mayerson, A. B., Hundal, R. S., Dufour, S., Lebon, V., Befroy, D., Cline, G. W., Enocksson, S., Inzucchi, S. E., Shulman, G. I., & Petersen, K. F.
- Affiliations
- Yale University (US)
- Howard Hughes Medical Institute (US)
- Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2002-03-01
- Volume
- 51
- Issue
- 3
- Pages
- 797-802
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC2995527
- OpenAlex
- W2100514340
- Cited by
- 647
- References
- 53
- Citations by year
- 2026: 12 · 2025: 6 · 2024: 11 · 2023: 15 · 2022: 4 · 2021: 5 · 2020: 7 · 2019: 20 · 2018: 12 · 2017: 15 · 2016: 15 · 2015: 22 · 2014: 20 · 2013: 22 · 2012: 16
- FWCI
- 24.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Yale University
- Deutsches Krebsforschungszentrum
- U.S. Public Health Service
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK45735, R01DK049230, R01 DK-49230, K23DK002734, P30DK045735)
- National Center for Research Resources (M01RR000125, M01 RR-00125)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- rosiglitazone, thiazolidinediones, type 2 diabetes, insulin sensitivity, hepatic triglyceride content, extramyocellular lipids, plasma fatty acids, hyperinsulinemic-euglycemic clamp, microdialysis, lipid redistribution
- MeSH terms
- Rosiglitazone, Adipose Tissue, Blood Glucose, Body Composition, Calorimetry, Indirect, Diabetes Mellitus, Type 2, Fatty Acids, Glycerol, Glycated Hemoglobin, Humans, Hyperinsulinism, Insulin, Kinetics, Lipids, Lipolysis, Liver, Middle Aged, Magnetic Resonance Spectroscopy, Oxidation-Reduction, Thiazoles, Triglycerides, Glucose Clamp Technique, Microdialysis, Adipocytes, Muscle, Skeletal, Thiazolidinediones
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