Research
Hormonal
PPARγ agonists (glitazones) improve insulin sensitivity and lower glucose in type 2 diabetes by promoting fatty acid flux into adipose tissue, thereby reducing lipid interference with glucose utilization in muscle and liver.
Glitazones (like rosiglitazone and pioglitazone) treat type 2 diabetes by activating the PPARγ receptor. This shifts fatty acids into fat cells, allowing muscles and the liver to use glucose more effectively. They are insulin sensitizers, not insulin secretagogues.
StrongSupportsVERY_HIGH confidence
Our data provide evidence that the antidiabetic actions of PPARγ agonists are the consequence of coordinate regulation of gene expression in multiple insulin-sensitive tissues... The net effect of this fatty acid repartitioning is an increase in glucose oxidation in muscle and a decrease in glucose production by the liver.
Why this rating
Extensive evidence from binding assays, gene profiling, and animal models confirms the mechanism and efficacy.
Source
Peroxisome Proliferator-Activated Receptors: From Genes to Physiology
Steven A. Kliewer · Recent Progress in Hormone Research · 2001
DOI 10.1210/rp.56.1.239
narrative_reviewCited 426×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- PPARα agonists (fibrates) lower serum triglycerides and raise HDL cholesterol by directly binding to the PPARα receptor, thereby inducing genes involved in fatty acid oxidation and peroxisome proliferation.Good
- PPARs function as metabolic sensors that bind directly to a variety of natural fatty acids and oxidized fatty acid metabolites (eicosanoids), coupling fatty acid flux to the transcriptional regulation of lipid and glucose homeostasis genes.Good
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