Research

Hormonal

Muscle-specific PPARγ is not required for the antidiabetic effects of thiazolidinediones (TZDs); TZDs improve glucose homeostasis and insulin sensitivity in the absence of muscle PPARγ.

If you are taking a TZD (like rosiglitazone or pioglitazone), you do not need to worry that your muscle PPARγ status determines whether the drug will work for your blood sugar. The drug's ability to improve insulin sensitivity does not depend on the PPARγ receptor being present in your skeletal muscle. The benefit is likely mediated through other tissues, such as adipose tissue or the liver.

GoodRefutesHIGH confidence
Thus, muscle PPARγ is not required for the antidiabetic effects of TZDs, but has a hitherto unsuspected role for maintenance of normal adiposity, whole-body insulin sensitivity, and hepatic insulin action.
Andrew W. Norris et al. · Journal of Clinical Investigation · 2003

Why this rating

High-quality animal model (conditional knockout) with rigorous metabolic phenotyping (clamps), though not directly translatable to human clinical trials without further validation.

Source

Muscle-specific PPARγ-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones

Andrew W. Norris et al. · Journal of Clinical Investigation · 2003

DOI 10.1172/jci17305

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DOI resolved against Crossref · corpus check 2026-06-10

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