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.
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.
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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