Hormonal
PPARγ ligands (thiazolidinediones) improve systemic insulin sensitivity and lipid profiles in type 2 diabetes by promoting adipocyte differentiation and sequestering free fatty acids into adipose tissue, thereby reducing ectopic lipid accumulation in muscle and liver.
For individuals with type 2 diabetes, PPARγ-activating medications (like TZDs) work by encouraging the body to store fat in adipose tissue rather than in the liver and muscles. This shift reduces insulin resistance and improves blood sugar control, provided the patient has functional fat tissue.
TZDs reduce circulating FFA levels and improve insulin sensitivity in muscle and liver due to promotion of adipocyte differentiation and FFA uptake.
Why this rating
Supported by multiple mouse models, human genetic studies, and clinical use of drugs like rosiglitazone and pioglitazone.
Source
PPARadigms and PPARadoxes: expanding roles for PPARγ in the control of lipid metabolism
Robert Walczak et al. · Journal of Lipid Research · 2002
DOI 10.1016/s0022-2275(20)30159-0
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