Research
Hormonal
Phosphorylation of PPARγ at Ser273 selectively activates diabetic gene programs (causing insulin resistance) without affecting adipogenic or osteogenic programs, whereas Ser112 phosphorylation promotes osteogenesis.
This is a molecular mechanism. It explains why some diabetes drugs cause insulin resistance despite lowering blood sugar. Researchers are trying to block this specific phosphorylation to make better drugs.
GoodSupportsHIGH confidence
Briefly, in HFD induced obesity, protein kinase cyclin-dependent kinase 5 (Cdk5) is activated and in turn phosphorylates PPARγ at Ser273. This form of post-translational modified PPARγ selectively transactivates target genes involved in insulin resistance, without significant changes in adipogenic or osteogenic gene program.
Why this rating
Supported by multiple mechanistic studies cited.
Source
Deciphering the Roles of PPARγ in Adipocytes via Dynamic Change of Transcription Complex
Xinran Ma et al. · Frontiers in Endocrinology · 2018
DOI 10.3389/fendo.2018.00473
narrative_reviewCited 182×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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