From
Dr. Michael Helmrath
A shift in PKM2 oligomeric state instructs adipocyte inflammatory potential.
pubmed.ncbi.nlm.nih.gov shows its articles on its own site.
Read the article on pubmed.ncbi.nlm.nih.gov ↗Article · Nov 2026 · 1 min read
In brief
In brief
This study reveals how type I interferon signaling alters white adipocyte metabolism by shifting PKM2 oligomeric state, driving inflammatory responses that contribute to obesity-related systemic inflammation. The findings identify a novel metabolic-immune axis linking glycolysis reprogramming to adipose tissue dysfunction in obesity.
Written by the GCMD Library team from the article.
Processes that promote white adipocyte inflammatory function remain incompletely defined. Here, we demonstrated that type I interferon-dependent (IFN-I-dependent) skewing of adipocyte glycolysis, nicotinamide adenine dinucleotide (NAD+) utilization, and pyruvate kinase isozyme M2 (PKM2) function may contribute to increased systemic and tissue inflammation and disease severity in obesity. Notably, …
Statements in this article
Type I interferon-dependent skewing of adipocyte glycolysis, NAD+ utilization, and PKM2 function contributes to increased systemic and tissue inflammation and disease severity in obesity.
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