Exercise-Induced cytokines, diet, and inflammation and their role in adipose tissue metabolism.
Level 5 - mechanism / opinion, no new human data
Narrative/mechanistic review synthesizing molecular pathways without quantitative meta-analysis
PubMed 39221051 · doi:10.1002/hsr2.70034
What was done
The authors conducted a literature search across multiple databases to review the mechanistic roles of exercise-induced cytokines (including IL-6, IL-15, BDNF, irisin, myostatin, FGF21, follistatin, and ANGPTL4), dietary factors, and inflammation in regulating adipose tissue metabolism.
What was found
The abstract reports qualitative mechanistic pathways without quantitative summary statistics or numerical effect sizes. Identified pathways include IL-6 promoting fatty acid oxidation and reducing lipogenesis via AMPK activation; IL-15 upregulating PPARδ to stimulate fat catabolism; BDNF enhancing AMPK-dependent fat oxidation; irisin inducing browning of white adipose tissue and thermogenesis; and distinct roles for myostatin, FGF21, follistatin, and ANGPTL4 in modulating lipid uptake, adipogenesis, and oxidation.
Why it matters
Clarifying how specific exercise-derived signaling molecules interact with adipose tissue helps map biological pathways that could inform lifestyle or targeted therapeutic interventions for obesity management.
Limits
The abstract provides no quantitative data, effect sizes, or counts of included studies. As a broad narrative review, it synthesizes diverse preclinical and clinical mechanistic literature without meta-analytic pooling, risk-of-bias evaluation, or head-to-head clinical trial comparisons.
Cited by
- supports The surge of interleukin-6 released during exercise acts as a signal that activates AMP-activated protein kinase (AMPK) to stimulate fat mobilization and lower blood sugar.