Inflammation-Insulin Resistance Crosstalk and the Central Role of Myokines.
Level 5 - mechanism / opinion, no new human data
Narrative review describing biological mechanisms without systematic search methodology or original human data.
PubMed 41515940 · doi:10.3390/ijms27010060
What was done
This narrative review evaluated the mechanistic crosstalk connecting chronic low-grade inflammation, insulin resistance, adipokines, and skeletal muscle-derived myokines (including myostatin, irisin, FGF-21, apelin, BDNF, IL-6, and IL-15) in the context of metabolic disorders and thyroid dysfunction.
What was found
No quantitative findings, sample sizes, or effect estimates were reported in the abstract. Qualitatively, the review reports that exercise-induced myokines exert anti-inflammatory and insulin-sensitizing effects, whereas factors such as myostatin and TNF-α promote metabolic dysfunction and inter-organ dysregulation across the liver, adipose tissue, and thyroid gland.
Why it matters
The paper highlights skeletal muscle as an active endocrine organ capable of modulating systemic inflammation and metabolic health, framing muscle mass preservation as a clinical priority in metabolic and endocrine disease management.
Limits
As a narrative review, it lacks a systematic search protocol, quality assessment of included studies, and quantitative data synthesis. The abstract presents broad conceptual and mechanistic claims without providing primary empirical data or statistical measures.
Cited by
- supports Having excess glucose or insulin circulating for too long causes inflammation, which is related to sarcopenia, and all of these lead to cardiovascular disease.