Hormonal
Obesity-induced infiltration of proinflammatory immune cells (macrophages and T cells) into skeletal muscle adipose depots (IMAT/PMAT) drives local inflammation, which impairs myocyte insulin signaling and contributes to systemic insulin resistance.
In obesity, fat storage around muscle fibers triggers an immune response that blocks insulin from working effectively in muscle cells. This is a biological inflammatory process, not just a dietary failure. Addressing the underlying inflammation through weight loss and metabolic health improvements can help restore insulin sensitivity.
Increasing evidence suggests that inflammation occurs in skeletal muscle in obesity and is mainly manifested by increased immune cell infiltration and proinflammatory activation in intermyocellular and perimuscular adipose tissue. By secreting proinflammatory molecules, immune cells may induce myocyte inflammation, adversely regulate myocyte metabolism, and contribute to insulin resistance via paracine effects.
Why this rating
The paper is a comprehensive review citing numerous human and rodent studies, though it notes some inconsistencies in specific myokine data.
Source
Skeletal muscle inflammation and insulin resistance in obesity
Huaizhu Wu et al. · Journal of Clinical Investigation · 2017
DOI 10.1172/jci88880
More from this paper
- Chronic elevation of the myokine IL-6 in obesity contributes to insulin resistance, contrasting with its acute anti-inflammatory and insulin-sensitizing effects during exercise.Good
- Influx of free fatty acids (FFAs) and triglyceride-rich lipoproteins into skeletal muscle induces inflammation and insulin resistance via activation of TLR4, PKC, and JNK pathways.Good
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