Research
Hormonal
Low-grade inflammation driven by adipose tissue expansion (secreting TNF-a, IL-6, leptin) directly contributes to insulin resistance and muscle protein catabolism, accelerating the progression of sarcopenic obesity.
Managing inflammation through lifestyle (diet, activity) is part of treating SO, as fat tissue actively secretes hormones that break down muscle and block insulin.
GoodSupportsHIGH confidence
Specifically, adipocytes promote macrophage recruitment... then adipocytes and immune cells secrete more adipokines such as leptin, chemerin, resistin, and more cytokines such as tumor necrosis factor-α (TNF-α), interleukins (ILs), interferon-γ (INF-γ)... creating a circumstance of low-grade inflammation. Previous studies have indicated that an inflammatory state plays a significant role in the progression of SO...
Why this rating
Supported by multiple cited studies linking inflammatory markers (IL-6, CRP, MCP-1) to SO.
Source
Diabetes and Sarcopenic Obesity: Pathogenesis, Diagnosis, and Treatments
Mina Wang et al. · Frontiers in Endocrinology · 2020
DOI 10.3389/fendo.2020.00568
narrative_reviewCited 221×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Sarcopenic obesity (SO) creates a synergistic, vicious cycle with diabetes where insulin resistance accelerates muscle catabolism and loss of muscle mass worsens insulin sensitivity, leading to significantly higher all-cause mortality and metabolic disorder risks than either condition alone.Good
- Dietary interventions for sarcopenic obesity should prioritize increased protein intake (1-1.5 g/kg/day) and chronic (not acute) caloric restriction combined with resistance training to prevent muscle loss during weight loss.Moderate
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