Immune cells may hold the key to fighting obesity-induced muscle dysfunction
One of the many ways obesity harms the human body is through damage to skeletal muscle. This progressive muscle decline, also known as sarcopenia, reduces strength, mobility and the ability to live independently. Unfortunately, most therapies for obesity and related conditions like type 2 diabetes focus solely on managing weight and blood glucose rather than addressing the loss of muscle mass and…
Obesity can lead to damage in skeletal muscles, causing a decline known as sarcopenia that reduces strength and mobility. Current obesity therapies focus on weight and blood glucose management, not muscle loss. Recent research indicates immune cells, particularly M2 macrophages, may help coordinate muscle repair by releasing signaling molecules.
Deleting transforming growth factor-beta 1 (TGF-β1) from a specific M2 macrophage subpopulation protects muscle from obesity-related dysfunction. Mice engineered to delete TGF-β1 in these cells performed better in tests of endurance, grip strength, and glucose tolerance compared to control mice, despite similar body weights. The deletion activated muscle-supporting cells, increased muscle-building hormones, and improved fat tissue signaling, enhancing mitochondrial function and energy metabolism.
These findings suggest TGF-β1 contributes to obesity-induced muscle decline through mechanisms that limit regeneration and impair mitochondrial function. Blocking TGF-β1 in humans could potentially improve muscle mass and function in sarcopenia patients, offering hope for better quality of life as obesity-related muscle loss becomes more common in aging populations.
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