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Leptin Signaling Suppression in Macrophages Improves Immunometabolic Outcomes in Obesity. | LitMetric

AI Article Synopsis

  • Obesity leads to low-grade inflammation, increasing the risk of insulin resistance, with leptin being a key player by regulating food intake and being elevated in obese individuals.
  • Leptin enhances macrophage responses to inflammation, promoting cytokine production and changes in mitochondrial function, thereby intensifying the inflammatory response.
  • Intervening in leptin signaling pathways may offer new strategies for treating obesity-related inflammation and improving insulin resistance.

Article Abstract

Obesity is a major concern for global health care systems. Systemic low-grade inflammation in obesity is a major risk factor for insulin resistance. Leptin is an adipokine secreted by the adipose tissue that functions by controlling food intake, leading to satiety. Leptin levels are increased in obesity. Here, we show that leptin enhances the effects of LPS in macrophages, intensifying the production of cytokines, glycolytic rates, and morphological and functional changes in the mitochondria through an mTORC2-dependent, mTORC1-independent mechanism. Leptin also boosts the effects of IL-4 in macrophages, leading to increased oxygen consumption, expression of macrophage markers associated with a tissue repair phenotype, and wound healing. In vivo, hyperleptinemia caused by diet-induced obesity increases the inflammatory response by macrophages. Deletion of leptin receptor and subsequently of leptin signaling in myeloid cells (ObR-/-) is sufficient to improve insulin resistance in obese mice and decrease systemic inflammation. Our results indicate that leptin acts as a systemic nutritional checkpoint to regulate macrophage fitness and contributes to obesity-induced inflammation and insulin resistance. Thus, specific interventions aimed at downstream modulators of leptin signaling may represent new therapeutic targets to treat obesity-induced systemic inflammation.

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Source
http://dx.doi.org/10.2337/db21-0842DOI Listing

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