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During Obesity and Diabetes, Microbiota and Receptors that Resemble Nod keep Metabolism and Inflammation in Check

Han Fang

Obesity and metabolism are intertwined factors that significantly impact human health. Obesity, characterized by excess body fat, leads to metabolic dysregulation and increases the risk of chronic diseases, such as type 2 diabetes and cardiovascular disorders. Metabolism encompasses the complex set of chemical processes that convert food into energy and other essential substances within the body. Understanding the relationship between obesity and metabolism is crucial for unraveling the underlying mechanisms contributing to weight gain and its impact on overall health. Metabolic alterations observed in obesity include insulin resistance, dyslipidemia, and chronic inflammation.Adipose tissue, hormonal regulation, and the gut microbiota play pivotal roles in energy balance, appetite regulation, and metabolic homeostasis. Genetic factors influence obesity and metabolism, with numerous genes identified through genome-wide association studies. Lifestyle modifications, including diet and exercise, are crucial for managing obesity and improving metabolic health. Further research is needed to explore epigenetics, the gut-brain axis, and environmental influences. Addressing the obesity epidemic and promoting metabolic health require a multidisciplinary approach involving healthcare professionals, policymakers, and individuals themselves. By promoting healthy lifestyle habits and personalized interventions, we can mitigate the impact of obesity on individuals and societies, leading to improved health outcomes.

During obesity, the host’s metabolism and immunity are affected by the gut microbiota. The innate immune system’s bacterial sensors transmit signals from specific bacterial components, or postbiotics, that may have opposing effects on metabolic inflammation in the host. Although they both recruit receptor-interacting protein kinase 2 (RIPK2), NOD-like receptors (NLRs) like Nod1 and Nod2 have distinct effects on blood glucose control. Nod1 links metabolic inflammation and insulin resistance to signals from the bacterial cell wall, whereas Nod2 can boost immune tolerance, insulin sensitivity, and better control of blood glucose during obesity. Inflammasomes that contain a pyrin domain belonging to the NLR family (NLRP) can also produce distinct metabolic outcomes. NLRP3 appears to have a bias toward IL- 1-mediated metabolic inflammation and insulin resistance, whereas NLRP1 protects against obesity and metabolic inflammation possibly due to a bias toward IL-18 regulation.