हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।
ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं
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.