Vol. 10, Issue 11, Part E (2024)

Abstract
Hypothalamic inflammation is increasingly recognized as a critical factor in the development and progression of diabetes mellitus, particularly type 2 diabetes. The hypothalamus, a central regulator of energy homeostasis, plays a crucial role in maintaining glucose and lipid metabolism. Chronic inflammation within the hypothalamus can disrupt these regulatory processes, leading to insulin resistance and impaired glucose tolerance, both hallmark features of diabetes mellitus. Key drivers of hypothalamic inflammation include high-fat diets, obesity, and elevated circulating levels of free fatty acids, which activate inflammatory pathways such as the nuclear factor-kappa B (NF-κB) and c-Jun N-terminal kinase (JNK) signaling cascades. These pathways result in the production of pro-inflammatory cytokines and chemokines, further exacerbating neuronal dysfunction and metabolic disturbances. Moreover, hypothalamic inflammation has been linked to the dysregulation of appetite and energy expenditure, contributing to the vicious cycle of obesity and metabolic syndrome that often precedes diabetes. Understanding the mechanisms underlying hypothalamic inflammation offers potential therapeutic avenues for preventing and managing diabetes mellitus, with emerging research focusing on anti-inflammatory strategies and interventions targeting hypothalamic function. As the global prevalence of diabetes continues to rise, addressing hypothalamic inflammation may hold promise for improving metabolic health and mitigating the burden of this chronic disease.