Abstract

Obesity is a complex metabolic disorder characterized by excessive adipose tissue accumulation, which contributes to chronic inflammation and metabolic dysfunction. Adipocytes, the primary cells within adipose tissue, play a crucial role in maintaining metabolic homeostasis through their ability to store and release energy in response to physiological cues. However, in obesity, adipocytes undergo significant alterations, including increased cellular stress within the endoplasmic reticulum (ER). The endoplasmic reticulum is a central organelle involved in protein folding and lipid biosynthesis, critical for adipocyte function. Under conditions of obesity, excessive lipid accumulation and nutrient overload can overwhelm ER capacity, leading to ER stress. This triggers the unfolded protein response (UPR), an adaptive mechanism aimed at restoring ER function and cellular homeostasis. However, chronic or unresolved ER stress contributes to adipocyte dysfunction, characterized by impaired insulin signaling, dysregulated lipid metabolism, and increased secretion of pro-inflammatory cytokines. Stress within the ER of adipocytes thus emerges as a pivotal mechanism linking obesity to adipose tissue dysfunction and associated metabolic complications. This abstract explores current research on the role of ER stress in adipocyte dysfunction within obese adipose tissue, highlighting its impact on systemic metabolic health and potential therapeutic strategies targeting ER stress pathways. Understanding the intricate interplay between stress responses in adipocytes and metabolic dysfunction is essential for developing targeted interventions to mitigate the adverse effects of obesity on health.