The article discusses the structural and functional differences between subcutaneous and visceral adipose tissue. Subcutaneous fat, which makes up about 80% of the body's total fat, is primarily composed of small, young adipocytes that actively absorb free fatty acids (FFAs) from the bloodstream and store triglycerides. In contrast, visceral fat, which accounts for 10-20% of body fat in men and 5-8% in women, contains larger, insulin-resistant adipocytes with high lipolytic activity. Visceral fat is more metabolically active and is characterized by increased vascularity, blood supply, and innervation compared to subcutaneous fat. Visceral fat is directly connected to the liver via the portal system, leading to the direct entry of FFAs and adipokines into the liver. This results in the activation of hepatic immune mechanisms, the production of pro-inflammatory mediators like C-reactive protein (CRP), and the development of insulin resistance. Visceral adipocytes are also more sensitive to catecholamine-induced lipolysis and less responsive to anti-lipolytic effects of insulin. Adipocytes in both types of fat tissue produce adipokines that influence energy balance, appetite, and insulin sensitivity. Subcutaneous fat is a significant source of leptin, while visceral fat is a major source of adiponectin. Visceral fat also produces other inflammatory cytokines and chemokines, contributing to the inflammatory state associated with obesity and diabetes. The accumulation of visceral fat is linked to hyperglycemia, hyperinsulinemia, hypertriglyceridemia, impaired glucose tolerance, and increased levels of lipoproteins rich in apolipoprotein B. Excess visceral fat increases the risk of cardiovascular disease, hypertension, and acute ischemic stroke. It is also a significant predictor of mortality, independent of body mass index (BMI). Despite these risks, visceral fat is more responsive to weight loss interventions compared to subcutaneous fat. Moderate weight loss can reduce inflammatory markers and improve adipokine levels, such as increasing plasma adiponectin levels. The article concludes that further research into the molecular and cellular mechanisms of adipocytes and adipokines is crucial for developing new therapeutic strategies to treat metabolic diseases.The article discusses the structural and functional differences between subcutaneous and visceral adipose tissue. Subcutaneous fat, which makes up about 80% of the body's total fat, is primarily composed of small, young adipocytes that actively absorb free fatty acids (FFAs) from the bloodstream and store triglycerides. In contrast, visceral fat, which accounts for 10-20% of body fat in men and 5-8% in women, contains larger, insulin-resistant adipocytes with high lipolytic activity. Visceral fat is more metabolically active and is characterized by increased vascularity, blood supply, and innervation compared to subcutaneous fat. Visceral fat is directly connected to the liver via the portal system, leading to the direct entry of FFAs and adipokines into the liver. This results in the activation of hepatic immune mechanisms, the production of pro-inflammatory mediators like C-reactive protein (CRP), and the development of insulin resistance. Visceral adipocytes are also more sensitive to catecholamine-induced lipolysis and less responsive to anti-lipolytic effects of insulin. Adipocytes in both types of fat tissue produce adipokines that influence energy balance, appetite, and insulin sensitivity. Subcutaneous fat is a significant source of leptin, while visceral fat is a major source of adiponectin. Visceral fat also produces other inflammatory cytokines and chemokines, contributing to the inflammatory state associated with obesity and diabetes. The accumulation of visceral fat is linked to hyperglycemia, hyperinsulinemia, hypertriglyceridemia, impaired glucose tolerance, and increased levels of lipoproteins rich in apolipoprotein B. Excess visceral fat increases the risk of cardiovascular disease, hypertension, and acute ischemic stroke. It is also a significant predictor of mortality, independent of body mass index (BMI). Despite these risks, visceral fat is more responsive to weight loss interventions compared to subcutaneous fat. Moderate weight loss can reduce inflammatory markers and improve adipokine levels, such as increasing plasma adiponectin levels. The article concludes that further research into the molecular and cellular mechanisms of adipocytes and adipokines is crucial for developing new therapeutic strategies to treat metabolic diseases.