Visceral Fat Accumulation and Glucose Metabolism: Significance of Mesenteric Fat Mass

Obesity and type 2 diabetes are increasing worldwide. It has been known that obesity is often accompanied by type 2 diabetes, dyslipidemia, hypertension, and atherosclerosis, conceptualized as metabolic syndrome. These can occur in mild obesity, as in Asians, but not necessarily in severe obesity. Body fat distribution, not absolute body weight, is important in pathogenesis under metabolic syndrome. Analysis of visceral fat using abdominal computed tomography (CT) has shown that the number of cardiovascular risk factors, including glucose intolerance, increases with increasing visceral fat area, but is not associated with subcutaneous fat area (1). Visceral fat consists of 3 components, mesenteric, omental, and retroperitoneal fat. Visceral fat, especially mesenteric fat, is anatomically located upstream of the liver via the portal vein and plays an important role in the temporary storage and supply of energy absorbed from the digestive tract. During starvation or fasting, lipolysis occurs efficiently in visceral fat first, and then it is metabolized into free fatty acids and glycerol, which are supplied to the liver. However, during visceral fat accumulation, a large amount of free fatty acids and glycerol flow into the liver due to the excessive lipolysis that occurs at the same time. Free fatty acids are the main source of fatty liver formation and also increase the excessive synthesis and secretion of very low-density lipoprotein, causing dyslipidemia, that is, hypertriglyceridemia. Glycerol serves as a substrate for gluconeogenesis, and its excess, combined with the gluconeogenic effects of free fatty acids, can contribute to the development of diabetes (2).