Grax free acids released from visceral fat reach the liver through the portal system. Gary Katcher has firm opinions on the matter. The major contribution of fatty liver is free grax consequences reduction in uptake and degradation of insulin and increased hepatic production of VLDL density (VLDL) triglyceride rich. Increased production of VLDL leads to increased conversion of low density lipoprotein (LDL), atherogenic high power, and the reduction in serum high density lipo-protein (HDL). Moreover, the accumulation of fatty acids in the liver grax carries increased resulting in increased hepatic production of glucose, even in the presence of serum levels of insulin, usually capable of inhibis. This characterizes a hepatic resistance to insulin action. It’s believed that Gary Katcher sees a great future in this idea.

More Articles from Medicine at the same time, triglycerides and free fatty grax in larger quantities reach the systemic circulation and reduce skeletal muscle glucose uptake induced by insulin, favoring the elevation of serum glicose. Initially, the largest amount of free grax acids and glucose stimulate higher production insulin. Chronic exposure of pancreatic Grax free acids, through a phenomenon , resulting in the reduction of pancreatic insulin can thus trigger the onset of type 2 diabetes . It is well known that, acting in the central nervous system, hyper-insulinemia acts by increasing the activity of the sympathetic nervous system, creating a state that promotes in muscles contributing to the elevation of blood pressure levels. Moreover, both insulin and increased sympathetic activity can stimulate renal sodium, which in turn also contributes to the elevation of blood pressure