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The main role of brain in glucose homeostasis was put forward hundred of years ago. Recent studies show that brain process information from the adiposity signals such as leptin and insulin, which flows in proportion to body fat mass, and combines this inputs with nutrient signals. In response, the brain conveys signals to regulate feeding behavior and metabolism of substrate in a manner that encourages homeostasis of energy stores and fuel metabolism (Hotamisligil 54).
Both Insulin and leptin play a key role in the fundamental control of peripheral metabolism of glucose. Studies carried out on mice established that hypothalamic insulin receptor function causes hepatic insulin resistance and damaged reticence of hepatic glucose output. Peripheral and brain insulin are both important for typical insulin action. These studies also established that insulin and leptin encourages the expression of SOCS-3, and reduced neuronal expression of the same (Shah 1).
Obesity-related nutrients have a major effect on insulin action (Shah 2). Central integration of oleic acids enhances hepatic insulin sensitivity. Similar effects are experienced after infusion of an inhibitor CPT-1, which enhances hypothalamic fatty Acyl-CoA by reducing oxidation of obesity-associated nutrients (Hotamisligil 54). Central CPT-1 inhibition triggers neuron in the brain stem region that controls the parasympathetic outflow and increased hepatic insulin sensitivity through a process that entail activation of vagal efferent that supply the liver. Continuous increase in circulation of obesity associated nutrients results to ectopic fat storage such as triglycerides in the liver and muscles. Accumulation of ectopic lipid has also been attributed to insulin resistance (Sjoholm, and Thomas 611-612).
Given the explosion of candidate molecules, systems and pathway shown above, it is evident that many factors causes insulin resistance. Numerous endocrine, inflammatory and neural pathways simultaneously adjust signaling pathways that are cell intrinsic and functional in a range of metabolic tissues such as liver. These pathways and modulators are involved in chronic diseases such as tumors and autoimmune disorders.