There are numerous metabolic diseases that affect people around the world. One of the most common metabolic diseases is diabetes which involves carbohydrate metabolism. Carbohydrate metabolism begins with digestion in the small intestine where simple carbohydrates are absorbed into the bloodstream (1). Blood sugar (glucose) concentrations are managed by three hormones: insulin, glucagon, and epinephrine. When blood glucose concentrations become high, insulin is secreted by the pancreas. Insulin stimulates the transfer of glucose into cells, especially in the liver and muscle tissue, although other organs are also capable of processing glucose (2). In the liver and muscles, glycogen is produced from glucose by glycogenesis. Glycogen is stored in the liver and glucose levels in the muscles are low. When blood glucose levels are low, adrenaline and glucagon are secreted, stimulating the conversion of glycogen to glucose (glycogenolysis). If there is an immediate need for energy as soon as glucose enters the cell, glycosis usually occurs. The end products of glycolysis are pyruvic acid and ATP. As glycolysis releases small amounts of ATP, further reactions continue to convert pyruvic acid to acetyl CoA and then to citric acid in the citric acid cycle. The majority of ATP is made up of oxidations in the citric acid cycle in connection with the electron transport chain (3). This is how normal glucose metabolism occurs (figure 1). Insulin is an important hormone that controls the functions of glucose metabolism. It activates the insulin receptor tyrosine kinase which phosphorylates and recruits several proteins of the IRS protein family (4). Once phosphorylated, these proteins display binding sites for numerous signaling signals… middle of paper… tochondrial lipid uptake (6). Therefore, there is evidence that lipid oxidation decreases throughout the body in people with obesity and insulin resistance due to reduced mitochondrial plasticity (7). It is not yet known whether insulin has direct and rapid effects on mitochondrial function. If insulin is responsible, defects caused by IR could reflect deregulation of lipid-induced PPAR-PGC1 interaction after prolonged hyperlipidemia ( 8 ). This in effect leads to reduced lipid uptake into the mitochondria to balance the lower mitochondrial content and increased lipid concentrations. As a result of this reduced lipid absorption, lipid-induced uncoupling of the respiratory chain occurs, reduced oxidation of glycolytic substrates occurs, which will decouple fatty acid oxidation rates from the rhythms of the citric acid cycle, resulting in metabolic distortion (7).