Essay On Carbohydrates

There are numerous metabolic diseases that affect people all around the world. One of the most common metabolic diseases is diabetes which involves carbohydrate metabolism. Carbohydrate metabolism starts with digestion in the small intestine where simple carbohydrates are absorbed into the blood stream (1). Blood sugar (glucose) concentrations are managed by three hormones: insulin, glucagon, and epinephrine. When glucose concentrations in the blood become elevated, insulin is secreted by the pancreas. Insulin stimulates the transfer of glucose into the cells, especially in the liver and muscle tissue, although other organs are also able to process glucose (2).
In the liver and muscles, glycogen is produced from glucose by glycogenesis. Glycogen is stored in the liver and muscles glucose levels are low. When blood glucose levels are low, epinephrine and glucagon are secreted stimulating the conversion of glycogen to glucose (glycogenolysis). If there is an immediate need for energy upon glucose entering the cell, then glycoysis usually takes place. The end products of glycolysis are pyruvic acid and ATP. Since glycolysis releases small amounts ATP, further reactions continue to convert pyruvic acid to acetyl CoA and then citric acid in the citric acid cycle. The majority of the ATP is made from oxidations in the citric acid cycle in connection with the electron transport chain (3). This is how normal glucose metabolism takes place (figure-1).
Insulin is a major hormone controlling functions of glucose metabolism. It activates insulin receptor tyrosine kinase which phosphorylates and recruits different proteins from the IRS family of proteins (4). Once phosphorylated these proteins display binding sites for numerous signaling pat...

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...tochondrial lipid uptake (6). Therefore, evidence that lipid oxidation decreases throughout the body in people with obesity and insulin resistance as a result of impaired mitochondrial plasticity (7). It still remains unknown if insulin has direct and rapid effects on mitochondrial function. If insulin is responsible, the defects caused by IR might reflect deregulation of the lipid‑induced PPAR–PGC1 interaction after prolonged hyperlipidemia (8). This in effect leads to reduced lipid uptake into mitochondria in order to balance for lower mitochondrial content and increased lipids concentrations. As a result of this reduced lipid uptake, lipid induced uncoupling of the respiratory chain takes place, there is reduced oxidation of glycolytic substrates, which will detach fatty acid oxidation rates from citric acid cycle rates, resulting in metabolic distortion (7).