High blood glucose levels trigger the release of Insulin from the pancreatic islets. It then acts on plasmalemmal receptors of a number of different types of cells, most importantly hepatic, muscle and adipose tissue cells. On all of these cells, insulin functions to stimulate the uptake of glucose where it can be metabolized and stored as glycogen or used in the synthesis of proteins or fats.
In fat cells, insulin stimulates glucose uptake which results in increased catabolism of sugar to glycerol. it also activates endothelial cell lipoprotein lipase which triggers the release of FFAs from chylomicrons. the fatty acids are then transported into fat cells where along with glycerol they form triglycerides. These are then added to lipid droplets within adipose cells. this lipid synthesis is stimulated by insulin because it activates enzymes involved such as citrate lipase, acetyl- CoA carboxylase, fatty acid synthase and glycerol-3-phosphate dehydrogenase.
Insulin also acts on the liver to activate glycogen synthetase which is an enzyme that works to stimulate glycogen formation from glucose. It also indirectly stimulates the conversion of intracellular glucose to glucose-6-PO4 which prevents the release of glucose from hepatocytes.
In muscle cells, insulin prompts the active transport of glucose and amino acids which thus enhances protein synthesis.
Insulin is also plays a role in potassium homeostasis whereby insulin stimulates potassium uptake by cells and can result in extracellular hypokalemia (Hadley and Levine 243).
The secretion of insulin is controlled by a number of physiological regulators including endocrine, neural and metabolic factors with blood glucose being the most important. As mentioned above, increased blood glucose levels stimulate the release of insulin. Insulin secretion is also stimulated by amino acids and is important in using these for protein synthesis. Catecholamines such as adrenal epinephrine inhibit insulin secretion during stress. this is important so that glucose can be used by tissues that are active during stress response.
Insulin is also involved in an important feedback loop with glucagon whereby increased glucagon stimulates insulin secretion from the beta cells of the pancreas and insulin then subdues glucagon secretion from the alpha cells. (Hadley and Levine 252-253)
Diabetes Mellitus is a disease characterized by high glucose levels in the blood resulting from a lack or resistance to insulin. It causes symptoms such as frequent urination and increased thirst. Left untreated, increased blood glucose greatly damages blood vessels leading to complications such as heart disease, possible amputations, blindness and death.
Type 1 diabetes also known as insulin-dependent diabetes mellitus occurs when there is a decrease in the number of insulin containing beta cells within the pancreas. This may occur due to a hereditary predisposition or to the development of islet cell surface antibodies, however the signals responsible for production of these antibodies are unknown. There is evidence to suggest that type 1 juvenile onset diabetes can be caused by a virus or symptoms can manifest as a result of damage sustained by infections such as mumps or rubella. Onset of Type 1 diabetes usually occurs early in life. Juvenile onset diabetes occurs in youth where symptoms develop suddenly. Type 1 diabetes is typically treated with regulated insulin injections. Insulin can not be taken orally since it is a protein and would be digested. (Hadley and Levine 255-256).
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Type 2 diabetes is also known as non-insulin dependent diabetes mellitus arrises not from a lack of insulin as in type 1, but a reduced sensitivity of target tissues to the action of insulin. This is referred to as insulin resistance. Patients with Type 2 diabetes often have hyperinsulinemia, which is an elevation in blood insulin levels as a result of over secretion from the pancreas due to elevated blood glucose. Since target tissues are less sensitive to insulin, blood glucose levels remain high despite the increases in insulin . Type 2 diabetes was formerly referred to as adult onset diabetes because it was typically found in middle age adults who were obese or overweight. However, due to the increase incidence of obesity in children, there has been an increase in occurrence of type 2 diabetes in younger individuals. Therefore Type 2 diabetes is no longer referred to as an adult onset disease. Type 2 diabetes is responsible for approximately 90% of diabetes cases. It is often the result of poor lifestyle choices including bad diet and lack of exercise. This results in frequent high blood glucose levels and either not enough insulin to make up for it or an increased insensitivity of cells to insulin. Type 2 diabetes can thus be treated by improving one's lifestyle by managing diet and increasing exercise. (Hadley and Levine 256-257).
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References:
Hadley, Mac E., and Jon E. Levine. Endocrinology. 6th ed. Upper Saddle River, NJ: Pearson, 2006. 241,243, 252-253, 255-257. Print.
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