Biology of Diabetes
Glucose is the body’s key source of energy hence is an essential nutrient in the body. Insulin on the other hand signals both alpha and beta cells to increase glucose uptake in case the body is experiencing hyperglycemia. The insulin is generated by the pancreas. An individual is said to be suffering from Diabetes when the glucose uptake function is impaired. This can only happen in either of two cases. In the first case, the insulin production process may be hampered. This results in the failure of the uptake of glucose by alpha and beta cells. Alternatively, the uptake itself may be hampered through the body’s inability to react appropriately to the insulin produced.
Glucagon has effects opposite those of insulin. Glucagon’s objective is to increase the production of fatty acids while insulin aids the conversion of fatty acids into triglycerides (Research and Education Association Editors, 2013).Diabetes is thus caused by a chain of reactions that result in destruction of insulin functioning in the body. This implies that most of those who suffer from diabetes have a series of underlying metabolic alterations (Alan, 2009).
Diabetes Mellitus is characterized by the insufficiency in the amount of insulin in the blood. This is where insulin production is impaired. The impacts of diabetes mellitus as such are many. For instance, the greatest impact is frailty as a result of reduced energy supply. Without insulin, the uptake of glucose is impaired leading to excretion of glucose with urine and reduced availability of glucose for energy production. In addition to this, diabetes patients also face dehydration as increased excretion of glucose results in increased loss of water and sodium from the body. The cause of diabetes insipid on the other hand is not yet known. However, both types of diabetes can be managed pharmacologically.
Research & Education Association Editors, Research and Education Association. Biology Problem Solver. New York: Research & Education Assoc, 2013.
Sinclair, Alan. Diabetes in Old Age. Chichester, UK: Wiley-Blackwell, 2009. Print.
CITATION Res13 l 1033 (Research & Education Association Editors)
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