Basic a condition in which there is an

Basic comprehension of normal insulin metabolism must be grasped in order for an understanding of the malfunctioning mechanisms leading to T2DM can be made. Insulin is a hormone that is produced in the ?-cells of the pancreas. In a healthy pancreas, there is a continuous release of insulin into the bloodstream in small pulsatile increments which increase with the ingestion of food. This facilitates a stable glucose range of approximately 3.5-8mmol/L.

With normal endogenous insulin secretion, post-prandial plasma insulin concentrations rise rapidly and peak at approximately one hour. As carbohydrate absorption from the gastrointestinal tract decreases, there is a decline in insulin concentrations towards pre-prandial values. Insulin works to lower blood glucose levels (BGL) by promoting the transport of glucose from the bloodstream across the plasma cell membrane to the cytoplasm of the cell. Four major metabolic abnormalities play a role in the development of T2DM; insulin resistance, decreased insulin production, excessive hepatic glucose production, and a dysfunction of adipokines. Insulin resistance is a condition in which there is an insufficient number of insulin receptors or these receptors are unresponsive. Both can also be seen simultaneously. This subsequently leads to hyperglycaemia as glucose is unable to enter the cells and BGL rises. A compensatory overproduction of insulin occurs in the early stages of insulin resistance (Diabetes Australia, 2015).

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This leads to a fatigue in ?-cells, and decreases the ability of the pancreas to produce insulin. Excessive hepatic glucose production refers to the inappropriate release of glucose by the liver that does not correspond to blood levels, causing constant hyperglycaemia. Adipokines, or adipose tissue, play a role in altered glucose and fat metabolism and is thought to cause chronic inflammation – which affects insulin sensitivity.

Although the exact cause is unknown, T2DM is a progressive condition that is associated with modifiable lifestyle risk factors (Diabetes Australia, 2015).


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