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Type 1 Diabetes

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Insulin Resistance and Beta Cell Dysfunction in
Type 2 Diabetes Mellitus
Andrea Kingsley
North Island College

Insulin Resistance and Beta Cell Dysfunction in Type 2 Diabetes Mellitus

Type 2 diabetes (T2D) is a disease that alters the health of individuals worldwide (Nolan, Damn, & Prentik, 2011). T2D requires a genetic predisposition, which, in combination with environmental factors and lifestyle leads to its development (McCance, 2012). Insulin resistance is a key factor responsible for the progression, which may lead to beta cell dysfunction (Schofield & Sutherland, 2012).
In the pre-diabetic phase, glucose levels remain normal but once beta cell dysfunction occurs, sufficient amounts of insulin secretion decreases (Ismail-Beigi, 2012). The purpose of this paper is to relate beta cell dysfunction and insulin resistance to the development of type 2 diabetes. In this paper I discuss both the pathogenesis and risk factors of the disease. I examine how the cells of the pancreas respond to increased glucose levels and how this progresses. I also consider the treatment and prevention of the disease.
Defining Diabetes Mellitus
Diabetes mellitus can be defined as a disorder that results in chronic hyperglycemia (McCance, 2010). T2D is characterized by insulin resistance and elevated glucose production, (Mannino & Sesti, 2012), associated with excessive lipid accumulation in tissue (Corpeleijn et al., 2008).
Etiology
T2D is a result of both genetic and environmental factors (McCance, 2010). It is an autosomal dominant disorder, although there is no pattern that determines the outcome (Irland, 2011). There are several genes that have been identified that correlate with the development of T2D, most of which code for beta cell mass and function (McCance, 2010). The progression to T2D requires environmental factors as well as physical

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