Epidemiology and effects of Type 2 diabetes mellitus

Epidemiology of T2DM

The epidemiology of a disease or condition is evaluated in terms of its prevalence (the number of individuals affected by the condition) and incidence (the number of new cases recorded). The global prevalence of diabetes in the year 2000 was estimated to be 2.8%, with such estimates projected to increase to 4.4 % (366 million) by 2030 (Wild, Roglic, Green, Sicree & King, 2004). More recent data by WHO estimates the number of people with diabetes to be 346 million (WHO, 2011). T2DM is estimated to contribute up to 90% of diabetes cases (WHO, 2011; Campbell, 2000). In the U.S., approximately 8.3% of the population (25.8 million) is estimated to have diabetes with 18.8 million having been diagnosed whereas 7.0 million remain undiagnosed (Centers for Disease Control, 2011). The prevalence of diabetes increases in specific subgroups as compared to the general population. For instance, its prevalence increases in older population (≥ 65 years), obese individuals, individuals with a family history of the disease, and non-Caucasians (ADA, 2000; Lee, Brancati & Yeh, 2011; Strayer & Schub, 2011).

In respect to the incidence of diagnosed diabetes, it was estimated that up to 1.9 million cases of diabetes were diagnosed in 2010 in the US (CDC, 2011). The global incidence rate is likely to continue increasing with observations that in Asia and Africa, diabetes cases are likely to double by 2030 (Campbell, 2000; Wild et al. 2004, WHO, 2011). Diabetes is linked to 3.4 million deaths, with 80 % of diabetes deaths being recorded in underdeveloped and developing nations (WHO, 2011).

Effects on body systems

Effects of T2DM on body systems arise due to the inability of cells to respond to ingested glucose. Such reduced sensitivity to insulin results in the inability of cells to absorb glucose from the blood thus resulting into a scenario of high glucose concentration in blood amidst low concentration within the cell, after the consumption of a high carbohydrate diet (Lehninger, Nelson & Cox 2005, p. 909). Such a scenario signals for initiation of oxidation of fatty acids in the liver to compensate for energy requirements (Lehninger, Nelson & Cox 2005, p. 909). However, the acetyl-CoA produced by the β – oxidation is not completely oxidized due to the inhibition of the tricaboxylic acid cycle by a high NADH/NAD+ concentration (Lehninger, Nelson & Cox 2005, p. 907). The resultant accumulation of acetyly-CoA results into its conversion into ketone bodies, with the volatile ketone body, acetone, being exhaled in the breath of patients with uncontrolled diabetes (Lehninger, Nelson & Cox 2005, p. 909). Excessive production of ketone bodies could result into diabetic ketoacidosis due to a lowering of plasma pH following the ionization of such ketones in the blood (Lehninger, Nelson & Cox 2005, p. 909).

Apart from initiating the oxidation of fatty acids in the liver, T2DM impairs various other metabolic process. For instance, in T2DM glucagon secretion by α-pancreatic cells is not suppressed by high glucose concentrations in the blood (Casey, 2011). Accordingly, unlike in the case of healthy individuals, high levels of glucagon in the blood persist even with high glucose concentrations. Such glucagon levels signal for the mobilization of glycogen in the liver thus increasing the level of glucose in the blood – hyperglycemia (Casey, 2011; Zinman, 2011). Other hormones whose function is impaired by T2DM include amylin (regulates glucagon secretion, gastric emptying and satiety) and incretins (e.g. glucagon-like peptide, GLP -1, which reduces pancreatic β-cell workload) (Casey, 2011; Zinman, 2011). go to conclusion here.

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