chemicals informative if their results were reported in terms of TCDD toxic equivalents (TEQs) or concentrations of specific congeners.


Diabetes mellitus is a group of heterogeneous metabolic disorders characterized by hyperglycemia and quantitative or qualitative deficiency of insulin action (Orchard et al., 1992). Although all forms share hyperglycemia, the pathogenic processes involved in its development differ. Most cases of diabetes mellitus are in one of two categories: type 1 diabetes is characterized by a lack of insulin caused by the destruction of insulin-producing cells in the pancreas (b cells), and type 2 diabetes is characterized by a combination of resistance to the actions of insulin and inadequate secretion of insulin (called relative insulin deficiency). In old classification systems, type 1 diabetes was called insulin-dependent diabetes mellitus or juvenile-onset diabetes mellitus, and type 2 was called non–insulin-dependent diabetes mellitus or adult-onset diabetes mellitus. The modern classification system recognizes that type 2 diabetes can occur in children and can require insulin treatment. Long-term complications of both types can include cardiovascular disease (CVD), nephropathy, retinopathy, neuropathy, and increased vulnerability to infections. Keeping blood sugar concentrations within the normal range is crucial for preventing complications.

About 90% of all cases of diabetes mellitus are of type 2. Onset can occur before the age of 30 years, and incidence increases steadily with age. The main risk factors are age, obesity, abdominal fat deposition, a history of gestational diabetes (in women), physical inactivity, ethnicity (prevalence is greater in blacks and Hispanics than in whites), and—perhaps most important—family history. The relative contributions of those features are not known. Prevalence and mortality statistics in the US population for 2006 are presented in Table 10-1.

The etiology of type 2 diabetes is unknown, but three major components have been identified: peripheral insulin resistance (thought by many to be primary) in target tissues (muscle, adipose tissue, and liver), a defect in β-cell secretion of insulin, and overproduction of glucose by the liver. In states of insulin resistance, insulin secretion is initially higher for each concentration of glucose than in people who do not have diabetes. That hyperinsulinemic state is a compensation for peripheral resistance and in many cases maintains normal glucose concentrations for years. Eventually, β-cell compensation becomes inadequate, and there is progression to overt diabetes with concomitant hyperglycemia. Why the β cells cease to produce sufficient insulin is not known. The onset of type 2 diabetes can be preceded by a set of clinical findings that are collectively called metabolic syndrome. A number of definitions of the syndrome have been proposed, but it typically includes a combination of high waist circumference, low high-density lipoprotein cholesterol, high triglycerides, high blood pressure, and high fasting glucose.

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