Nutrition and Oral Medicine (Nutrition and Health)

Chapter 11 / Diabetes Mellitus 187polyuria, polydipsia, polyphagia, weight loss, and fatigue occur in the setting of newonsetdiabetes in young patients whose disease is caused by profound insulin deficiency(Type 1) (5). T1DM, or insulin-dependent diabetes mellitus (IDDM), constitutes approx3–5% of all cases of diabetes mellitus and is related to autoimmune-mediated destructionof the insulin-producing -pancreatic islet cells. Thus, these patients are prone to diabeticketoacidosis, an acute and potentially life-threatening metabolic complication, and arecompletely dependent on exogenous insulin to sustain life. Ketoacidosis may developrapidly and lower the pH of the blood, leading to coma and death. The onset of signs andsymptoms of diabetes in these patients is relatively abrupt and usually occurs at a youngage (mean of 15 yr), although T1DM may arise at any age. The destruction of the -cellsin T1DM has been linked to the presence of certain major histocompatibility locusantigens (HLA), some of which are also associated with other autoimmune diseases (5).These autoimmune diseases include Hashimoto’s thyroiditis (hypothyroidism) andAddison’s disease (primary chronic adrenal insufficiency). The only genes definitelyassociated with T1DM are those of the major HLA. In T1DM, 95% of persons affectedexpress either HLA-DR3 or HLA-DR4, or both, compared with 40% of the generalpopulation (6). Thus, the overall clinical management of the individual with Type 1diabetes must take into careful consideration the potential for the development of otherautoimmune-mediated endocrine diseases characterized by hypofunction.2.2. Type 2 Diabetes MellitusType 2 diabetes mellitus (T2DM) accounts for approx 95% of all cases of diabetes. Theinsulin levels of affected patients may be normal, increased, or decreased, but there is noprofound insulin deficiency. However, over many years, the majority of individuals withT2DM show a continual decrease in their insulin levels. The etiology and pathogenesisof T2DM may be more heterogeneous with multiple biochemical or molecular lesions(5). These lesions may include impaired insulin secretion; a defect at the insulin receptor;a defect distal to the insulin receptor; or a defect in the hepatic uptake of glucose, contributingto insulin intolerance. These patients are not prone to ketoacidosis under basalconditions and are not completely dependent on exogenous insulin to sustain life. However,insulin treatment for patients with T2DM (25–30% of cases) can improve controlof hyperglycemia.The hyperglycemia in T2DM is not caused by autoimmune destruction of -cells; itis rather a failure of those cells to meet an increased demand for insulin (impaired insulinsecretion). Obesity is an overwhelming risk factor and is frequently associated withT2DM (6). Obesity and its associated high serum cholesterol can also further exacerbateaccelerated atherosclerosis that is frequently a preexisting component of clinical diabetes.The diagnosis of T2DM usually occurs after age 40. Eighty percent of adult diabeticsare obese or have a history of obesity. Among adults who are at least 25% over their idealbody weight, one out of five has elevated fasting blood sugar levels, and three out of fivehave abnormal oral glucose tolerance tests (5). Obesity increases insulin levels anddecreases the concentration of insulin receptors or their sensitivity in tissue, includingskeletal muscle and fat (clinical insulin resistance). Exercise increases the number ofinsulin receptors and improves insulin sensitivity, whereas a sedentary lifestyle is associatedwith glucose intolerance. Regular exercise with weight loss is associated with adecreased incidence of T2DM after adjusting for body mass index (5).