Diabetes mellitus (DM) is best defined as a syndrome characterized by inappropriate fasting or postprandial hyperglycemia, caused by absolute or relative insulin deficiency and its metabolic consequences, which include disturbed metabolism of protein and fat. This syndrome results from a combination of deficiency of insulin secretion and its action. Diabetes mellitus occurs when the normal constant of the product of insulin secretion times insulin sensitivity, a parabolic function termed the “disposition index” (Figure 19-1), is inadequate to prevent hyperglycemia and its clinical consequences of polyuria, polydipsia, and weight loss. At high degrees of insulin sensitivity, small declines in the ability to secrete insulin cause only mild, clinically imperceptible defects in glucose metabolism. However, irrespective of insulin sensitivity, a minimum amount of insulin is necessary for normal metabolism. Thus, near absolute deficiency of insulin must result in severe metabolic disturbance as occurs in type 1 diabetes mellitus (T1DM). By contrast, with decreasing sensitivity to its action, higher amounts of insulin secretion are required for a normal disposition index. At a critical point in the disposition index curve (see Figure 19-1), a further small decrement in insulin sensitivity requires a large increase in insulin secretion; those who can mount these higher rates of insulin secretion retain normal glucose metabolism, whereas those who cannot increase their insulin secretion because of genetic or acquired defects now manifest clinical diabetes as occurs in type 2 diabetes (T2DM).
n a metabolic disorder caused primarily by a defect in the production of insulin by the islet cells of the pancreas, resulting in an inability to use carbohydrates. Characterized by hyperglycemia, glycosuria, polyuria, hyperlipemia (caused by imperfect catabolism of fats), acidosis, ketonuria, and a lowered resistance to infection. Periodontal manifestations if blood sugar is not being controlled may include recurrent and multiple periodontal abscesses, osteoporotic changes in alveolar bone, fungating masses of granulation tissue protruding from periodontal pockets, a lowered resistance to infection, and delay in healing after periodontal therapy. See also blood glucose level(s).
Can type 2 diabetes be cured? In the early stages of type 2 diabetes, it is possible to manage the diabetes to a level where symptoms go away and A1c reaches a normal level – this effectively “reverses” the progression of type 2 diabetes. According to research from Newcastle University, major weight loss can return insulin secretion to normal in people who had type 2 diabetes for four years or less. Indeed, it is commonly believed that significant weight loss and building muscle mass is the best way to reverse type 2 diabetes progression. However, it is important to note that reversing diabetes progression is not the same as curing type 2 diabetes – people still need to monitor their weight, diet, and exercise to ensure that type 2 diabetes does not progress. For many people who have had type 2 diabetes for a longer time, the damage to the beta cells progresses to the point at which it will never again be possible to make enough insulin to correctly control blood glucose, even with dramatic weight loss. But even in these people, weight loss is likely the best way to reduce the threat of complications.
Unlike many health conditions, diabetes is managed mostly by you, with support from your health care team (including your primary care doctor, foot doctor, dentist, eye doctor, registered dietitian nutritionist, diabetes educator, and pharmacist), family, and other important people in your life. Managing diabetes can be challenging, but everything you do to improve your health is worth it!
John P. Cunha, DO, is a U.S. board-certified Emergency Medicine Physician. Dr. Cunha's educational background includes a BS in Biology from Rutgers, the State University of New Jersey, and a DO from the Kansas City University of Medicine and Biosciences in Kansas City, MO. He completed residency training in Emergency Medicine at Newark Beth Israel Medical Center in Newark, New Jersey.
Jump up ^ Palmer, Suetonia C.; Mavridis, Dimitris; Nicolucci, Antonio; Johnson, David W.; Tonelli, Marcello; Craig, Jonathan C.; Maggo, Jasjot; Gray, Vanessa; De Berardis, Giorgia; Ruospo, Marinella; Natale, Patrizia; Saglimbene, Valeria; Badve, Sunil V.; Cho, Yeoungjee; Nadeau-Fredette, Annie-Claire; Burke, Michael; Faruque, Labib; Lloyd, Anita; Ahmad, Nasreen; Liu, Yuanchen; Tiv, Sophanny; Wiebe, Natasha; Strippoli, Giovanni F.M. (19 July 2016). "Comparison of Clinical Outcomes and Adverse Events Associated With Glucose-Lowering Drugs in Patients With Type 2 Diabetes". JAMA: the Journal of the American Medical Association. 316 (3): 313–24. doi:10.1001/jama.2016.9400. PMID 27434443.
What does the research say about proactive type 2 diabetes management? Research shows that proactive management can pay off in fewer complications down the road. In the landmark UKPDS study, 5,102 patients newly diagnosed with type 2 diabetes were followed for an average of 10 years to determine whether intensive use of blood glucose-lowering drugs would result in health benefits. Tighter average glucose control (an A1c of 7.0% vs. an A1c of 7.9%) reduced the rate of complications in the eyes, kidneys, and nervous system, by 25%. For every percentage point decrease in A1c (e.g., from 9% to 8%), there was a 25% reduction in diabetes-related deaths, and an 18% reduction in combined fatal and nonfatal heart attacks.
The ADA recommends using patient age as one consideration in the establishment of glycemic goals, with different targets for preprandial, bedtime/overnight, and hemoglobin A1c (HbA1c) levels in patients aged 0-6, 6-12, and 13-19 years.  Benefits of tight glycemic control include not only continued reductions in the rates of microvascular complications but also significant differences in cardiovascular events and overall mortality.