Type II Diabetes
The more prevalent type of diabetes is referred to as Type II or non-insulin-dependent diabetes mellitus (NIDDM). In the United States, about 5.2% of the population (13 million people) has diabetes; 90% of these cases are non-insulin dependent diabetes (NIDDM). Of these people, 90% can be classified as overweight or obese. Although this type of diabetes used to occur mostly in adults over 40 years of age, it is now being diagnosed in children as young as 10 years of age.
In NIDDM, insulin levels are typically elevated, indicating that the beta cells are functioning to produce what should be sufficient amounts of insulin, but a number of factors have caused the body’s cells to lose sensitivity to the hormone. Thus, blood sugar levels remain dangerously elevated.
Unlike Type I diabetes, which always results in a deficiency in insulin, there are a number of ways in which Type II diabetes manifests. In some patients, there is a decreased production of insulin, but this is not always the case. NIDDM with insulin resistance occurs when the body produces insulin, but becomes desensitized to it and thus fails to react. Some Type II patients may even have increased insulin production to compensate for this resistance.
Hyperinsulinemia is a frequently overlooked precursor to NIDDM, in which excessive secretions of insulin causes a condition similar to mild insulin shock, but more chronic in nature.
Causes of NIDDM
There are many proposed explanations of the mechanisms involved in the development of NIDDM. This type of diabetes is consistently associated with a diet high in refined foods, obesity, and a sedentary lifestyle.
Diet
A low-fiber diet that is high in refined sugars and fats can contribute to the development of reactive hypoglycemia. Refined carbohydrates cause a rapid rise in blood sugar levels, and the resulting insulin surges may lead to hypoglycemia. In response, the adrenal glands secrete epinephrine, cortisol, and other stress hormones to return blood sugar levels back to normal. If patients continually assault their bodies with this type of refined diet, it may result in both pancreatic and adrenal exhaustion.
Obesity
Obesity is a significant risk factor for developing NIDDM. Type II patients comprise about 90% of all diabetics, and of these, the vast majority are overweight or obese. In fact, excess weight is the primary predictor of Type II diabetes. A 2001 American random telephone survey of nearly 200,000 subjects concluded that being overweight or obese was significantly associated with diabetes, among other diseases. When compared with normal-weight subjects, those with a body mass index (BMI) of 40 or higher were more than seven times more likely to have been diagnosed with diabetes.
Research indicates that obesity often precedes the oversecretion of insulin. Oversecretion of insulin leads to resistance of the cells to the actions of insulin. This results in increased production of insulin by the pancreas and an ensuing vicious cycle that results in hyperinsulinemia, or high insulin levels in the blood. This can start early in life. Obesity in childhood and adolescence is significantly associated with insulin resistance, dyslipidemia, and elevated blood pressure in young adulthood. The good news, however, is that weight loss by obese young people has been shown to result in a decrease in insulin concentration and improvement in insulin sensitivity. On the basis of our current knowledge, it is, therefore, reasonable to suggest that lifestyle modification and weight control reduces the risk of developing Type II diabetes mellitus later in life.
Glucose Oxidation
Another postulated mechanism of how obesity contributes to the development of NIDDM is via a problem with the metabolism of glucose at the cellular level. Glucose metabolism is regulated by an enzyme known as pyruvate-dehydrogenase (PDH), and inhibited by isomers of another enzyme, pyruvate-dehydrogenase kinase (PDK). Increased levels of PDK may cause insulin resistance and increased fatty acid oxidation in NIDDM patients. Recent studies have found that obesity can cause increased levels of PDK, which impairs glucose oxidation and thus results in increased fatty acid oxidation.
Fortunately, this type of diabetes often responds exceptionally well to changes in diet, and in a large number of people can be prevented and even reversed entirely by making healthful lifestyle modifications.
Hepatic Insulin Sensitizing Substance
Glucose homeostasis is regulated both by the pancreas and the counter-regulatory responses of the adrenal gland and liver. The hormones involved include glucagon, catecholamines, growth hormone, and cortisol. The role of the liver in NIDDM has been demonstrated in both animal and human studies. Receptors on hepatic parasympathetic nerves release nitric oxide, which causes the release of hepatic insulin sensitizing substance (HISS). HISS sensitizes skeletal muscle to absorb insulin. Animal studies have shown that the blockade of nitric oxide release causes a secondary blockade of HISS, which results in insulin resistance.
Low Birth Weight
Low birth weight and poor infant nutrition create lifelong health risks and are contributing factors in the development of NIDDM. Inadequate calories during fetal growth may be diverted to the development of organs other than the pancreas, or may encourage genes to become thriftier in maximizing available calories. This is problematic in later periods of caloric abundance. The abnormal development of pancreas and adipose tissues resulting from decreased fetal nutrition thus contributes to hyperglycemia in adulthood.
Key Terms
Blood sugar: A measure of the amount of glucose in the blood. Control of blood glucose is the most vital component of diabetes management.
Glucagon: A hormone secreted by the pancreas, which increases the concentration of glucose in the blood.
Glycogen: A storage form of carbohydrate, which the body can convert to back to glucose when needed.
Insulin: A hormone secreted by the pancreas (beta cells), which is essential for the proper metabolism of glucose.
Insulin resistance: A cellular blunting of the effects of insulin on the ability to metabolize glucose.
