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The etiology of type II diabetes mellitus (non-insulin- dependent diabetes mellitus, NIDDM) is even less clearly understood. Two factors have been identified:

a) Impaired insulin release-basal secretion of insulin is often normal, but rapid release of insulin follows a meal is greatly impaired, resulting in failure of normal handling of a carbohydrate load. In most patients, some level of insulin secretion is maintained, so that abnormality of glucose metabolism is limited and ketoacidosis is uncommon. In these patients, insulin secretion can be stimulated by drugs such as sulfonylureas. Exogenous insulin is therefore not essential in treatment. It also have been suggested that inheritance of a defective pattern of insulin secretion is responsible for familial tendency of diabetes. The genetic factor is very strong in type II diabetes, with a history of diabetes present in about 50% of first degree relatives.

b) Insulin resistance-a defect in tissue response to insulin is believed to play a major role. This phenomenon is called insulin resistance and is caused by defective insulin receptors on target cells. Insulin resistance occurs in association with obesity and pregnancy. In normal individuals who become obese or pregnant, B cells secrete increased amounts of insulin to compensate. Patients who have genetic susceptibility to diabetes cannot compensate because of their inherent defect in insulin secretion. Thus, type II diabetes is frequently precipitated by obesity and pregnancy. In a few patients with extreme insulin resistance, antibodies against receptors have been demonstrated in plasma. These antibodies are mostly of IgG class and act against insulin receptors, causing decreased numbers of insulin receptors and defective binding of insulin to receptors.

Other specific types of diabetes mellitus includes maturity-onset diabetes of young (MODY), diabetes due to mutant insulin, diabetes due to mutant insulin receptors, diabetes mellitus associated with a mutation of mitochondrial DNA and obese type 2 patients.