Diabetes mel´litus  (DM) a chronic syndrome of impaired carbohydrate, protein, and fat metabolism owing to insufficient secretion of insulin or to target tissue insulin resistance. It occurs in two major forms: type 1 d. mellitus, which differ in etiology, pathology, genetics, age of onset, and treatment. nephrogenic diabetes insipidus  inherited or acquired diabetes insipidus caused by failure of the renal tubules to reabsorb water in response to antidiuretic hormone, without disturbance in the renal filtration and solute excretion rates. non–insulin-dependent diabetes mellitus  (NIDD) (NIDDM) type 2 d. preclinical diabetes  former name for impaired glucose tolerance. subclinical diabetes  former name for impaired glucose tolerance. Type I diabetes mellitus  type 1 d. type 1 diabetes mellitus  one of the two major types of diabetes mellitus, characterized by abrupt onset of symptoms (often in early adolescence), insulinopenia, and dependence on exogenous insulin; it is due to lack of insulin production by the pancreatic beta cells. With inadequate control, hyperglycemia, protein wasting, and ketone body production occur; the hyperglycemia leads to overflow glycosuria, osmotic diuresis, hyperosmolarity, dehydration, and diabetic ketoacidosis, which can progress to nausea and vomiting, stupor, and potentially fatal hyperosmolar coma.

The associated angiopathy of blood vessels (particularly microangiopathy) affects the retinas, kidneys, and arteriolar basement membranes. Polyuria, polydipsia, polyphagia, weight loss, paresthesias, blurred vision, and irritability also occur. Type II diabetes mellitus  type 2 d. type 2 diabetes mellitus  one of the two major types of diabetes mellitus, peaking in onset between 50 and 60 years of age, characterized by gradual onset with few symptoms of metabolic disturbance (glycosuria and its consequences) and control by diet, with or without oral hypoglycemics but without exogenous insulin required. Basal insulin secretion is maintained at normal or reduced levels, but insulin release in response to a glucose load is delayed or reduced. Defective glucose receptors on the pancreatic beta cells may be involved. It is often accompanied by disease of blood vessels, particularly the large ones, leading to premature atherosclerosis with myocardial infarction or stroke syndrome

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