NIDDM

There are multiple causes of diabetes. Whereas the molecular bases of some forms of diabetes are well understood, in many cases etiologies are unknown. It is customary to divide diabetes into two main forms insulin-dependent diabetes mellitus (IDDM), also referred to as Type I or juvenile-onset diabetes, and noninsulin-dependent diabetes mellitus (NIDDM), also called Type II or maturity-onset diabetes (3). 

NIDDM is a much more common disease than IDDM, accounting for about 85—90% of all cases of diabetes meUitus. Whereas NIDDM may be present at any age, the incidence increases dramatically with advanced age over 10% of the population reaching 70 years of age has NIDDM. Patients with NIDDM do not require insulin treatment to maintain life or prevent the spontaneous occurrence of diabetic ketoacidosis. Therefore, NIDDM is frequendy asymptomatic and unrecognized, and diagnosis requires screening for elevations in blood or urinary sugar. Most forms of NIDDM are associated with a family history of the disease, and NIDDM is commonly associated with and exacerbated by obesity. The causes of NIDDM are not well understood and there may be many molecular defects which lead to NIDDM. 

Three classes of oral therapeutic agent are available for treating patients with diabetes mellitiis (NIDDM) the arylsulfonylureas (known simply as sulfonylureas), biguanides, and a-glycosidase inhibitors. Since 1977, only the sulfonylureas have been approved for use in the United States, although the other classes are used elsewhere. 

Relative potency alone does not determine dmg selection because maximal effectiveness is similar for all agents. A single daily dose of any sulfonylurea, except tolbutamide, is sometimes adequate to control blood glucose in NIDDM patients. 

Type 2 Diabetes (Previonsiy non-lnsnlin-Dependent Diabetes Mellitns, NIDDM)... 

Thorens B, Waeber G (1993) Glucagon-like peptide-I and the control of insulin secretion in the normal state and in NIDDM. Diabetes 42 1219-1225... 

Type 2—Noninsulin-dependent diabetes mellitus (NIDDM). Fonner names of this type of diabetes mellitus include maturity-onset diabetes, adult-onset diabetes, and stable diabetes. 

A L and WILLETT w c (1997a) Dietary fiber, glycemic load and risk of NIDDM in men. Diabetes Care. 20 (4) 545-50. 

De Fronzo, R. (1988). The triumvirate B cell, muscle, liver. A collusion responsible for NIDDM. Diabetes 34, 667-687. 

Non-insulin-dependent diabetes mellitus (NIDDM)-well controlled... 

NIDDM Non-insulin dependent diabetes mellitus PCR Polymerase chain reaction... 

Mutations in GK (Hx IV) causes maturity-onset diabetes of the young (MOD Y), a form of non-insulin-dependent diabetes mellitus (NIDDM) characterized by onset before 25 years of age and an autosomal dominant inheritance (PI 2). This suggests that the mutations in other forms of Hx may also contribute to the development of NIDDM. Among them, Hx II is a particularly attractive candidate, although this isozyme is not expressed in red blood cells. Hx II has been analyzed extensively in the muscle of prediabetic insulin-resistant individuals. But studies have shown that Hx II mutation alone is unlikely to have a significant role in the development of peripheral insulin resistance and NIDDM (L6). 

Auboeuf D, Rieusset J, Fajas L, Vallier P, Frering V, Riou JP, et al. Tissue distribution and quantification of the expression of mRNAs of peroxisome proliferator-activated receptors and liver X receptor-alpha in humans no alteration in adipose tissue of obese and NIDDM patients. Diabetes 1997 46 1319-1327. 

Frati AC, Gordillo BE, Altamirano P, Ariza CR, Cortes-Franco R and Chavez-Negrete A. 1990a. Acute hypoglycemic effect of Opuntia streptacantha Lemaire in NIDDM. Diabetes Care 13 155 156. 

It has already been noted above that hyperglycemia may affect nitric oxide production in different ways. Mohan and Das [129] demonstrated that NO prevented (3-cell damage in the model of alloxan-induced diabetes in rats. However, far more important data on the role of nitric oxide in diabetes development were obtained in the study of diabetic patients. Thus, Kedziora-Kornatowska [130] showed that there is difference in superoxide and NO production by the granulocytes from NIDDM patients NO production was increased in diabetic patients with and without diabetic nephropathy, while superoxide production was increased or decreased in the same patients, respectively. 

A 53-year-old female with NIDDM is started on a sulfonylurea. Which of the following is one mechanism of action of sulfonylureas ... 

Type 2 Peripheral tissue resistance to the action of insulin Insulin secretory defects Includes those formerly classified as adult onset diabetes, type II DM or non-insulin dependent diabetes mellitus (NIDDM). Ketosis is rare. 

Another form of diabetes is non-insulin-dependent diabetes mellitus (NIDDM, or adult diabetes, or type II diabetes). In this case, insulin is produced and a normal insulin level is detected in blood. But for various reasons its effect is reduced. This may be caused by a reduced number of insulin receptors on cells, or reduced effectiveness in binding to these receptors. The cause is complex and may involve genetic make-up, changes in lifestyle, nutritional habits, and environmental factors. 

In patients with type 1 insulin-dependent diabetes mellitus not adequately treated with insulin, fatty add release from adipose tissue and ketone synthesis in the liver exceed the ability of other tissues to metabolize them, and a profound, life-threatening ketoaddosis may ocxnir. An infection or trauma (causing an increase in cortisol or epinephrine) may predpitate an episode of ketoaddosis. Patients with type 2 non-insulin-dependent diabetes meUitus (NIDDM) are much less likely to show ketoaddosis. The basis for this observation is not completely understood, although type 2 disease has a much slower, insidious onset, and insulin resistance in the periphery is usually not complete. Type 2 diabetics can develop ketoacidosis after an infection or trauma. In certain populations with NIDDM, ketoaddosis is much more common than previously appredated. 

Tomino, Y., Makita, Y., Shike, T., et al. (1999) Relationship between polymorphism in the angiotensinogen, angiotensin-converting enzyme or angiotensin 11 receptor and renal progression in Japanese NIDDM patients. Nephron. 82, 139-144. 

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