Insulin resistance forms

Diabetes mellitus is defined as hyperglycaemia (fasting > 7 mM and/or 2 h postprandial >11.1 mM) due to absolute or relative lack of insulin. The most common forms are type 1 diabetes (prevalence 0.25%), with absolute lack of insulin, and type 2 diabetes (prevalence 4-6%) which is due to the combination of insulin resistance and insufficient insulin secretion. 

Insulin resistance occurs when the normal response to a given amount of insulin is reduced. Resistance of liver to the effects of insulin results in inadequate suppression of hepatic glucose production insulin resistance of skeletal muscle reduces the amount of glucose taken out of the circulation into skeletal muscle for storage and insulin resistance of adipose tissue results in impaired suppression of lipolysis and increased levels of free fatty acids. Therefore, insulin resistance is associated with a cluster of metabolic abnormalities including elevated blood glucose levels, abnormal blood lipid profile (dyslipidemia), hypertension, and increased expression of inflammatory markers (inflammation). Insulin resistance and this cluster of metabolic abnormalities is strongly associated with obesity, predominantly abdominal (visceral) obesity, and physical inactivity and increased risk for type 2 diabetes, cardiovascular and renal disease, as well as some forms of cancer. In addition to obesity, other situations in which insulin resistance occurs includes... 

An individual can also become insulin resistant because of the development of antibodies gainst insulin. These patients have impaired receptor function and become so unresponsive to insulin that the daily dose requirement may be in excess of500 units per day (U/ d), rather than the usual 40 to 60 U/d. High-potency insulin in a concentrated form (U500 see the Summary Drug Table Insulin Preparations) is used for patients requiring more than 200 U/d. 

Type 2 DM is the most prevalent form of diabetes and accounts for approximately 90% to 95% of all diagnosed cases. Type 2 DM is usually slow and progressive in its development and often is preceded by pre-diabetes. Rising blood glucose levels result from increasing insulin resistance and impaired insulin secretion leading to a situation of relative insulin deficiency. 

Insulin is the one agent that can be used in all forms of DM for blood sugar control. Insulin is the essential treatment for patients with type 1 DM and can overcome insulin resistance in patients with type 2 DM. Insulin is available commercially in various formulations that vary markedly in terms of onset and duration of action and the source from which a product is obtained. Insulins can be divided into four separate classes based on their length of action. Most formulations are available as U-100, indicating a concentration of 100 units/mL. Insulin is typically refrigerated, and most vials are good for 28 days at room temperature. Specific details of insulin products are listed in Table 40-9. 

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). 

Oral antidiabetic agents might be indicated in noninsulin dependent diabetes mellitus (NIDDM), i.e. diabetes Type II where insulin resistance caused by down-regulation of insulin receptors or a failure of the pancreas to release insulin even though it is formed, play a role. However, oral antidiabetic... 

The sulfonylureas are ineffective for the management of type I and severe type II diabetes mellitus, since the number of viable -cells in these forms of diabetes is small. Severely obese diabetics often respond poorly to the sulfonylureas, possibly because of the insulin resistance that often accompanies obesity. 

Correct answer = A. Elevated blood glucose occurs in type 1 diabetes as a result of a lack of insulin. In type 2 diabetes, hyperglycemia is due to a defect in p cell function and insulin resistance. Both forms of the disease show complex genetics. Ketoacidosis is more common in type 1 disease. 

Noninsulin-dependent (type 2) diabetes is the prevalent form of diabetes mellitus found in populations chronically exposed to inorganic arsenic from the environment (Rahman et al, 1998 Tseng, 2002). Type 2 diabetes is characterized by insulin resistance of internal organs and peripheral tissues that results in impaired glucose utilization, and, consequently, in abnormally high blood glucose levels between and especially after meals. Insulin resistance and P-cell dysfunction can be induced by chronic arsenic exposure and these defects may be responsible for arsenic-induced diabetes mellitus (Tseng, 2004). 

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