Glucose metabolic syndrome

Metabolic Syndrome Insulin Receptor Glucose Transporters ATP-dependent K+ Channel Oral Antidiabetic Drugs... 

ATP III recognizes the metabolic syndrome as a secondary target of risk reduction after LDL-C has been addressed. This syndrome is characterized by abdominal obesity, atherogenic dyslipidemia (elevated triglycerides, small LDL particles, low HDL cholesterol), increased blood pressure, insulin resistance (with or without glucose intolerance), and prothrom-botic and proinflammatory states. If the metabolic syndrome is present, the patient is considered to have a CHD risk equivalent. 

Defects in glucose uptake into muscle cells are characteristic of insulin resistance in type 2 diabetes and the metabolic syndrome. This phenomenon is likely to be due to reduced activity of a transporter that operates by what mechanism ... 

Potatoes have been valued around the world for centuries because they are an easily cultivated, easily prepared and readily assimilated source of carbohydrate energy. The ease with which potatoes are digested has, however, become a double-edged sword, as the interrelated epidemics of metabolic syndrome and type 2 diabetes become global crises linked to rising obesity. At the same time as carbohydrates have been blamed for obesity, glucose intolerance has become recognized as a core feature of the metabolic syndrome and type 2 diabetes (Seidell, 2000). 

Abdominal obesity is associated with a threatening combination of metabolic abnormalities that includes glucose intolerance, insulin resistance, hyperinsulinemia, dyslipidemia (low HDL and elevated VLDL), and hypertension. This clustering of metabolic abnormalities has been referred to as syndrome X, the insulin resistance syndrome, or the metabolic syndrome. Individuals with this syndrome liave a significantly increased risk for developing diabetes mellitus and cardiovascular disorders. For example, men with the syndrome are three to four times more likely to die of cardiovascular disease. 

Joss EE, Zurbrugg RP, Tonz O, Mullis PE. Effect of growth hormone and oxandrolone treatment on glucose metabolism in Turner syndrome. A longitudinal study. Horm Res 2000 53(l) l-8. 

Bruning, J. C., Michael, M. D., Winnay, J. N., Hayashi, T., Horsch, D., Accili, D., et al. (1998) A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 2, 559-569. 

Any relationship between obesity and stroke is likely to be confounded by the positive association of obesity with hypertension, diabetes, hypercholesterolemia and lack of exercise, and the negative association with smoking and concurrent illness. Nevertheless, stroke is more common in the obese, and abdominal obesity appears to be an independent predictor of stroke (Suk et al. 2003). The constellation of metabolic abnormalities including central obesity, decreased high density lipoprotein, elevated triglycerides, elevated blood pressure and impaired glucose tolerance is known as the metabolic syndrome and is associated with a three-fold increase risk of type 2 diabetes and a two-fold increase in cardiovascular risk (Eckel et al. 2005 Grundy et al. 2005). 

Adipocytes have vitamin D receptors, and there is evidence that vitamin D may act as a suppressor of adipocyte development (Kawada et al., 1996). It has been suggested that vitamin D inadequacy may be a factor in the development of the metabolic syndrome ( syndrome X, the combination of insulin resistance, hyperlipidemia, and atherosclerosis associated with abdominal obesity). Sunlight exposure, and hence vitamin D status, may be a factor in the difference in incidence of atherosclerosis and myocardial infarction between northern and southern European countries in addition to effects on adipocyte development, calcitriol also enhances insulin secretion through induction of calbindin-D (Section 3.3.7.1), and there is some evidence vitamin D supplements can improve glucose tolerance (Boucher, 1998). 

Combination antiretroviral therapy is associated with redistribution of body fat in some patients ( lipodystrophy syndrome ), and protease inhibitors may disturb lipid and glucose metabolism. Appropriate laboratory tests to monitor these effects should be performed. 

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