Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperglycemic crises in type 2 diabetes are not rare and are becoming increasingly recognized as part of the spectrum of the presentation of previously undiagnosed diabetes mellitus and the decompensation of established diabetes mellitus. Contributing factors and associations are being elucidated but remain far from clear, particularly in DKA states. Medications commonly used in the treatment of many comorbid illnesses in patients with diabetes can themselves predispose to HHS. Endocrinopathies can contribute to insulin resistance and directly increase the glycemic load, leading to hyperglycemia. Medications such as the protease inhibitors may in the future lead to a better understanding of the pathophysiology of the metabolic derangements seen in the development of type 2 diabetes mellitus.
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PMID:Hyperglycemic crises in diabetes mellitus type 2. 1172 1

Our nation's battle with the bulge has contributed to the current co-epidemics of obesity and metabolic syndrome. The US Surgeon General's office reports that these disease risks may soon cause as much disease and death as cigarette smoking (HHS, 2001). In the United States, one in four adults has metabolic syndrome, which includes about 15 million persons with type 2 diabetes (Ford, 2002). About 50 percent of the estimated 47 million individuals with metabolic syndrome also have insulin resistance, which is a major factor in type 2 diabetes (Ford, 2002; Blackburn, 2001). Overweight and obese adults have a 50 to 100 percent increased risk for premature death compared to those of normal weight (HHS, 2001). The co-epidemics of obesity and metabolic syndrome are costly, as well, having an estimated price tag in 2000 of over $117 billion (HHS, 2001). This article will define the co-epidemics of obesity and metabolic syndrome and describe recommended prevention and management procedures to be adopted in home care.
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PMID:Metabolic syndrome & obesity: co-epidemics could overwhelm home health care. 1290 69

Lowering of low-density lipoprotein cholesterol with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) is clearly efficacious in the treatment and prevention of coronary artery disease. However, despite increasing use of statins, a significant number of coronary events still occur and many of such events take place in patients presenting with type 2 diabetes and metabolic syndrome. More and more attention is being paid now to combined atherogenic dyslipidemia which typically presents in patients with type 2 diabetes and metabolic syndrome. This mixed dyslipidemia (or "lipid quartet"): hypertriglyceridemia, low high-density lipoprotein cholesterol levels, a preponderance of small, dense low-density lipoprotein particles and an accumulation of cholesterol-rich remnant particles (e.g. high levels of apolipoprotein B)--emerged as the greatest "competitor" of low-density lipoprotein-cholesterol among lipid risk factors for cardiovascular disease. Most recent extensions of the fibrates trials (BIP - Bezafibrate Infarction Prevention study, HHS - Helsinki Heart Study, VAHIT--Veterans Affairs High-density lipoprotein cholesterol Intervention Trial and FIELD--Fenofibrate Intervention and Event Lowering in Diabetes) give further support to the hypothesis that patients with insulin-resistant syndromes such as diabetes and/or metabolic syndrome might be the ones to derive the most benefit from therapy with fibrates. However, different fibrates may have a somewhat different spectrum of effects. Other lipid-modifying strategies included using of niacin, ezetimibe, bile acid sequestrants and cholesteryl ester transfer protein inhibition. In addition, bezafibrate as pan-peroxisome proliferator activated receptor activator has clearly demonstrated beneficial pleiotropic effects related to glucose metabolism and insulin sensitivity. Because fibrates, niacin, ezetimibe and statins each regulate serum lipids by different mechanisms, combination therapy--selected on the basis of their safety and effectiveness - may offer particularly desirable benefits in patients with combined hyperlipidemia as compared with statins monotherapy.
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PMID:Atherogenic dyslipidemia in metabolic syndrome and type 2 diabetes: therapeutic options beyond statins. 1700 98

Fibrates primarily cause lowering of triglycerides and elevation of high density cholesterol levels. In WHO, HHS and VA-HIT trials fibrates were shown to decrease development of complications of cardiovascular diseases. Efficacy of fenofibrate in subjects with moderate risk and type 2 diabetes combined with mild dyslipidemia was studied in the placebo controlled FIELD study. Administration of fenofibrate was associated with insignificant 11% decrease of cardiovascular events (19% decrease after adjustment for statin use) and significant 24% decrease of nonfatal myocardial infarctions. Among effects on secondary end points were significant decreases of coronary revascularizations (-21%), strokes (-11%) and requrements in laser therapy for diabetic retinopathy (-30%). Fenofibrate also caused significant slowing of progression of albuminuria and nephropathy. Fenofibrate can be used in subjects with high coronary risk and metabolic syndrome combined with atherogenic dyslipidemia (total cholesterol/high density lipoprotein cholesterol >4 mmol/l), as well as in patients with moderate and pronounced hypertriglyceridemia or normal or elevated high density lipoprotein cholesterol. One of important indications for administration of fenofibrate is type 2 diabetes without ischemic heart disease but with microvascular complications. Fenofibrate can be also used in combination with other lipid lowering drugs (e.g. statins) in primary and secondary prevention for facilitation of achievement of target lipid levels.
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PMID:[Expediency of the use of fibrates for primary and secondary prevention of cardiovascular complications.]. 1731 Sep 61

Evidence of the effectiveness of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) within continuum of atherothrombotic conditions and particularly in the treatment and prevention of coronary heart disease (CHD) is well established. Large-scale, randomized, prospective trials involving patients with CHD have shown that statins reduce the clinical consequences of atherosclerosis, including cardiovascular deaths, nonfatal myocardial infarction and stroke, hospitalization for acute coronary syndrome and heart failure, as well as the need for coronary revascularization. Direct testing of varying degrees of low-density lipoprotein (LDL)- cholesterol lowering has now been carried out in 4 large outcomes trials: PROVE IT-TIMI 22, A to Z, TNT and IDEAL. However, the question whether more aggressive LDL-cholesterol lowering by high-dose statins monotherapy is an appropriate strategy is still open: higher doses of statins are more effective mainly for the prevention of the nonfatal cardiovascular events but such doses are associated with an increase in hepatotoxicity, myopathy and concerns regarding noncardiovascular death. Moreover, despite the increasing use of statins, a significant number of coronary events still occur and many such events take place in patients presenting with type 2 diabetes and metabolic syndrome. More and more attention is now being paid to combined atherogenic dyslipidemia which typically presented in patients with type 2 diabetes and metabolic syndrome. This mixed dyslipidemia (or 'lipid quartet') - hypertriglyceridemia, low high-density lipoprotein (HDL)-cholesterol levels, a preponderance of small, dense LDL particles and an accumulation of cholesterol-rich remnant particles - emerged as the greatest 'competitor' of LDL-cholesterol among lipid risk factors for cardiovascular disease. Most recent extensions of the fibrates trials (BIP, HHS, VAHIT and FIELD) give further support to the hypothesis that patients with insulin-resistant syndromes such as diabetes and/or metabolic syndrome might be the ones to derive the most benefit from therapy with fibrates. However, different fibrates may have a somewhat different spectrum of effects. Other lipid-modifying strategies included using of niacin, ezetimibe, bile acid sequestrants, CETP inhibitors and omega-3 fatty acids. Particularly, ezetimibe/statins combinations provide superior lipid-modifying benefits compared Tenenbaum/Fisman/Motro/Adler 128 with any statins monotherapy in patients with atherogenic dyslipidemia. Atherogenic dyslipidemia is associated with increased levels of chylomicrons and their remnants containing 3 main components: apolipoprotein B-48, triglycerides and cholesterol ester of intestinal origin. Reduction in accessibility for one of them (specifically cholesteryl ester lessening due to ezetimibe administration) could lead to a decrease of the entire production of chylomicrons and result in a decrease of the hepatic body triglycerides pool as confirmed in number of clinical studies. However, the ENHANCE study showed no difference in the progression of carotid atherosclerosis between ezetimibe/simvastatin vs. simvastatin alone over a 2-year period. Conclusions regarding ezetimibe/statins combinations should not be made until the three large clinical outcome trials will be completed within the next 2-3 years. In addition, bezafibrate as a pan-PPAR activator has clearly demonstrated beneficial pleiotropic effects related to glucose metabolism, insulin sensitivity and pancreatic beta cell protection. Because fibrates, niacin, ezetimibe, omega-3 fatty acids and statins each regulate serum lipids by different mechanisms, combination therapy - selected on the basis of their safety and effectiveness, could be more helpful in achieving a comprehensive lipid control as compared with statins monotherapy.
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PMID:Optimal management of combined dyslipidemia: what have we behind statins monotherapy? 1823 Sep 60