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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperlipidemia is commonly observed in patients with type 2 diabetes and is also characteristic of the metabolic syndrome. We discuss the lipoprotein abnormalities in type 2 diabetes and the relation of triglyceride, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol to insulin resistance and diabetes. We also present a case study of a diabetic woman with hyperlipidemia and coronary artery disease.
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PMID:Management of patients with diabetic hyperlipidemia. 1267

The objective of this study was to examine the effect of the antihyperglycemic agents metformin (insulin sensitizer) and glibenclamide (insulin secretory agent) on the serum level of C-reactive protein (CRP) in well-controlled type 2 diabetics with metabolic syndrome. The participants were diabetic patients being followed in the medical outpatient clinic of King Abdulaziz University Hospital. The inclusion criteria were type 2 diabetics with the metabolic syndrome, well-controlled blood glucose on metformin alone or glibenclamide alone, and exclusion of major medical illness. Patients were divided into two groups according to the antihyperglycemic agent used. CRP level was measured 4-wk apart and the mean was calculated. The following data were collected from the study groups: age, sex, body mass index (BMI), duration of diabetes, smoking history, presence of hypertension, hyperlipidemia, and mean CRP level. A total of 110 patients were studied, 65 using metformin and 45 using glibenclamide. CRP level was significantly lower in patients using metformin for blood glucose control compared with those using glibenclamide, 5.56 and 8.3 mg/L, respectively (p = 0.01). A significantly higher level was observed in hypertensive and hyperlipidemic patients compared with normotensive and normolipidemic, 5.3 vs 3.2 mg/L and 7.1 vs 4.3 mg/L, respectively (p = 0.02, 0.01). There was a statistically significant correlation between CRP and BMI (r = 0.37) and age (r = 0.36) (all p = 0.01). The data showed that metformin decreases the level of circulating CRP, a marker of inflammation, more than glibenclamide.
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PMID:Effect of metformin and sulfonylurea on C-reactive protein level in well-controlled type 2 diabetics with metabolic syndrome. 1272 99

The incidence of diabetes has reached epidemic proportions across the world. In patients with diabetes, there is a two to four times increased risk of developing coronary artery disease (CAD). Diabetes seems to eliminate the protective benefits of hormones in women against CAD. Patients with type II diabetes also have hypertension, dyslipidemia, obesity, endothelial dysfunction and prothrombotic factors, called 'the metabolic syndrome'. Not only the incidence of CAD is higher in diabetes, the mortality of the diabetic patients after a cardiac event is significantly increased as compared to non-diabetics, including sudden death. Although in the past 35 years there has been a decline in the rate of death due to CAD in the general population, this has not been seen among patients with diabetes. Primary prevention can play an important role in decreasing the incidence of CAD in diabetic patients. Aggressive treatment of hyperlipidemia and hypertension is essential. Recent knowledge about the protective effects of aspirin, statins, angiotension converting enzyme inhibitors, and glitazones in the diabetic patients, if used appropriately will go a long way in primary and secondary prevention of CAD in patients with diabetes.
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PMID:Current concepts of cardiovascular diseases in diabetes mellitus. 1276 34

Insulin resistance and hyperinsulinemia are the critical characteristics of the metabolic syndrome that is associated with abdominal obesity and are the early manifestations of its progression to type 2 diabetes. These metabolic abnormalities are becoming recognized as a major contributor to cardiovascular disease. The experimental studies required to elucidate the underlying mechanisms and to develop effective preventative strategies will require the use of appropriate animal models and these are available. The evidence from such research indicates that a wide range of interventions (including peroxisome proliferator activator receptor agonists, insulin-sensitizing agents, statins, fibrates, angiotensin-converting enzyme inhibitors, estrogen receptor modulators, lipid-based nutriceuticals, and ethanol) can markedly reduce or prevent vasculopathy and ischemic cardiac lesions in animal models. Overall, the results suggest that early damage to the vascular wall, both in function and presenting as atherosclerotic lesions, is secondary to long-term hyperinsulinemia and, especially, to postprandial peaks in plasma insulin levels, and is exacerbated by the accompanying hyperlipidemia. Effective treatment will, of necessity, be preventative and will necessitate diagnostic approaches that can identify asymptomatic individuals at high risk for vascular damage and eventual progression to type 2 diabetes. Therapeutic targets in this population include insulin sensitivity and the associated signal transduction pathways, the peroxisome proliferator activator receptor-alpha and -gamma systems, and the complex pathways leading from acetyl CoA and the citric acid cycle to the synthesis of fatty acid and the storage of triglyceride. These pharmacological approaches offer the prospect of preventing a significant proportion of cardiovascular disease.
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PMID:Reduction and prevention of the cardiovascular sequelae of the insulin resistance syndrome. 1276 60

Type 2 diabetes mellitus and the closely related metabolic syndrome are associated with significant risk for cardiovascular disease. Recent evidence suggests that both conditions are increasing in epidemic proportions. Dyslipidemia is characterized by increased triglyceride-rich lipoproteins; low high-density lipoprotein cholesterol; small, dense low-density lipoprotein particles; increased postprandial lipemia; and abnormal apolipoprotein A1 and B metabolism. All these lipoprotein disturbances accelerate atherosclerosis in these patients. It is likely that many patients will need combinations of lipid-modifying therapy to achieve American Diabetes Association (ADA), Adult Treatment Panel III, and American Heart Association (AHA)/American College of Cardiology (ACC) guidelines to help prevent cardiovascular disease and death.
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PMID:Therapeutic approaches to dyslipidemia in diabetes mellitus and metabolic syndrome. 1285 29

Diabetic nephropathy has become the single largest cause of end-stage renal disease (ESRD) worldwide. Until recently, it was thought that once a patient developed overt proteinuria, diabetic nephropathy was irreversible and inevitably progressed to ESRD. However, the reversal of lesions caused by diabetic nephropathy (e.g., glomerular basement membrane thickening and mesangial matrix increase) has been demonstrated in a series of patients who underwent a pancreas transplantation 10 years prior to the reversal. Remission of nephrotic range proteinuria has also been reported in some patients with type 1 diabetes from the Collaborative Study Group during a median follow-up of 3 years of angiotensin-converting enzyme (ACE) inhibitor administration; no deterioration of renal function was observed in these patients. Remission and regression in nephropathy of type 1 diabetes patients have also been reported when blood pressure was controlled aggressively. Recent clinical trials have demonstrated that angiotensin II receptor blocker (ARB) preserved renal function and slowed the progression of nephropathy to ESRD in patients with type 2 diabetes. Since many patients with type 2 diabetes manifest with a metabolic syndrome, multifactorial intensive treatment is necessary; such treatment includes behavior modifications, dietary intervention, exercise, and smoking cessation. In this population, pharmacological therapy targeting hyperglycemia, hypertension (including ARB/ACE inhibitor), and hyperlipidemia in cases of type 2 diabetes is also necessary.
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PMID:Remission and regression of diabetic nephropathy. 1292 17

Especially the macrovascular risk and the reduced life expectancy emphasize that besides the optimal glycemic control in diabetes, the associated factors of metabolic syndrome, namely hypertension and hyperlipidemia, have to be treated with equal intensity. This will minimize additional diseases (e. g., atherosclerosis, nephropathy, retinopathy) and take some of the strain from our health care system in the long run. This article contains the current guidelines for the optimal treatment of hypertension and hyperlipidemia in diabetic patients.
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PMID:[Normalization of blood pressure and lipids in patients with diabetes]. 1293 2

Inflammation is a major factor in atherothrombotic disease. Levels of high-sensitivity C-reactive protein (hs-CRP), a marker of systemic inflammation and a mediator of atherothrombotic disease, have been shown to correlate with cardiovascular disease risk. Recent findings in 27,939 healthy women in the Women's Health Study indicate that hs-CRP (1) is a stronger predictor of risk than low-density lipoprotein (LDL) cholesterol, (2) predicts elevated risk in subjects without overt hyperlipidemia, and (3) adds prognostic information to risk scoring and LDL cholesterol categories. Other data from this cohort show that hs-CRP level adds prognostic information to the diagnosis of the metabolic syndrome. Taken together with other data in men on the association of hs-CRP with vascular risk, a strong argument is provided for screening in the primary prevention population. With regard to potential treatment, statins have been found to reduce hs-CRP levels, and data from statin treatment trials raise the possibility that subjects with elevated hs-CRP levels may derive greater benefit from treatment than do patients without elevated hs-CRP. The Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER) trial is planned to examine the effects of rosuvastatin treatment in preventing cardiovascular events in 15,000 healthy subjects with elevated hs-CRP levels in the absence of overt hyperlipidemia.
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PMID:High-sensitivity C-reactive protein and cardiovascular risk: rationale for screening and primary prevention. 1294 72

Metabolic abnormalities associated with the metabolic syndrome are also present in patients with type 2 diabetes mellitus and in those with familial combined hyperlipidemia (FCHL). These abnormalities include central obesity, insulin resistance with hyperinsulinemia, hypertension, increased plasma triglycerides, and decreased high-density lipoprotein cholesterol levels. Other characteristics associated with FCHL include the presence of small, dense low-density lipoprotein cholesterol and increased apolipoprotein B. Patients with these abnormalities are at an increased risk for premature coronary artery disease. Treatment of the dyslipidemia associated with type 2 diabetes and FCHL with a combination of a statin and a thiazolidinedione or niacin offers the most comprehensive modality to correct the various lipid abnormalities.
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PMID:Lipoprotein distribution in the metabolic syndrome, type 2 diabetes mellitus, and familial combined hyperlipidemia. 1295 24

Obesity, a state of increased adipose tissue mass, is a major cause for type 2 diabetes, hyperlipidemia, and hypertension, resulting in clustering of risk factors for atherosclerosis. Heterozygous PPARgamma knockout mice and KKA(y) mice administered with a PPARgamma antagonist were protected from high-fat diet-induced adipocyte hypertrophy and insulin resistance. Moderate reduction of PPARgamma activity prevented adipocyte hypertrophy, thereby diminution of TNFalpha, resistin, and FFA and upregulation of adiponectin and leptin. These alterations led to reduction of tissue TG content in muscle/liver, thereby ameliorating insulin resistance. Insulin resistance in the lipoatrophic mice and KKA(y) mice were ameliorated by replenishment of adiponectin. Moreover, adiponectin transgenic mice ameliorated insulin resistance and diabetes, but not the obesity of ob/ob mice. Furthermore, targeted disruption of the adiponectin gene caused moderate insulin resistance and glucose intolerance. In muscle, adiponectin activated AMP kinase and PPARgamma pathways, thereby increasing beta-oxidation of lipids, leading to decreased TG content, which ameliorated muscle insulin resistance. In the liver, adiponectin also activated AMPK, thereby downregulating PEPCK and G6Pase, leading to decreased glucose output from the liver. In conclusion, PPARgamma plays a central role in the regulation of adipocyte hypertrophy and insulin sensitivity. The upregulation of the adiponectin pathway by PPARgamma may play a role in the increased insulin sensitivity of heterozygous PPARgamma knockout mice, and activation of adiponectin pathway may provide novel therapeutic strategies for obesity-linked disorders such as type 2 diabetes and metabolic syndrome.
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PMID:[The mechanisms by which PPARgamma and adiponectin regulate glucose and lipid metabolism]. 1450 Nov 64


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