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

Early antihypertensive intervention in diabetes often means intervention in a cluster of cardiovascular risk factors including glucose intolerance per se, hyperlipidemia, obesity and hypertension, which are not just coexistent but may be causally linked together by the resistance of peripheral tissues to the action of insulin. Blood pressure lowering treatment should therefore be metabolically neutral in order to avoid aggravation of this risk factor syndrome. Clinical studies applying CE-inhibitors in type II diabetes are critically reviewed under this aspect. The majority of the available studies in type II diabetes report a reduction of insulin resistance and a marginal improvement of metabolic control. The order of magnitude in HbA1 reduction is nearly 10% of the glycosylated haemoglobin, reduction of fasting and postprandial blood glucose approximates 1 mmol/l. From a more extended view, considering essential hypertension as insulin resistant and thus possibly "prediabetic" state, this marginal metabolic effect gets further support from recent studies in essential hypertension consistently reporting an improvement of metabolic parameters of similar magnitude. This might become a central argument in the discussion about individualized and metabolically neutral antihypertensive treatment in essential hypertension.
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PMID:Clinical studies with CE-inhibitors in diabetes. 220 31

Underlying causes of hypertension are found in less than 5% of cases but they are frequently surgically remediable. Elementary biochemical tests are usually sufficient to exclude most renal and endocrine causes of hypertension. However, young patients with very high blood pressures merit more detailed investigation in specialized centres. As coexistent hyperlipidaemia or glucose intolerance substantially worsen the prognosis for a given level of blood pressure, these two risk factors are worth assessing in all hypertensive patients. Their presence may also alter the choice of antihypertensive drug therapy. About 25% of the population have raised blood pressure at first screening and about 10% are in need of drug therapy, so this represents an appreciable load on biochemical laboratories. Most patients, however, need only a single biochemical profile on one occasion, and should be exclusively managed in general practice.
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PMID:Biochemical investigation of hypertension. 189 56

We studied the prevalence of diabetes mellitus in Singapore and compared it to the study conducted ten years previously. A rise in prevalence rates from 2.0% to 4.7% was demonstrated. Impaired glucose tolerance (IGT) was studied for the first time, and a prevalence rate of 0.9% was found. Findings on chronic complications of diabetes were also reported. A high frequency of coronary heart disease and hypertension were detected in both diabetic and IGT subjects. Obesity and hyperlipidaemia were identified as important risk factors. This study demonstrates the scope and impact of diabetes mellitus as a major healthcare problem in Singapore. Strategies directed at prevention and control of this disease needs to be implemented so as to check its rising trend.
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PMID:Diabetes mellitus and its chronic complications in Singapore: an increasing healthcare problem. 222 12

We investigated whether or not obesity is related to increased factor VII activity. We studied 70 obese subjects (aged 25 to 50 years, 25 males and 45 females, body mass index (BMI): mean +/- SD = 32.44 +/- 5.44) and 33 non-obese subjects (aged 25 to 50 years, 12 males and 21 females, BMI: mean +/- SD = 21.80 +/- 1.70). None of them were smokers or affected by hyperlipidemia, diabetes mellitus, impaired glucose tolerance or arterial hypertension. Factor VII activity was measured by the coagulometric method. We found higher factor VII activity in obese subjects (115.74 +/- 26.10%) than in healthy subjects (98.55 +/- 23.49%, p less than 0.005). Increased factor VII levels could determine a thrombophilic state involved in the genesis of cardiovascular accidents in obesity.
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PMID:[Factor VII and cardiovascular risk in obese subjects]. 224 59

The JCR:LA-cp rat is a strain incorporating the corpulent (cp) gene. When homozygous for the cp gene, the rats are hyperphagous, hyperinsulinemic, hyperlipidemic and obese. The corpulent male rats develop atherosclerotic and myocardial lesions from an early age, while corpulent female and lean rats do not develop lesions. The hyperlipidemia is due to elevated levels of VLDL resulting in moderately raised cholesterol levels and markedly elevated triacylglycerol levels. The VLDL concentrations are similar in corpulent male and female rats at an early age with both having much higher levels than lean rats. As the animals age, the VLDL hyperlipidemia in the corpulent male increases at 3 months and then decreases slowly and rises again at 12 months of age. The corpulent female rats show higher triacylglycerol and phospholipid concentrations than the males at 3 months age and reach values over 1000 mg/100 ml by 9 months of age, then decrease at 12 months of age. The cholesterol concentrations of the corpulent females are greater than those of the males from 9 months of age. Thus, in the period of life up to middle age, the cardiovascular disease incidence does not correlate with the degree of hyperlipidemia. The disease progression does correlate with the severity of insulin resistance and glucose intolerance, which is more severe in the corpulent male than female rats. The results suggest that the hyperlipidemia must be a necessary condition for development of atherosclerotic disease in this strain of rats, but it is not a sufficient condition.
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PMID:Effect of age on serum lipids and lipoproteins of male and female JCR:LA-corpulent rats. 229 27

The antidiabetic effects of pioglitazone (5-[4-[2-(5-ethyl-2-pyridyl)ethoxy]benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) were examined in normal, obese, and/or diabetic animals. When orally administered to genetically obese and diabetic yellow KK mice (2.4-24.5 mg/kg/d), and Zucker fatty rats (0.1-10 mg/kg/d) for 4 days, pioglitazone markedly decreased hyperglycemia, hyperlipidemia, hyperinsulinemia, and glucose intolerance characterized as insulin resistant states in these animals. Pioglitazone potentiated insulin-mediated glucose metabolism in the diaphragm and adipose tissues of yellow KK mice and enhanced the glycemic response to exogenous insulin in Zucker fatty rats. Four-day administration of pioglitazone (1 mg/kg/d) to aged and obese beagle dogs with moderate insulin resistance decreased plasma glucose and lipids in the fasting state, and postprandial rises in plasma triglyceride. Pioglitazone decreased plasma lipids but did not alter the plasma glucose level in young normal rats. Pioglitazone did not alter plasma glucose and lipid levels in streptozocin-diabetic rats. These results indicate that pioglitazone is effective on abnormal glucose and lipid metabolism associated with insulin resistance by enhancing insulin action on peripheral tissues. Therefore, pioglitazone is expected to be useful in treating obese non-insulin-dependent diabetes.
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PMID:Effects of pioglitazone on glucose and lipid metabolism in normal and insulin resistant animals. 233 55

Hyperlipidemia, long recognized as a difficult and common problem following organ transplantation, may be the underlying cause of the accelerated atherosclerosis observed in heart transplant recipients and children with renal transplants. In addition, hyperlipidemia may play a role in late renal graft loss. The cause of post-transplant hyperlipidemia is unclear. In patients treated with azathioprine and prednisone, hypertriglyceridemia is the commonest finding and probably results from an increased consumption of calories from carbohydrate and fat following resolution of uremia, in conjunction with glucose intolerance secondary to steroid administration. In patients treated with cyclosporine, hypercholesterolemia is the most common form of hyperlipidemia. Cyclosporine is a lipophilic drug that is transported in the plasma, largely in association with lipoproteins, and may require the low-density lipoprotein (LDL) receptor for internalization into cells. Hypercholesterolemia may result from interference with the basic cholesterol feedback mechanism via the LDL receptor. In addition, cyclosporine affects bile acid synthesis and worsens glucose tolerance, both factors that may promote hyperlipidemia. The first therapeutic approach to hyperlipidemia in the transplant recipient is dietary calorie-fat restriction and supplementation with soluble fiber. Ongoing clinical trials of the available pharmacologic lipid-lowering agents are addressing the safety and efficacy of these agents in the setting of immunosuppression; until that time, they should be used cautiously and in low doses.
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PMID:Hyperlipidemia after organ transplantation. 248 50

Acute pancreatitis often results in a hyperdynamic, consumptive state. Hallmarks of this condition are decreased peripheral resistance with increased cardiac output. Hemodynamic and cardiovascular changes are accompanied by metabolic alterations. Increased protein catabolism, increased ureagenesis, glucose intolerance, increased lipolysis, and reduced servoregulation are metabolic changes commonly seen in this syndrome. To preserve organ structure and function, biochemical processes must be metabolically supported. Substrate needs change as stress level increases. The per cent of total calories provided as protein must increase. Branched-chain-enriched amino acid solutions have been shown to improve nitrogen utilization in hypermetabolic patients and may therefore be beneficial for the patient with acute pancreatitis. Glucose utilization decreases and free fatty oxidation increases. A mixed fuel system that provides fat, protein, and glucose is suggested for these patients. IV fat has been shown to be a safe energy substrate for patients with pancreatitis in the absence of hyperlipidemia. Failure to use fat as an energy substrate in conjunction with TPN may result in hepatic steatosis and excess carbon dioxide production. The decision of whether to use the parenteral or enteral route to nutritionally support the patient with pancreatitis remains controversial. TPN may allow maintenance of pancreatic rest. The role of enteral feedings is less clear. However, it has been shown that the further down the alimentary tract the feeding is infused, the less pancreatic stimulation occurs. Therefore, it seems wise to support the patient with TPN during severe acute pancreatitis. Jejunal enteral feedings should be initiated as a transitional feeding when the acute inflammatory episode begins to subside.
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PMID:Nutritional support in acute pancreatitis. 250 54

Studies were made on the diabetic state and the pathogenesis of myocardial disorders in KK mice with the following results: (1) KK mice showed glucose intolerance, hyperinsulinemia and hyperlipidemia; (2) their electrocardiograms (ECGs) showed a marked left-axis deviation of the QRS vector; (3) they showed epicardial calcification and myocardial disorders; (4) the Ca content of their myocardiums was much higher, and the Mg contents in the erythrocytes and myocardiums were much lower than those of control mice; (5) the addition of Mg to the drinking water of KK mice normalized these changes, and suppressed their myocardial disorders, but did not normalize their ECG changes. These results suggested that Mg deficiency plays an important role in the development of myocardial disorders in KK mice.
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PMID:Myocardial disorders caused by magnesium deficiency in diabetic KK mice. 261 21

Abnormalities of Zn metabolism are well documented in patients with chronic renal disease, especially those with nephrotic disease and uremia. The causes of Zn deficiency in kidney disease are not clear. Decreased dietary Zn intake and intestinal absorption, increased endogenous Zn secretion, and increased urinary Zn excretion (as in the nephrotic syndrome and in renal transplant recipients) all may contribute to altered Zn metabolism. Zn depletion may account for decreased taste, sexual and gonadal dysfunction, hyperprolactinemia, glucose intolerance, hyperlipidemia, growth retardation in children, neuropathy, anemia, abnormalities of neutrophil and lymphocyte function, and delayed wound healing. The benefit of pharmacologic doses of Zn, in the treatment of such manifestations, requires further evaluation under controlled conditions. Before use of Zn routinely for therapeutic purposes in uremic subjects, the cause(s) of abnormal Zn metabolism should be identified.
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PMID:Zinc in kidney disease. 267 56


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