Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two sensitive and accurate methods for the determination of apo B using polyclonal antibody for human purified LDL are reported. Modified one step EIA by sandwich method is highly sensitive and serum has to be diluted by 1,000-3,000 times, but suited for the diagnosis of hypo or abetalipoproteinemia, detailed analyses of lipoprotein subfractions and in vitro study of lipoprotein metabolism. Latex method is moderately sensitive (serum dilution: 100 times), automated, simple and accurate with CV, 1.5-2.5%. Serum apo B assay is useful not only for the diagnosis of hyperlipidemia, hypolipidemia, but also for the analyses of atherogenic lipoproteins which are frequently associated with large vessel atherosclerotic changes in diabetes, obesity and coronary, cerebral or peripheral vascular diseases. A family pedigree of elevated apo B with frequent association of diabetes (type 2 b) and prominent hypercholesterolemia with autoimmune apo B antibody has been described. In obesity, either hyperinsulinemia or hyperglycemia plays a role in the elevation of VLDL and IDL probably through hepatic overproduction of VLDL. The size of VLDL tends to be larger in VLDL while IDL and LDL seem to become smaller judging from relative lipid contents to apo B.
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PMID:[Highly sensitive apo B assay and its clinical significance]. 223 45

In 102 patients with ischemic heart disease the severity of stenosis was classified into 7 grades (0, 25, 50, 75, 90, 99, 100%) in accordance with the AHA reporting system. The coronary angiograms were compared at first and second catheterization (intervals 2-84 months) and progression was considered present if the stenosis in the second study showed more than one grade increase in comparison with the first study. Fifty six patients met criteria for progression. Risk factors were obtained within the first second catheterization. Drug and diet therapy were evaluated by interview. No significant difference could be found between the progression (P) group and the nonprogression (N) group in relation to family history and obesity. A history of hypertension was more common in the P group. In respect to blood sampling, the values of total cholesterol, Apo B, CII, E and Apo B/AI were significantly higher in the P group than those in the N group at first and second catheterization. The percentage of patients showing abnormal levels of blood sugar and lipid were higher in the P group than the N group although the percentage of patients with drug and diet therapy were higher in the P group than in the N group. The percentage of patients with diet therapy for hyperglycemia and hyperlipidemia were higher in the P group, however weight increase was more common in the P group. These data suggest that sufficient diet and drug therapy is necessary for patients with risk factors.
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PMID:[Prevention of progression of coronary atherosclerosis by drug and diet therapy]. 223 14

Forty-two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked fibrosis with disturbed architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5-yr observation period, and in the patients with extensive fibrosis the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis. We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol-induced liver disease but usually slowly progressive and of low-grade severity. However, the disorder may ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."
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PMID:The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years. 1503 Sep 72

In 127 patients, we investigated the influence of hyperlipemia on observed fructosamine values. An in vitro influence of the lipids on the fructosamine reading could be excluded for cholesterol, HDL-cholesterol and triglycerides. However, in patients with type I diabetes, both, cholesterol and triglycerides significantly (p less than 0.05) correlated with fructosamine. This may be explained by in vivo effects of hyperglycemia on lipids or lipoproteins. For a given level of hyperglycemia, fructosamine is slightly more sensitive than HbA1c.
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PMID:[The effect of hyperlipoproteinemia on serum fructosamine]. 232 87

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

Glucose has several disadvantages such as low pH, high osmolality and hyperglycemia. Rapid glucose absorption contributes to hyperlipidemia, obesity and ultrafiltration failure in peritoneal dialysis patients. Two commercially available plasma substitutes 10% hydroxyethylstarch (HES) and 6% dextran were studied for ultrafiltration and absorption patterns. 18 ml of each solution were instilled into the peritoneal cavity of 6 non-uremic rats. HES yielded a significantly (p less than 0.02) greater ultrafiltration after 6 h of dwell, whereas 2.3% glucose solution showed the typical ultrafiltration pattern of an easily absorbable osmotic agent. With 6% dextran ultrafiltration was markedly lower. At the end of cycle time the mean absorption rates for HES were 62.7% and 41.5% for dextran. It is concluded that HES is a potent osmotic agent due to sustained colloidal ultrafiltration. However, despite their high molecular weights both solutions were markedly absorbed probably by lymphatics. However, accumulation in tissues and undefined metabolic pathways might prove disadvantageous in patients with ESRD.
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PMID:Ultrafiltration and absorption characteristics of hydroxyethylstarch and dextran during long dwell peritoneal dialysis exchanges in rats. 248 83

A new congenic strain of rat, the SHR/N-corpulent, provides a good model for noninsulin-dependent diabetes and was used in the present study. Corpulent rats as compared to their lean littermates are obese, hyperlipidemic, and severely hyperinsulinemic, and show an age-dependent loss of glucose tolerance. Mild fasting hyperglycemia is seen only in corpulent rats fed sucrose. Since dietary sucrose is more lipogenic than starch and since insulin and glucagon are involved in lipid and carbohydrate metabolism, we studied the effect of the type of dietary carbohydrate on insulin and glucagon levels and their receptors in lean and corpulent SHR/N rats. A significant phenotypic effect was observed (corpulent greater than lean) on plasma levels of triglyceride, cholesterol, and insulin. Dietary sucrose increased these parameters in corpulent rats but not in lean rats. Insulin and glucagon binding to liver plasma membranes was lower in corpulent rats than in lean; decreases were due to fewer receptors without a significant change in affinity. Thus, in corpulent rats, in addition to hyperinsulinemia, fewer glucagon receptors and their failure to be regulated by plasma glucagon levels appear to contribute to the hyperlipidemia. Furthermore, the hyperglycemia observed in sucrose-fed corpulent rats may be due to extreme resistance to insulin despite lower plasma glucagon and fewer glucagon receptors.
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PMID:Effect of dietary carbohydrates on insulin and glucagon receptors in a new model of noninsulin-dependent diabetes-SHR/N-corpulent rat. 255 55

The serum sodium concentration reflects the osmolality of the extracellular fluid and provides no direct information about total body sodium content. Patients with hyponatremia may have decreased, normal, or increased total body sodium content. The first step in the approach to the patient with hyponatremia is measurement of plasma osmolality. Hyponatremia with normal plasma osmolality results from hyperlipemia or hyperproteinemia whereas hyponatremia with increased plasma osmolality results from hyperglycemia or mannitol infusion. Patients with hyponatremia and decreased plasma osmolality may be hypovolemic, hypervolemic, or normovolemic. The volume status of the patient is best determined by history, physical examination, and a few ancillary tests (e.g., total plasma protein concentration, hematocrit, blood pressure, central venous pressure). The clinical signs of hyponatremia are related more to the rapidity of onset than to the severity of the associated plasma hypoosmolality and reflect influx of water into the central nervous system. The main goals of treatment in hyponatremia are to manage the underlying disease and, if necessary, to increase serum sodium concentration and plasma osmolality.
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PMID:Hyponatremia. 264 63

The potential role of omega-3 fatty acids in the prevention of atherosclerotic disease in the nondiabetic population currently engenders interest, enthusiasm, and controversy. Some apparently beneficial effects of omega-3 fatty acids on platelet function, eicosanoid formation, plasma triglyceride levels, and blood pressure have been described in patients with diabetes mellitus. However, enthusiasm for the use of omega-3 fatty acids in diabetes has been dampened by reports of potentially deleterious effects of these agents, including increased plasma glucose, glycosylated hemoglobin, plasma total cholesterol and LDL cholesterol, and serum apolipoprotein B levels. These adverse effects have been achieved with large, perhaps excessive, doses of omega-3 fatty acids, in the range of 4-10 g/day. The magnitude of these adverse effects has been small (typically 10-36%). It cannot be assumed that the effects of omega-3 fatty acids are the same in patients with diabetes mellitus as in nondiabetic subjects or patients with primary hyperlipidemia. First, the biosynthesis and composition of fatty acids is abnormal in diabetic animals and possibly in diabetic patients. Second, many potential mechanisms implicated in the pathogenesis of atherosclerosis are present in diabetic but not necessarily in nondiabetic subjects. Third, the mechanisms of many of the risk factors in diabetic patients differ from the mechanisms of these abnormalities in nondiabetic subjects, reflecting the effects of insulin deficiency, hyperglycemia, and their sequelae. Finally, because diabetes is a heterogeneous group of diseases, the effects of omega-3 fatty acids must be addressed separately for patients with insulin-dependent diabetes mellitus, non-insulin-dependent diabetes mellitus, and possibly other forms of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Omega-3 fatty acids in diabetes mellitus. Gift from the sea? 265 24

Experimental and clinical evidence points to the existence of a cardiomyopathy associated with diabetes mellitus that is not due to coronary atherosclerosis. The condition is characterized by distinct clinical presentations and physiologic and biochemical abnormalities. Potential mechanisms for the development of diabetic cardiomyopathy are complex but are probably associated, in part, with hyperglycemia and hyperlipidemia. Primary hypertension is also associated with the development of myocardial abnormalities. Many of these changes are similar to those seen in diabetic cardiomyopathy. It is now clear that the co-existence of hypertension and diabetes mellitus produces a more severe cardiomyopathy than that produced by hypertension or diabetes alone. Potential mechanisms for interaction are numerous. Treatment of hypertension in diabetic patients must be targeted to more specific needs. Antihypertensive drugs should not worsen cardiac risk factors or glucose control and should have favorable effects on left ventricular function. The calcium antagonists and angiotensin-converting enzyme inhibitors have pharmacologic profiles that make them attractive as monotherapy for diabetic patients.
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PMID:Myocardial disease in hypertensive-diabetic patients. 268 10


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