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

Type II diabetes mellitus may affect as many as 20% of the elderly US population. In the absence of data to support the need to maintain a specific level of glucose beyond that necessary to relieve symptoms, choice of therapy is problematic. Clearly, supervised dietary therapy for the obese type II diabetic patient represents a safe and cost-effective treatment. For those patients who fail dietary therapy because they fail to lose weight or regain lost weight, or because blood glucose levels remain high despite weight loss, further therapy must be individualized. The only rational criteria for drug treatment supportable by currently available data are (1) persistent symptoms associated with hyperglycemia, (2) ketonuria in the unstressed state, and (3) certain cases of hyperlipidemia, especially with triglyceride levels greater than 1000 mg/dl. In these clinical settings, drug therapy is necessary to eliminate symptoms, prevent development of ketoacidosis, and reduce the risk of pancreatitis, respectively. Consideration of drug therapy should also be made in the case of very elevated blood glucose levels, even in the absence of symptoms, when dehydration and risk of severe hyperosmolarity exist. The issues regarding insulin versus sulfonylureas have not been examined specifically in the elderly population. Extrapolating from published studies that generally include patients older than 65 years leads to the following conclusions: Caution regarding adverse side effects of insulin (hypoglycemia, theoretic risk of hyperinsulinemia) and sulfonylureas (hypoglycemia, drug interactions, increased risk of cardiovascular death) must be balanced against the theoretic benefit of treatment in the absence of symptoms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insulin treatment in the elderly diabetic patient. 222 55

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

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

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

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

The sympathetic nervous system helps regulate both physiologic and metabolic functions. Norepinephrine usually mediates the physiologic functions, including heart rate, myocardial contractility, vasomotor tone, and blood pressure. Epinephrine produces the metabolic effects--including hyperglycemia, hyperlactacidemia, hyperlipemia, increased oxygen consumption, and serum potassium changes. Many of the metabolic effects are common to hypertension. Understanding the metabolic effects of the catecholamines could lead to understanding their role in disease states and thus to knowing the usefulness and risks of drugs that either mimic or block their action. The data presented were selected for their relevance to the metabolic abnormalities commonly encountered among hypertensive patients. The sympathetic nervous system's effects on glucose homeostasis, lipoprotein metabolism, potassium homeostasis, hyperinsulinemia, and hypertension are discussed.
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PMID:Metabolic factors and the sympathetic nervous system. 268 91

Salmon (Oncorhynchus kisutch) somatostatin (sSS; 4 or 8 ng/g body wt) or synthetic Gillichthys urotensin II (UII; 2 or 4 ng/g body wt) were injected intraperitoneally into juvenile freshwater coho salmon. Both sSS and UII caused a dose-dependent increase in plasma free fatty acids (FFA) which diminished with time. sSS induced an initial (1 hr) transient hyperglycemia. By contrast, UII tended to induce hypoglycemia, this effect being significant 5 hr after injection of the higher dose. Both sSS and UII depressed plasma insulin titers 1 hr after injection. By 3 hr, the sSS-associated insulin depression was no longer observed. UII treatment induced a hyperinsulinemia which was present 3 and 5 hr after peptide administration. Although no decreases in liver total lipid concentration or in mesenteric fat total tissue mass were observed, lipolytic enzyme activity within each depot was significantly enhanced by both peptides. Neither sSS nor UII altered 3H2O incorporation into fatty acids or neutral lipids. However, enhanced lipogenesis, particularly by UII, was indicated by increased NADPH production resulting from glucose-6-phosphate dehydrogenase activity. Both sSS and UII enhanced glucose mobilization, as indicated by decreased liver glycogen content and increased liver glucose-6-phosphatase activity. UII, but not sSS, stimulated glycogen synthetase activity. These results suggest that both sSS and UII stimulate hyperlipidemia by enhancing depot lipase activity and that although both factors are potentially gluconeogenetic, sSS seems to be glycogenolytic and hyperglycemic, whereas UII may channel glucose to FFA synthesis.
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PMID:Effects of somatostatin-25 and urotensin II on lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 288 97

Young and mature, genetically obese and non-obese, spontaneously hypertensive rats (SHR) were injected with saline (controls) or naloxone for 12 weeks. Naloxone stilled the hyperphagia to a normal intake in the obese SHR (Obese/SHR) so that young Obese/SHR did not develop their usual massive obesity and mature Obese/SHR that had become massively obese were reduced to leanness. The naloxone-treated young, obese and non-obese SHR (controls) exhibited marked reduction of the weight of their pituitary and adrenal glands, whereas the pituitary and adrenal glands of naloxone-treated mature, obese and non-obese/SHR were greatly increased in weight. The elevated systolic blood pressure of the obese and non-obese rats was reduced after chronic treatment with naloxone. Naloxone treatment caused reduction of blood ACTH, corticosterone, and beta endorphin levels but elevated growth hormone levels. The characteristic hyperinsulinemia, hyperlipidemia, hyperglycemia, elevated BUN levels, and the Cushingoid spectrum of degenerative changes found in Obese/SHR did not appear in naloxone-treated rats.
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PMID:Anti-opiate (naloxone) suppression of Cushingoid degenerative changes in obese/SHR. 299 79

A catabolic and hypolipemic effect of glucagon has been described in normal animals. We therefore studied the role of glucagon in genetically obese, hyperlipemic rats. Twelve genetically obese hyperlipemic LA/N-cp/cp (corpulent) rats and 12 lean littermates were fed either 54% starch or 54% sucrose for 12 weeks. Plasma glucagon and insulin levels and glucagon and insulin binding to liver membranes were measured. Comparing all corpulent and lean animals regardless of diet, a significant (P less than 0.0001) phenotypical effect (cp/cp greater than lean) was observed in plasma insulin levels (464 +/- 54 vs 70.3 +/- 7.6 muu/ml, mean +/- SEM). Insulin binding (2.68 vs 16.1%/50 micrograms protein) and glucagon binding (25.6 vs 47.3%/50 micrograms protein) were both significantly lower (P less than 0.0001) in corpulent rats as compared to their lean littermates. Sucrose feeding had marginal effect on plasma insulin or insulin binding. It, however, decreased glucagon binding in corpulent rats but not in their controls. A significant negative correlation was observed between plasma insulin and insulin binding, while a positive correlation was seen for plasma glucagon and glucagon binding. A significant negative correlation was observed between plasma glucagon and lipogenic enzymes (glucose-6-phosphate dehydrogenase and malic enzyme) in liver and between glucagon binding and these enzymes. We propose that in these genetically obese rats, in addition to hyperinsulinemia, impaired glucagon activity as manifested by decreased glucagon binding to target cells may be an important contributor to the hyperlipemia and obesity. A further decrease in glucagon binding in rats fed sucrose indicates that sucrose, per se, may be an additional contributory factor.
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PMID:Genetic obesity and dietary sucrose decrease hepatic glucagon and insulin receptors in LA/N-corpulent rats. 300 53

This study was designed to evaluate the effects of soy fiber, a natural source of dietary fiber that consists of both cellulosic and noncellulosic dietary fiber, on human plasma lipoprotein lipids and glucose tolerance in patients with primary hyperlipidemia. Supplementing 25 g of soy fiber per day provided a significant additional reduction of plasma total-cholesterol by 13 mg/dl (P less than 0.04) and LDL cholesterol by 12 mg/dl (P less than 0.05) beyond that previously achieved by treatment with an NIH Type II-A low-fat, low-cholesterol diet for 12 weeks in Type II-A hypercholesterolemic patients. There were no effects on HDL cholesterol or apoprotein A-I and A-II levels. The hypocholesterolemic effect was greater than in the hyperlipidemic patients with impaired glucose tolerance. Soy fiber supplementation also significantly reduced insulin responses to oral glucose challenge by 20% in Type II-A hypercholesterolemic and by 16.5% in Type IV hypertriglyceridemic patients. Results from this study suggest that supplementing the diet with soy fiber may be beneficial in dietary management of hyperlipidemia in patients with hypercholesterolemia and particularly in hyperlipidemic patients with hyperinsulinemia and impaired glucose tolerance.
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PMID:Soy fiber improves lipid and carbohydrate metabolism in primary hyperlipidemic subjects. 302 11


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