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

We assessed the analytical performance of the co-immobilized hexokinase (EC 2.7.1.1) and glucose-6-phosphate dehydrogenase (EC 1.1.1.49) method for D-glucose analysis on the Technicon SMAC. The enzyme-containing coils were usable for one month, or 12 000 tests. Bilirubin, hemoglobin, lipemia, creatinine, uric acid, citric acid, and ascorbic acid did not interfere. Results with this method were compared to those by the National Glucose Reference Method. The upper limits of the total error estimate (a combination of random and systematic errors) were 76, 74, and 125 mg/liter at concentrations of 500, 1200, and 3000 mg/liter, respectively. The error estimates were less than allowable errors based on medical usefulness; thus the method was judged to perform acceptably with respect to the Reference Method. We also present performance data for the routine SMAC glucose oxidase (EC 1.1.3.4)/Peroxidase (EC 1.11.1.7) 3-methyl-2-benzothianolinone hydrazone-N,N-dimethylaniline method, the direct hexokinase method with the Du Pont aca, and the glucose oxidase oxygen-rate method with the Beckman Glucose Analyzer.
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PMID:Evaluation of the co-immobilized hexokinase/glucose-6-phosphate dehydrogenase method for glucose, as adapted to the Technicon SMAC. 65 1

The effect of addition of different carbohydrates (starch, glucose, fructose) to the feed was investigated using the experimental animal. Additionally, the admixture of cholesterol and of cholesterol plus cholic acid was tested. Fructose (70% of the feed) causes a slight increase in serum triglyceride concentration and a very slight increase in triglyceride concentration in the liver. Fructose and to a lesser degree glucose cause an increase in pyruvate kinase activity in the liver. The activity of glucose-6-phosphate dehydrogenase is increased slightly following high-dosed glucose, whereas the increase is very pronounced following fuctose-rich feed. The admixture of cholesterol (with cholic acid) causes a decrease in glucose-6-phosphate dehydrogenase activity up to 70%. The activity of glutamate dehydrogenase is decreased also following cholesterol admixture. A fructose-rich diet causes a slight degree of hyperlipemia with a metabolic situation similar to a latent diabetic state. This effect is greatly intensified by the addition of cholesterol and cholic acid to the diet of the rats. Especially striking was the increase in serum-free-fatty-acid concentrations in all groups of animals. This is speculated to be a sign of insulin deficiency. The so-called "carbohydrate-induced hypertriglyceridemia" is obviously intensified within a short period by the admixture of cholesterol plus cholic acid to the experimental diet.
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PMID:[Effect of various dietary carbohydrates on supplementary cholesterol]. 89 66

Rainbow trout, Oncorhynchus mykiss, were used to evaluate the effects of carbohydrate loading on plasma levels of pancreatic hormones and associated changes in metabolic indexes in a carnivorous fish. Glucose (3,000 mg/dl, 10 microliters/g body wt) was injected intraperitoneally into fish (mean wt 54 +/- 5 g) that were killed 0.5-24 h after administration. Glucose injection resulted in hyperglycemia with maximum glucose levels of 306 +/- 13 mg/dl observed 60 min after injection. Glucose administration also resulted in hyperlipidemia. Plasma fatty acids increased twofold in glucose-injected animals. Alterations in plasma metabolites reflected changes in energy stores. Although total lipid concentration was unaffected by glucose injection, lipolytic enzyme activity in the liver was enhanced. Biosynthetic capacity, as indicated by NADPH production from glucose-6-phosphate dehydrogenase, was decreased by glucose injection. Liver glycogen content was reduced in glucose-injected animals 1 h after injection. Glucose injection was attended by increases in the plasma levels of gene II somatostatin-25 (predominant form of pancreatic somatostatin in salmonids) and of glucagon. Insulin levels were initially suppressed after glucose injection. These results indicate that metabolic adjustments caused by glucose administration can be related to the regulatory action of pancreatic hormones. Furthermore, these results suggest that the somatostatin-secreting cells of the trout are sensitive to glucose and that somatostatin-suppressed insulin secretion contributes to the glucose intolerance of trout.
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PMID:Insulin suppression is associated with hypersomatostatinemia and hyperglucagonemia in glucose-injected rainbow trout. 167 8

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial beta-oxidation was unaffected and peroxisomal beta-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC 1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and glutathione peroxidase (EC 1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC 3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.
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PMID:Metabolic effects of coconut, safflower, or menhaden oil feeding in lean and obese Zucker rats. 176 Apr 46

We developed an assay for serum magnesium (Mg) by coupling phosphoglucomutase (EC 2.7.5.1) with glucose-6-phosphate dehydrogenase (EC 1.1.1.49). The kinetic generation of NADPH by the action of the above two enzymes upon glucose-1-phosphate (G-1-P) and glucose-1,6-diphosphate (G-1,6-P) was proportional to the concentration of Mg in serum, and was monitored at 340 nm. The average within-run and day-to-day imprecision (% CVs), as determined from 10 replicate analyses for three sera with different Mg concentrations, were 0.8 to 2.1% and 1.9 to 2.7%, respectively. For 60 clinical samples, including several with lipemia and hemolysis, our method showed good agreement with atomic absorption spectrophotometry and the Xylidyl Blue method. We also present data showing that the method is highly sensitive, rapid, relatively free of interference, and amenable to automation.
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PMID:Development of an enzymatic method for the assay of serum magnesium using phosphoglucomutase and glucose-6-phosphate dehydrogenase. 183 12

Juvenile coho salmon (Oncorhynchus kisutch) were placed on five dietary regimes: fed 1 week, fasted 1 week, fed 3 weeks, fasted 3 weeks, and fasted 1 week/refed 2 weeks. Plasma levels of glucose, fatty acids, insulin, glucagon, and glucagon-like peptide (GLP) and the activities of key metabolic enzymes were determined. Plasma glucose levels in the fed control groups were 98.4 +/- 3.4 (SEM) and 104.8 +/- 4.7 mg/dl at 1 and 3 weeks, respectively. Plasma glucose in the fasted 1 week group was significantly elevated to 128.8 +/- 9.2 mg/dl. Animals fasted 3 weeks or fasted 1 week/refed 2 weeks displayed plasma glucose levels similar to those of fed animals. Fasted groups possessed significantly less liver glycogen than fed or fasted/refed groups. Plasma fatty acids were elevated only after 3 weeks of fasting (from 0.39 +/- 0.04 microEq/ml to 0.61 +/- 0.06 microEq/ml). This response was reflected in elevated liver lipase activity (from 6.02 +/- 0.44 nmol fatty acid released/hr/mg protein to 14.22 +/- 0.90 units). No significant alterations in liver lipogenesis, assessed by glucose-6-phosphate dehydrogenase activity and by 3H2O incorporation into fatty acids, were observed. Gluconeogenic flux, determined indirectly through kinetic parameters of pyruvate kinase, was enhanced in animals fasted 3 weeks and in animals recovering from a 1-week fast. Plasma insulin levels were highest in fed groups (7.7 +/- 2.3 and 5.9 +/- 1.4 ng/ml at 1 week and 3 weeks, respectively) and were significantly depressed in fasted groups. Plasma levels of glucagon and GLP were also depressed in fasted groups. These results indicate that plasma glucose levels are maintained in salmon during fasting and that fasting-induced hyperlipidemia is mediated by lipolytic enzyme activity. Insulin, glucagon, and GLP may interact with these enzyme systems to coordinate nutritional metabolism of fish.
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PMID:Effects of nutritional state on in vivo lipid and carbohydrate metabolism of coho salmon, Oncorhynchus kisutch. 205 44

To determine whether the estrogen-induced hyperlipidemia is affected by fasting, male growing chicks were administered subcutaneously a single dose of 17 beta-estradiol (25 mg/kg body wt), and the hormone treatment lasted for 2 days with or without feed (Experiment 1). In the second experiment, chicks were initially fasted for 1 or 3 days, and then treated with the same dosage of 17 beta-estradiol as in Experiment 1 for 2 days without feed. Plasma and liver lipids, and the activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, and hormone-sensitive lipase in the adipose tissue were determined. Compared with fed control chicks, estrogen treatment in fed birds resulted in a marked elevation of plasma lipids, especially triglyceride during the 2-day period (137 vs 2263 mg/dl). In fasted chicks, the present finding that estrogen also induced a marked hyperlipidemia is noteworthy. Upon estrogen treatment (Experiment 1), the level of plasma triglyceride in fasted birds increased about 16 times over that of the fasted control group (133 vs 2093 mg/dl). Even in chicks fasted for 5 days (Experiment 2), estrogen treatment resulted in a persistent hypertriglyceridemia (75 vs 1369 mg/dl). In fed chicks, estrogen treatment also induced a fatty liver with massive accumulation of triglyceride, but the liver of estrogen-treated/fasted chicks appeared to be normal. In both fed and fasted chicks, malic enzyme was found to be the major NADPH producing enzyme in the liver. Upon fasting, both malic enzyme and glucose-6-phosphate dehydrogenase activities decreased significantly (P less than 0.05). In fed chicks, the total activities of both enzymes increased with estrogen treatment, whereas the effect of hormone on these enzymes was less obvious in fasted chicks. The hormone-sensitive lipase activity in the adipose tissue was much lower in fed chicks compared with that of fasted birds (0.15 vs 0.33 nmol of oleic acid released/min/mg protein). Estrogen treatment in fed chicks had no effect on the hormone-sensitive lipase activity, but its activity was enhanced by the hormone treatment in fasted chicks. The present finding that hyperlipidemia persisted in estrogenized chicks during the fasting seems to indicate the complex nature of this hormonal influence on lipid metabolism.
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PMID:Estrogen induces hyperlipidemia in fasted chicks. 230 May 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

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

We have developed a kinetic fixed-time approach for the quantitative determination of serum glucose by use of the hexokinase/glucose-6-phosphate dehydrogenase method. To achieve a large measuring range, we have apparently increased the Michaelis constant of glucose-6-phosphate dehydrogenase through addition of the competitive inhibitor ATP. By this means, serum samples with glucose concentrations up to 55.5 mmol/l could be analyzed without pre-dilution. The method has been adapted to the ENI GEMSAEC analyzer and to the LKB 2086 Mark II analyzer. It yielded satisfactory results with regard to precision. A comparison of the kinetic procedure with the manual end-point method showed good agreement. No interferences from hemoglobin, bilirubin, or lipemia have been observed.
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PMID:Kinetic determination of serum glucose by use of the hexokinase/glucose-6-phosphate dehydrogenase method. 735 90


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