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Results for “LIPID METABOLISM”

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At least 19 recordsLinked to original sources

Glucose metabolism, lipid metabolism, and cardiovascular risk factors in adult Turner's syndrome. The impact of sex hormone replacement.

OBJECTIVE: To examine glucose metabolism, blood pressure, physical fitness, and lipid metabolism in adult untreated women with Turner's syndrome compared with a group of normal women and to examine the effects of female sex hormone substitution on these factors. RESEARCH DESIGN AND METHODS: A total of 26 patients with Turner's syndrome were examined before and during sex hormone replacement with 17 beta-estradiol and norethisterone, and an age-matched control group (n = 24) was examined once. A frequently sampled intravenous glucose tolerance test was applied with minimal model assessment. We also performed an oral glucose tolerance test, measurement of 24-h ambulatory blood pressure, and assessment of physical fitness and lipid metabolism. RESULTS: Insulin sensitivity (SI) and glucose effectiveness (SG) were similar in Turner's syndrome patients and control subjects, whereas the acute insulin response (P = 0.03) was lower in Turner's syndrome patients, and no change was seen during sex hormone treatment. Abnormal glucose tolerance was found in 50% of Turner's syndrome patients before and 78% during treatment with sex hormones. Fat-free mass (FFM; P = 0.0005) and physical fitness (P = 0.002) were lower in Turner's syndrome subjects compared with control subjects. During treatment, an increase in FFM (P = 0.001) and physical fitness (P = 0.02) was seen in Turner's syndrome patients. Blood pressure was increased in Turner's syndrome, and a decrease was seen in diastolic blood pressure during treatment with sex hormones. CONCLUSIONS: Turner's syndrome is associated with glucose intolerance, diminished first-phase insulin response, elevated blood pressure, reduced FFM, and physical fitness. Sex hormone administration causes a deterioration in glucose tolerance, increases FFM and physical fitness, and has beneficial effects on blood pressure. The deleterious effect on glucose tolerance may be mediated by norethisterone, a gestagen known to have androgenic effects.

Administration, Oral↗

Long-term feeding of dietary oils alters lipid metabolism, lipid peroxidation, and antioxidant enzyme activities in a teleost (Anabas testudineus Bloch).

Anabas testudineus (climbing perch), average body weight 21+/-1 g, were maintained in culture tanks and fed a 35% protein feed plus an additional supplementation of three dietary oils (20% each of coconut oil, palm oil, or cod liver oil). Body weight gain was similar among all groups. However, several hepatic lipogenic enzymes such as malic enzyme (ME), NADP-isocitrate dehydrogenase (ICDH), glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and beta-hydroxy-1-methyl glutaryl CoA reductase (HMG CoA reductase) were assayed, and they responded differently. Hepatic ME and G6PDH activities showed a significant decrease in the coconut oil and palm oil groups, but there was no significant change in ICDH activity. The 6PGDH activities were reduced, whereas HMG CoA reductase activity was increased in the palm oil-treated group. Cholesterol synthesis in the liver and muscle increased in the palm oil-treated group, but liver phospholipids did not show any significant change in fish supplemented with oils rich in saturated fatty acids. Triacylglycerol and free fatty acid concentrations were high in the coconut oil- and palm oil-supplemented groups. Lipid peroxidation products such as thiobarbituric acid-reactive substances and conjugated dienes decreased in the same two groups. Antioxidant potential was high in all groups as evidenced by increased activity of superoxide dismutase, glutathione peroxidase, and glutathione content. The results of this study indicate that in fish, dietary lipids depress hepatic lipogenic activity as well as lipid peroxidation products by maintaining high levels of antioxidant enzymes.

Animals↗

[Reclid effects on carbohydrate, lipid metabolism, lipid peroxidation and hemodynamics in patients with diabetes mellitus type 2].

Patients with diabetes mellitus type II have disorders in carbohydrate, lipid and other kinds of metabolism. This increases the risk of cardiovascular complications and atherogenesis. Therefore, it is advisable to use drugs preventing an excessive late phase of insulin secretion with resultant reduction of hyperinsulinemia. Reclid, the drug of this group, improves metabolic processes, insulin resistance, lipid metabolism, hemostasis and microcirculation. 3-month reclid therapy of patients with non-insulin-dependent diabetes mellitus produced a good hypoglycemic effect in 85% of the cases. This effect consisted in reduction of basal and postprandial glycemia, levels of glycosylated hemoglobin, 24-h glucosuria. In patients with diabetes mellitus type II reclid diminished the levels of total cholesterol, triglycerides, glycosylated hemoglobin. In patients with left ventricular diastolic dysfunction, reclid improved transmitral blood flow. Thus, reclid provides a good metabolic control in patients with non-insulin-dependent diabetes mellitus. Moreover, it positively affects mechanisms initiating cardiovascular complications in diabetic patients.

Carbohydrates↗

[Effect of phensuccinal on lipid metabolism, lipid peroxidation, and antioxidant system activity in rabbits with dithiazone-induced diabetes].

A three-month administration of phensuccinal improved glucose homeostasis, decreased the levels of total cholesterol, triglycerides, fatty acids, and low-density lipoproteins in the blood serum, and reduced the lipid peroxidation rate as compared to the untreated diabetic control. In addition, phensuccinal increased the content of the antiatherogenic high-density lipoprotein fraction and the related paraoxonase enzyme activity. The preventive effect of phensuccinal with respect to diabetic dyslipidemia development, together with the antioxidant action, show this compound to be a promising therapeutic means of preventing and/or reducing macrovascular complications in diabetic patients.

Aldehydes↗

[Hypokinesia, nutrition and lipid metabolism. Lipids and lipoproteins in the blood].

Long-term hypokinesia of August and Wistar Albino Glasgow rats caused some alterations in composition of total lipids and cholesterol esters both in blood serum and in individual lipoprotein fractions. The most distinct alterations were the following ones: I. increase in content of very low density lipoproteins (VLDL) and of low density lipoproteins (LDL), 2. decrease in the level of cholesterol esters in blood serum with a simultaneous increase of their content in VLDL and LDL as well as with alteration of their composition, 3. decrease of triglyceride content in VLDL and increase--in LDL, exhibiting the alteration in activity of lipolytic enzymes. Functional activity of muscles was very important for maintaining of the normal level of blood serum lipids and lipoproteins.

Animals↗

Systematic analysis of yeast strains with possible defects in lipid metabolism.

Lipids are essential components of all living cells because they are obligate components of biological membranes, and serve as energy reserves and second messengers. Many but not all genes encoding enzymes involved in fatty acid, phospholipid, sterol or sphingolipid biosynthesis of the yeast Saccharomyces cerevisiae have been cloned and gene products have been functionally characterized. Less information is available about genes and gene products governing the transport of lipids between organelles and within membranes or the turnover and degradation of complex lipids. To obtain more insight into lipid metabolism, regulation of lipid biosynthesis and the role of lipids in organellar membranes, a group of five European laboratories established methods suitable to screen for novel genes of the yeast Saccharomyces cerevisiae involved in these processes. These investigations were performed within EUROFAN (European Function Analysis Network), a European initiative to identify the functions of unassigned open reading frames that had been detected during the Yeast Genome Sequencing Project. First, the methods required for the complete lipid analysis of yeast cells based on chromatographic techniques were established and standardized. The reliability of these methods was demonstrated using tester strains with established defects in lipid metabolism. During these investigations it was demonstrated that different wild-type strains, among them FY1679, CEN.PK2-1C and W303, exhibit marked differences in lipid content and lipid composition. Second, several candidate genes which were assumed to encode proteins involved in lipid metabolism were selected, based on their homology to genes of known function. Finally, lipid composition of mutant strains deleted of the respective open reading frames was determined. For some genes we found evidence suggesting a possible role in lipid metabolism.

Antifungal Agents↗

Effect of anoxia and hypoxia on brain lipid metabolism.

Lipid metabolism in rat brain was investigated in mild hypoxia (5-7% O2 in nitrogen), which is associated with no apparent change in energy metabolism, and in severe anoxic conditions (ischemic anoxia), which are associated with a rapid decrease in ATP and oxygen content in brain. When brain slices were incubated with labeled glucose or acetate, the amount of labeled CO2 produced was no different in experimental and control conditions, but the incorporation of radioactivity into brain lipids was decreased in all hypoxic and anoxic conditions. Interestingly, the incorporation of label from [14C]glucose into phosphatidylinositols was specifically inhibited by both hypoxic conditions but not by conditions associated with anoxia. The incorporation of the same labeled precursor, i.e., [14C]glucose, into fatty acids was elevated in ischemic anoxia but reduced after mild hypoxia. Because of the obvious differences in oxygen utilization in brain in anoxic and hypoxic conditions, we believe that the observed disturbances in lipid metabolism may be due to factors other than those that arise from oxygen deficiency alone.

Acetates↗

Relation of urinary sodium excretion to blood pressure, glucose metabolism, and lipid metabolism in residents of an area of Japan with high sodium intake.

To evaluate the effects of prolonged intake of a high-sodium diet on glucose and lipid metabolism, we examined the relation of daily urinary sodium excretion to blood pressure, glucose metabolism, and lipid metabolism in 140 Japanese adults who lived in a region where the average daily consumption of sodium was high and stable during the past 15 yr; no subject had received any treatment for hypertension or metabolic disorders. Each subject was admitted to our health examination center for 2 d for measurement of blood pressure, sampling of blood, and glucose tolerance testing. A 24-h urine specimen was collected by each subject after discharge. Multiple regression analysis revealed that urinary sodium excretion was significantly independent of the mean blood pressure and was unrelated to the area under the serum glucose curve after glucose administration. The urinary sodium level was also unrelated to low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. The prevalence of hypertension in the group with a daily sodium excretion below 140 mEq (low sodium group) was 0%, while that in the group with a daily sodium excretion above 280 mEq (high sodium group) was 44%; this difference was significant (p < 0.01). No significant difference was observed in the prevalence of metabolic disorders between the two groups. Our results suggest that sodium intake has little influence on glucose and lipid metabolism but has a significant influence on blood pressure in normotensive and untreated hypertensive subjects who reside in an area with a relatively high sodium intake.

Adult↗

Estrogen replacement therapy continuously combined with four different dosages of dydrogesterone: effect on calcium and lipid metabolism.

Lipid and bone metabolism was studied in 165 healthy postmenopausal women treated with 2 mg 17 beta-estradiol continuously combined with one of four doses (2.5, 5, 10, or 15 mg) of dydrogesterone in a double blind randomized study design. Fasting blood and urine samples were drawn at baseline and after 3 and 6 months of treatment. Bone remodeling was significantly reduced in all four treatment groups, as indicated by the decrease in serum corrected calcium, phosphate, and alkaline phosphatase and the urinary calcium/creatinine ratio. A dose response of dydrogesterone on these indices was not found. With all four dosages of dydrogesterone, lipid profile (total cholesterol, high density lipoprotein cholesterol, low density lipoprotein cholesterol, and apolipoproteins) improved significantly; however, this was less pronounced with the highest dydrogesterone dose. Our data suggest that continuously applied dydrogesterone in combined hormone replacement therapy does not annihilate the beneficial effects on bone remodeling and lipid metabolism induced by estrogens.

Administration, Oral↗

[Effect of propofol and ketamine on lipid metabolism and lipid peroxidation in rats].

Ketamine (50 mg/kg, i.p.) increases the intensity of lipolysis in Wistar male rats, as manifested by increasing content of nonetherified fatty acids and cholesterol in the blood serum. This drug also enhances the lipid peroxidation (LPO) process, as manifested by the content of LPO products in the blood serum and in the liver and heart tissues. Propofol in the same dose also influences the lipid metabolism and LPO intensity, but to a lower extent.

Anesthetics↗

[Indicators of lipid metabolism and lipid peroxidation system in patients with different types of lesions of the vessels of the lower limbs].

A total of 66 patients were investigated with IR imager and television capillaroscopy for the blood circulation in the vessels of low extremities as well as for the values of lipid metabolism and the system of lipid peroxidation. According to the status of the vascular system in the low extremities the examinees were divided into the groups with the normal status of the vascular system, the groups with the signs of venous insufficiency, microcirculatory disorders and atherosclerosis of major vessels. With the disorders of microcirculation in low extremities staged increments in the atherogenic shifts in the exchange were demonstrated. It was suggested that atherosclerotic changes in the arteries could be preceded with the hemodynamic changes in the venous and capillary systems due to rheological disorders due to the development of hypercoagulation which accompanied dyslipoproteinemias and other atherogenic shifts in the metabolism.

Arteriosclerosis↗

Importance of apolipoproteins in lipid metabolism.

Lipids, which serve as a source of energy and are an important constituent of cell membrane structure, are readily stored in the body. By definition they are insoluble in water. Specific proteins called apolipoproteins interact with lipids to form soluble lipid-protein complexes called lipoproteins. It is in this form that the major lipids--cholesterol, triglyceride and phospholipid--circulate in plasma. Unesterified fatty acids, another major lipid group, are bound to albumin in the circulation. The plasma lipoproteins are complex macromolecules composed of lipids, apolipoproteins and carbohydrates. The relative proportions of these components differ markedly between lipoprotein classes. Hyperlipidemia is a term used for increased concentrations of plasma cholesterol and/or triglycerides. Any one plasma lipid is present in several types of lipoproteins. Thus, hyperlipidemia implies the presence of hyperlipoproteinemia. The latter has important therapeutic implications. Most of the recent attempts at classification have been directed at the lipoprotein level of plasma lipid organization. Decreased concentrations of lipids in plasma can be achieved by altering the rates of metabolism of lipoproteins. Decrease in lipoprotein synthesis, increased catabolism or impaired release from cells into the blood stream may all result in a decrease of plasma lipids. Drugs which affect one or more of these factors are used to treat hyperlipoproteinemia. In order to elucidate the mechanism of action of hypolipidemic drugs it is necessary to understand the lipoprotein defect at the molecular level. This requires a more detailed knowledge of lipoprotein metabolism than is presently available for most of the hyperlipoproteinemias. This paper will review some of the generally accepted properties of the plasma lipoproteins, describe some difficulties which hamper the understanding of lipoprotein metabolism, and identify possible mechanisms by which drugs may affect lipoprotein metabolism.

Apolipoproteins↗