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PubMed1979

[Hormonal contraception and lipid metabolism. Prospective and retrospective studies of lipid metabolic parameters during the use of contraceptives].

Remarkable changes of several parameters of lipid metabolism were observed in a retrospective study of women, who had used different oral contraceptives for a longer time, in comparison with women without any hormonal contraception. In contrast, under the conditions of a prospective double-blind study no statistically significant alterations of the same parameters were seen under the use of two oral contraceptives different in dosage. Nevertheless, oral contraceptives should not be prescribed to patients with hyperlipidaemia.

Adult↗
PubMed1979

In vitro lipid metabolism in the rat pancreas. I. Basal lipid metabolism.

1. The in vitro basal lipid metabolism of rat pancreatic fragments was compared with that in adipose tissue fragments and liver slices. 2. [1-14C]Acetate added to the media was mostly incorporated into palmitic acid and to a lesser extent into oleic acid. In addition, pancreatic tissue exhibited a marked capacity for elongation of polyunsaturated fatty acids by [1-14C]acetate and resulting desaturation when compared to adipose tissue and liver. 3. Data obtained in the presence of [U-14C]glucose, [1-14C]palmitate and 3H20 indicate that acetyl-CoA derived from glucose and from beta-oxidation of fatty acids contributed to de novo lipogenesis. 4. Oxidation of [1-14C]palmitic acid was 9-13 times higher in the pancreas than in adipose tissue or liver when expressed on a wet weight basis. 5. The fatty acid moiety of pancreatic glycerolipids could be derived from de novo synthesis, fatty acids added to the medium, or from fatty acids formed from the hydrolysis of endogenous lipids. The glycerol moiety could be derived either from glucose, or directly from glycerol through participation of glycerol kinase.

Acetates↗
PubMed2002

Metformin improves lipid metabolism and attenuates lipid peroxidation in high fructose-fed rats.

AIM: Insulin resistance, hyperinsulinaemia and disturbances in glucose metabolism can be produced in normal rats by feeding them a fructose-enriched diet. Metformin, an antidiabetic drug, enhances insulin sensitivity in type 2 diabetic patients. Previous studies have shown that metformin improves insulin sensitivity in fructose-fed rats. The aim of this study was to determine the effect of metformin treatment on overall lipid metabolism and lipid peroxidation in rats that were fed a fructose-enriched diet, which leads to insulin resistance. The relationship between hyperinsulinaemia and hyperglycaemia with lipid peroxide levels was also investigated. MATERIALS AND METHODS: The animals were divided into two batches. One batch received a standard diet and the other was fed a fructose-enriched diet (72 g/100 g feed). After 2 weeks, each batch of rats was subdivided into two groups. One group received metformin (50 mg/kg per day in water) and the other received the standard diet and served as control. RESULTS: High fructose feeding resulted in hyperinsulinaemia, hyperglycaemia and alterations in lipids and lipid metabolism, and plasma and tissue lipid peroxides were significantly elevated. Administration of metformin (50 mg/kg/day) was associated with significant normalization of plasma insulin level and lipid alterations. These rats also showed significantly higher lipoprotein lipase (LPL) and lecithin cholesterol acyl transferase (LCAT) activities in plasma than untreated, fructose-fed rats. Lipid peroxides content was also decreased in plasma and tissues. Significant positive correlations were observed between the levels of plasma insulin and plasma glucose with plasma lipid peroxides. CONCLUSIONS: We conclude that enhanced lipid peroxidation occurs in addition to disturbances in lipid metabolism in fructose-fed rats. Plasma insulin level probably contributes to this increased peroxidation. Improved insulin action in metformin-treated rats could be responsible for the amelioration of these abnormalities induced by fructose feeding.

Animals↗
PubMed1997

[The indices of lipid metabolism and of lipid peroxidation in acute intestinal obstruction and the administration of plasma substitute solutions].

The influence of the intravenously infusion of plasma substitute solution from the whey on the some indices of the lipid metabolism and the lipid peroxidation were studied in the experiments on the model of ileus. Resive data indicate the considerable alteration of the lipid peroxidation under ileus. The infusion therapy of the solution from the whey decreased the level of lipoperoxides and malondialdehyde in the liver and reduced the level of beta-lipoproteins in serum of blood.

Acute Disease↗
PubMed1994

Phenobarbital treatment enhances insulin-mediated glucose metabolism and improves lipid metabolism in the diabetic rat.

Previous studies with healthy volunteers and non-insulin-dependent diabetic (NIDDM) patients have shown a strong association between overall glucose metabolism and hepatic microsomal enzyme activity. In this study, the effects of 10-day oral administration of phenobarbital (PB), a potent inducer of the hepatic microsomal mixed-function oxidase system, on carbohydrate and lipid metabolism in the basal state and on glucose kinetics during submaximal hyperinsulinemic (5 mU.kg-1.min-1 insulin) clamps were investigated in nondiabetic rats and in rats made diabetic by the intravenous (IV) administration of either low-dose (40 mg/kg) or high-dose (55 mg/kg) streptozocin (STZ). In control rats receiving PB in drinking water (0.5 mg/mL), serum insulin and triglyceride levels were diminished without any change in glucose and cholesterol concentrations in the fed state. Administration of PB in drinking water (0.25 mg/mL) to both groups of diabetic rats decreased their water intake and serum triglyceride levels in the absence of an effect on glucose, insulin, and cholesterol concentrations in the fed state. However, fasting serum glucose levels and basal glucose turnover rates were lower in both groups of diabetic rats receiving PB. PB treatment increased the heparin-releasable lipoprotein lipase (LPL) activity of epididymal fat in both control and low-dose diabetic groups; this was not assessed in the high-dose diabetic group. Neither peripheral glucose utilization nor hepatic glucose production during submaximal insulin clamps was modified by PB treatment in nondiabetic rats. In contrast, PB administration enhanced insulin-mediated peripheral glucose utilization, as well as suppression of hepatic glucose production, in both low-dose and high-dose diabetic groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed2001

[Lipid metabolism. I. Role of insulin in lipid metabolism].

The triacylglyceroles that comprise the bulk of lipids in the diet are hydrolyzed to free fatty acids, monoacylglyceroles and glycerol in the intestinal tract. During absorption through the intestinal tract mucosa, triacylglyceroles are resynthesized from free fatty acids, and glycerol-3-phosphate is formed in the intestinal mucose. these globules, called chylomicrons, pass through the liver and adipose tissue, they are reduced in size by an enzyme, lipoprotein lipase (LPL). In the postabsorptive period, free fatty acids and glycerol are released from adipocytes by neural and hormonal stimulation. The free fatty acids can be burned by almost all tissues of the body except the brain. They are burned in the mitochondria by a process of b-oxidation to acetyl-CoA, which can then enter the citrate acid cycle for conversion to CO2, adenosine triphosphate, and water. When excessive quantities of glucose are ingested, the glucose can be converted to a storage form, triacylglycerol. Fatty acids are synthesized by a series of reactions in which acetyl-CoA and malonylo-CoA residues sequentially condense until the fatty acid chain is completed. The fatty acids are then combined with glycerol-3-phosphate, generated in the liver, to form the neutral triacylglyceroles. The insulin has effects on both the synthetic (estrification) and breakdown (lipolysis) pathways. The promotion of triacylglycerol storage in fat is one of the most important of the actions of insulin.

Adenosine Diphosphate↗
PubMed2004

[Hormonal dysregulation of lipid metabolism in pathogenesis of ischemic heart disease].

The aim of the study was to specify postprandial hyperlipidemia (PHL) and the level of hormones which regulate metabolism, lipids in particular, in patients with ischemic heart disease (IHD) vs those in healthy persons and patients with thyrotoxicosis as well as to clarify whether IHD pathogenesis correlates with fat metabolism disturbance. Lipid and apoprotein parameters of dyslipoproteinemia, concentrations of insulin, hydrocortisone, T3, T4 and thyrotropic hormone were tested before and 3, 6 hours after fat loading in IHD patients with angiographically documented coronary atherosclerosis, in healthy persons and patients with diffuse toxic goiter. In IHD patients postprandial PHL differed from that in healthy persons and thyrotoxicosis patients by higher and growing up to hour 6 after fat loading hypertriglyceridemia associated with lowering of antiatherogenic cholesterol of HDLP. In thyrotoxicosis both fasting and afterload lipid and apoprotein indices of the lipoprotein spectrum continued at low level except triglycerides the level of which returned to normal level. The hormonal spectrum in IHD patients was characterized by higher fasting insulin and its noticeable rise after fat loading. As healthy persons and patients with thyrotoxicosis had no significant changes in hormones levels after fat loading, it is suggested that development of atherogenic postprandial PHL caused primarily by hormone dysregulation of fat metabolism with a leading role of hyperinsulinemia contributes much to pathogenesis of IHD.

Adult↗
PubMed1998

S-adenosyl-L-methionine: role in phosphatidylcholine synthesis and in vitro effects on the ethanol-induced alterations of lipid metabolism.

Hepatic lipid metabolism is extremely modified by excessive ethanol consumption, but the cellular mechanisms of such alterations are still largely unexplored. S-Adenosyl-L-methionine (SAMe) is known as an important methylating agent and as a precursor of glutathione and it has been shown to prevent some of the toxic effects of ethanol in the liver. We therefore studied the effects of ethanol on cholesterol synthesis in a human hepatomal cell line (HepG2), the kinetics of SAMe, and its putative protective effects on the alterations of lipid metabolism induced by toxic concentrations of alcohol. Incubation of HepG2 cells with [3H]SAMe resulted in a progressive increase in the labelling of phosphatidylcholine and of its two intermediates during synthesis starting from phosphatidylethanolamine. This process is enzymatic, since it does not take place in heat-inactivated cells. Also, ethanol induced an increase in cholesterol and triglycerides syntheses and a decrease in phospholipid labelling. These alterations were not prevented by SAMe 10(-4) M, indicating that the protective effects of the drug are related to other mechanisms of action such as reduced formation of collagen, restoration of glutathione levels, and normalization of membrane functions.

Acetates↗
PubMed1983

[Relation between serum lipoprotein metabolism and biliary lipid metabolism].

This review concern with recent results regarding interrelationships between serum lipoprotein and bile acid metabolism. First, changes in bile acid metabolism in primary hyperlipoproteinaemia type II and type IV are described. In addition, influences of lipid-lowering drugs such as sitosterol, cholestyramine/colestipol, neomycin, nicotinic acid, clofibrate and thyroxin on serum lipoproteins and biliary lipid metabolism are discussed. Changes in lipoprotein metabolism in disorders of bile acid metabolism and effects of primary and secundary bile acids on lipoprotein metabolism, hepatic cholesterol metabolism and intestinal cholesterol absorption are described. In the final discussion interrelationships between very low density lipoprotein - triglycerides and cholic acid metabolism as well as low density lipoprotein and chenodeoxycholic acid metabolism are stressed. The positive correlation between serum triglycerides and lithogenicity of bile is underlined and the possible significance of high density lipoprotein-cholesterol as precursor of biliary cholesterol is discussed.

Bile↗
PubMed2005

Lipid metabolism mediated by adipocyte lipid binding protein (ALBP/aP2) gene expression in human THP-1 macrophages.

The critical initiating event in atherogenesis involves the invasion of monocytes through the endothelial wall of arteries, and their transformation from macrophages into foam cells. Human THP-1 monocytic cells can be induced to differentiate into macrophages by phorbol myristate acetate (PMA) treatment, and can then be converted into foam cells by exposure to oxidized low-density lipoprotein (oxLDL). We previously reported that adipocyte lipid binding protein (ALBP/aP2) is a gene that is highly up-regulated in foam cells in response to oxLDL. Here, we showed that overexpression of the ALBP gene using a lentiviral construct in macrophage foam cells enhanced the accumulations of cholesterol and triglyceride, probably due to an increased expression of the scavenger receptor type AI (SR-AI), which plays an important role in cell lipid metabolism. Moreover, we determined that the expression of acyl-coenzyme A: cholesterol-acyltransferase 1 (ACAT1) gene was up-regulated by the overexpression of ALBP gene, and on the other hand, the ATP-binding cassette A1 (ABCA1) gene and hormone sensitive lipase (HSL) gene, which mediate separately cholesterol efflux and cholesterol ester hydrolysis in the macrophage cells, were down-regulated by the overexpression of ALBP gene in these cells. Finally, our data indicated that oxLDL regulates expression of ALBP related to two peroxisome proliferator-responsive elements (PPREs) which are located in ALBP promoter region. These results have determined that ALBP gene expression accelerates cholesterol and triglyceride accumulation in macrophage foam cells and affects some key gene expression for lipid metabolism, suggesting some pivotal roles of ALBP in lipid metabolism for macrophage foam cell formation.

ATP Binding Cassette Transporter 1↗
PubMedDate not supplied

[Lipid metabolic disorders and lipid peroxidation in patients with the nephrotic syndrome].

Lipid metabolism was studied in 161 patients with renal diseases, 62 of them had nephrotic syndrome (NS). The measurements were made of cholesterol, triglycerides, dienic conjugates, B2-microglobulins in urine and blood, functional and morphological parameters, red cell resistance to peroxide hemolysis. It was found that NS patients, especially those with additional renal failure, displayed high-intensity lipoperoxidation (LPO). LPO intensity proved unrelated to NS etiology. NS-associated hyperlipidemia gives rise to multifunctional biomembrane instability responsible for antioxidant disorders.

Adult↗
PubMed1987

Medroxyprogesterone acetate and lipid metabolic changes.

Lipid metabolic changes under oral treatment with medroxyprogesterone acetate (MPA) were investigated in four groups of patients: group I; 10 patients aged 25-45 (mean 38) years received 50 mg MPA daily for pelvic endometriosis. Group II; 21 patients aged 55-77 (mean 62) years received 200 mg MPA daily for surgically treated endometrial carcinoma stage I. Group III; 14 praemenopausal patients aged 37-52 (mean 47) years received 1000 mg MPA daily for metastasized breast cancer. Group IV; 27 post-menopausal patients aged 53-78 (mean 68) years were treated with 1000 mg MPA daily for metastatic breast cancer as well. A fifth group of initially 86 patients aged 40-86 (mean 63) years after surgery for endometrial carcinoma stage I served as untreated control for groups II and IV. Cholesterol and triglyceride concentrations were measured enzymatically lipoproteins were determined by quantitative electrophoresis and precipitation and apolipoproteins A1 and B were quantified by kinetic rate nephelometry. Whereas in patients of group I no changes of lipid and lipoprotein parameters were observed, daily oral doses of 200 mg MPA and more led to a marked fall in alpha-lipoprotein-, HDL-cholesterol and apolipoprotein A1 levels. beta-Lipoprotein-, LDL-cholesterol and apolipoprotein B concentrations rose significantly in Groups III and IV. The relevance of these findings in terms of athero-genicity is discussed.

Adult↗