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Results for “LIPID METABOLISM”

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PubMedDate not supplied

[The role of disruption of lipid metabolism in mechanisms of the hepatotoxic effects of cisplatin].

Distinct alterations in the metabolism of lipids and phospholipids as well as activation of lipid peroxidation in liver tissue were detected in mice after administration of a new antitumoral drug cisplatin at a dose of LD50 (13.5 mg/kg) or after the course treatment within 5 days using 1/5 LD50. Content of malonic dialdehyde, diene conjugates and Schiff bases was increased, while the phospholipid composition was altered and concentration of membrane-toxic ingredients was increased. When the effects of cisplatin, administered at a dose of LD50 and during the course treatment, were analyzed more pronounced impairments of lipid metabolism were found during 7-15 days in mice treated with the drug at LD50. However, the drug toxic effect was manifested earlier during the course of treatment and in some cases it maintained for a long time (up to 30 days of the experiment). The data obtained suggest that correction of the cytostatic-induced impairments in liver tissue functions may be carried out by means of the anti-radical drugs.

Animals↗
PubMed1998

Perinatal expression of genes that may participate in lipid metabolism by lipid-laden lung fibroblasts.

Although a morphologically distinct population of lipid-laden interstitial cells (lipofibroblasts, LF), has been identified, the origins and functions of this population during lung development and disease remain undefined. Illumination of the developmental and functional characteristics of two other populations of lipid-laden mesenchymal cells, namely adipocytes and hepatic lipocytes, has fashioned tools that can be used to explore similar properties in pulmonary LFs. As the LF is transiently a very abundant cell in the perinatal lung, we elected to study the perinatal ontogeny of the expression of several genes that are involved in the acquisition of lipids by adipocytes, and may be involved in promoting the triglyceride accumulation that is the morphologic hallmark of the pulmonary LF. We found that the maximal expression of peroxisome proliferator-activated receptor-gamma (PPAR-gamma), at gestational day 21 in the LF, precedes the rise at birth, in the expression of genes that are involved in the hydrolysis of triglycerides at the plasma membrane (lipoprotein lipase, LPL), transport of fatty acids across the plasma membrane (fatty acid transporter, FAT) and in the cytoplasm (adipocyte lipid binding protein, ALBP). The steady-state levels of LPL, FAT, and ALBP mRNAs that were isolated from whole lung tissue showed a similar temporal pattern. The levels of the protein products of the LPL and ALBP genes changed in tandem with those of their precursor mRNAs in the LF, suggesting that these gene products are under pre-translational control. These findings indicate that characteristic adipocyte genes are also expressed in lipid-laden pulmonary fibroblasts and may participate in triglyceride accumulation and metabolism by these cells.

Animals↗
PubMed1990

Some aspects of metabolic adaptations in lipid metabolism during starvation are mimicked by epinephrine in rat adipocytes.

1. The effects of fasting on the neutral lipid synthesis to insulin and/or epinephrine in isolated fat cells have been examined using [1-14C]glucose. 2. The ability of adipocytes from starved rats to synthesize fatty acids from both labeled substrates was markedly diminished compared to adipocytes from control rats. 3. The response of lipogenic stimulation to insulin at all concentrations tested was greatly diminished in adipocytes from 24 hr starved rats. 4. [1-14C]glucose utilization rates in the absence or in the presence of insulin were not significantly different in adipocytes from 24 hr starved rats as compared with control adipocytes, although basal and insulin stimulated glyceride-glycerol synthesis were significantly higher in starved adipocytes. 5. Epinephrine acutely inhibited [1-14C]acetate incorporation into fatty acids for insulin-stimulated lipogenesis in control adipocytes, in contrast, this lipolytic agent strongly increased [1-14C]glucose conversion to triacylglycerols. 6. In both cases, the differences in lipid synthesis capacities found in both nutritional states were abolished by epinephrine.

Acetates↗
PubMed2002

A soy protein diet alters hepatic lipid metabolism gene expression and reduces serum lipids and renal fibrogenic cytokines in rats with chronic nephrotic syndrome.

Nephrotic syndrome (NS) is characterized by the presence of proteinuria and hyperlipidemia. However, ingestion of soy protein has a hypolipidemic effect. The present study was designed to determine whether the ingestion of a 20% soy protein diet regulates the expression of hepatic sterol regulatory element binding protein (SREBP)-1, fatty acid synthase (FAS), malic enzyme, beta-hydroxy-beta-methylglutaryl-CoA (HMG-CoA) reductase (r) and synthase (s), and LDL receptor (r), and to assess whether soy protein improves lipid and renal abnormalities in rats with chronic NS. Male Wistar rats were injected with vehicle or with puromycin aminonucleoside to induce NS and were fed either 20% casein or soy protein diets for 64 d. NS rats fed 20% soy protein had improved creatinine clearance and reduced proteinuria, hypercholesterolemia, hypertriglyceridemia, as well as VLDL-triglycerides and LDL cholesterol compared with NS rats fed the 20% casein diet. In addition, the soy protein diet decreased the incidence of glomerular sclerosis, and proinflammatory cytokines in kidney. Ingestion of the soy protein diet by control rats reduced the gene expression of SREBP-1, malic enzyme, FAS and increased HMG-CoAr, HMG-CoAs and LDLr. However, NS rats fed either casein or soy protein diets had low insulin concentrations with reductions in SREBP-1, FAS and malic enzyme expression compared with control rats fed the casein diet. NS rats fed the soy diet also had lower HMG-CoAr and LDLr mRNA levels than NS rats fed casein. In conclusion, the beneficial effects of soy protein on lipid metabolism are modulated in part by SREBP-1. However, in NS rats, the benefit may be through a direct effect of this protein on kidney rather than mediated by changes in expression of hepatic lipid metabolism genes.

Animals↗
PubMed2002

[Disturbance of lipid metabolism].

The disturbance of lipid metabolism is seen in some inherited diseases and also in patients with some kinds of underlying diseases. The presence of its disturbance can be detected by measuring the concentrations of cholesterol and triglyceride in serum. Although hyperlipidemia or hypolipidemia is the result of abnormal lipid metabolism, hyperlipidemia is of more concern to physicians because of the close association with atherosclerosis. Responsible genes for some primary (or hereditary) hyperlipidemic diseases have been confirmed as follows; LPL or apo C-II for primary chylomicronemia, LDL receptor for familial hypercholesterolemia and apo B-100 for familial defective apo B-100. However, the responsible gene remains controversial for familial combined hyperlipidemia, though AI/CIII/AIV cluster is one of the possible candidate genes. Secondary hyperlipidemia is caused by various diseases such as diabetes mellitus, renal diseases and cholestasis. This type of hyperlipidemia is improved by therapy for the underlying diseases. To date, the mechanism of lipid metabolism has been defined in a molecular basis. In fact, sterol regulatory element-binding protein (SREBP), peroxisome proliferator-activated receptor (PPAR) and ATP-binding cassette transporter subfamily A, member 1(ABCA1) were recently identified and it was demonstrated that these regulate lipid metabolism.

ATP Binding Cassette Transporter 1↗
PubMed1991

[Relation between hepatic lipid metabolism and the formation of lipid plaques in the rabbit aorta in an experimental model of atherosclerosis].

The objective of the work was to follow up on a model of experimental atherosclerosis induced in rabbits by a 1% cholesterol diet the mutual relationship of the deposition of total cholesterol as well as esterified and free fatty acids in the liver and the formation of lipid plaques in the rabbit aorta. The authors investigated also the influence exerted on this process by the s.c. administration of calcium antagonists--Verapamil 0.25 mg.kg-1.day-1 (Lek Ljubl., Jugoslavia), Dilthiazem 2 mg.kg-1.day-1 (Lachema CSFR) and Isradipine 2.5 mg.kg-1.day-1 (Isradipine--N Sandoz, Ltd, Switzerland). The interference of calcium antagonists with the lipid metabolism in the liver as well as the transport mechanism of lipids in the blood stream is differentiated. Verapamil administered in therapeutic doses promotes HDL-cholesterol formation and thus hastens the cholesterol transport from the blood stream into the liver where the latter cumulates. This may be one of the mechanisms of the antiatherogenic action of verapamil. On the other hand, isradipine and in particular dilthiazem administered in treble doses, as compared with therapeutic doses, slightly potentiated the formation of lipid plaques in the rabbit aorta and reduced the HDL-cholesterol level and thus also the cholesterol shift to the liver.

Animals↗
PubMed1990

[Effects of intra-partum stress on lipid metabolism. Adaptation of plasma lipid transport systems in neonates].

UNLABELLED: Intrapartum asphyxia modifies lipoprotein cholesterol distribution with possible repercussions related to membrane structures and its metabolic functions. We have studied plasma lipid profile and plasma lipoproteins cholesterol distribution in cord blood from 115 newborn infants and 72 pregnant women at delivery. RESULTS AND DISCUSSION: newborn infants with perinatal asphyxia (n, 48; pHua less than 7.20) have a higher cord blood triglyceridemia and lower plasma HDL-cholesterol, associated to high significant concentrations of atherogenic ratios (CT/HDLc, LDLc/HDLc) than normal newborn infants (n, 67; pHua = 7.20) [TG, 54.81 +/- 2.96 mg/dl vs 45.74 +/- 2.10 mg/dl (p less than 0.005); CT/HDLc, 24.00 +/- 1.30 mg/dl vs 29.62 +/- 1.12 mg/dl (p less than 0.05); LDLc/HDLc, 1.38 +/- 0.10 vs 1.07 +/- 0.06 (p less than 0.01)]. The highest triglycemia and atherogenic ratios in the acidotic newborn infants reveal deep changes in "esterified cholesterol/binding proteins" system, whereon "Apo A1-LCAT-Apo D" molecular complex binding HDL participate. More studies must be done to understand well this phenomenology. Furthermore, at delivery, pregnant women, that their newborn infants suffer an intrapartum hypoxia, had lower lipidemia than those who had newborn infants with intrapartum physiological stress.

Adaptation, Physiological↗
PubMed2006

Dietary conjugated linoleic acid lowered tumor necrosis factor-alpha content and altered expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of Zucker rats.

Type-2 diabetes is characterized by obesity-related insulin resistance. Insulin resistance and accompanying hyperinsulinemia have been reported to play an important role in pathogenesis of the metabolic syndrome. Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has attracted considerable attention because of its potentially beneficial biological effects. Previous studies showed that dietary CLA alleviates diabetes through improvement of glucose tolerance and insulin-stimulated glucose transport activity in skeletal muscle of diabetic rats. Skeletal muscle plays an important role both in insulin-mediated glucose metabolism and in lipid metabolism. In the present study, we evaluated comprehensively the effect of dietary CLA on the expression of genes related to lipid metabolism and insulin sensitivity in the skeletal muscle of obese, diabetic Zucker rats. After 8 weeks of feeding, expression of lipogenic genes was decreased in tendency, while expression of lipolytic genes was markedly increased by dietary CLA. Additionally, expression of genes-related insulin sensitivity, such as adiponectin receptor 1, was significantly enhanced, and mRNA level of peroxisome proliferator activated receptor-alpha, known as a transcriptional factor related lipid metabolism and insulin signaling in skeletal muscle, was markedly increased in CLA-fed rats. We also showed that dietary CLA significantly decreased the level of tumor necrosis factor-alpha (TNF-alpha), associated with the development of insulin resistance, in the skeletal muscle of Zucker rats. We suppose that the attenuated TNF-alpha accumulation in skeletal muscle may contribute to the alteration of expression of several genes and the alleviation of insulin resistance in CLA-fed Zucker rats.

Animals↗
PubMedDate not supplied

[Metabolic effects of ethanol and lipid metabolism in the rat liver].

Effect of ethanol intoxication of lipid metabolism in rat liver tissue was studied after daily intraperitoneal administration of 2g ethanol per kg of body mass within a week. Administration of ethanol led to an increase in content of total lipids, cholesterol and triacylglycerides in liver tissue as well as to elevation of relative content of lysophosphatidyl choline and cardiolipin and to a decrease of phosphatidyl choline. Under conditions of the intoxication incorporation of I-14C-acetate into triacylglycerides, phosphatidyl choline and phosphatidyl ethanolamine was decreased mainly as a result of a decrease in specific radioactivity of fatty acids of these lipids.

Alcoholic Intoxication↗
PubMedDate not supplied

[Mexidol corrects model post-reanimation changes in cerebral lipid metabolism].

The lipid spectrum of brain tissues in various stages of post-reanimation period was studied in rats upon clinical death modeled by cardiovascular fascicle ligation according to V. G. Korpachev. Reproduction of same model on the background of mexidol was characterized by (i) an increase in phosphatidylserine, (ii) normalization of the relative content of phosphatidylethanolamine and cholesterol, (iii) stabilization of the content of phosphatidylcholine, sphyngomyelin, lysophosphatidylethanolamine, and free fatty acids, and (iv) the absence of lysophosphatidylserine in late post-reanimation period (30 days) upon mexidol reperfusion. Mexidol also favored the development of protective and adaptive reactions on the level of lipid components of cerebral cell membranes in the early period upon reperfusion and prevented from the development of irreversible changes in cerebral phospholipid metabolism in the late post-reanimation period.

Animals↗