PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “LIPID METABOLISM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1991

[Indicators of lipid metabolism and the blood lipid peroxidation system in men with regard to hereditary predisposition to atherosclerotic vascular pathology].

Lipid metabolism and the blood lipid peroxidation system were examined in 56 military males living in rather similar conditions. The parameters in question were compared in the following groups: (1) control subjects, including healthy individuals without a family history of atherosclerotic vascular abnormalities; (2) healthy subjects with a family history of atherosclerosis; (3) patients with coronary heart diseases. There were significant differences only in single cases between the groups. The application of a system of grids setting upright the distribution curves for the parameters under study proved to be effective in finding significant differences between the groups, showing the value of the hereditary factors in the development of atherogenic lipid changes.

Adult↗
PubMed2006

Alcohol and lipid metabolism.

Hepatic lipid metabolism is controlled by several master transcription factors, in particular peroxisome proliferator-activated receptor-alpha (PPAR-alpha) and sterol response element binding protein-1 (SREBP-1). Peroxisome proliferator-activated receptor-alpha is a receptor for free fatty acids (FFA), and can activate genes involved in transport, oxidation, and export of FFA. Sterol response element binding protein-1 is a sensor for the level of cholesterol in the liver, and is able to activate genes involved in synthesis of cholesterol and FFA. Chronic ethanol treatment of cells or animals inhibited PPAR-alpha function and activated SREBP. In addition, ethanol inhibited adenosine monophosphate-dependent protein kinase (AMPK). The AMPK controls fatty acid metabolism by inhibiting acetyl-coenzyme A carboxylase, reducing malonyl-coenzyme A, and thereby permitting fatty acid transport into and oxidation in the mitochondrion. Adenosine monophosphate-dependent protein kinase was inhibited in alcohol-treated animals and cells. The mechanisms by which ethanol affects AMPK and the transcription factors are as yet incompletely understood.

AMP-Activated Protein Kinases↗
PubMed1993

Effect of metabolism modifiers on lipid metabolism in the pig.

Porcine somatotropin (pST) and certain beta-adrenergic agonists are potent metabolic modifiers that can improve performance in pigs. Pigs treated with either compounds utilize feed more efficiently and are leaner than controls. Comparative slaughter data clearly demonstrate that pST and some beta-agonists stimulate protein deposition. Porcine somatotropin decreases lipid deposition, but this is not the case for all beta-agonists. Somatotropin decreases lipid deposition through decreasing adipose tissue sensitivity to insulin, inhibiting lipogenesis, and perhaps stimulating lipolysis. Although lipolysis is increased during pST treatment of growing pigs, the greatest consequence is decreased lipogenesis. Although under controlled conditions certain beta-agonists stimulate lipolysis and inhibit lipogenesis, the limited metabolic studies suggest that at doses that are most efficacious for enhanced protein deposition, there are limited effects on lipid metabolism. In part, this may be due to desensitization of adipose tissue beta-adrenergic receptors and possibly a consequence of antagonism of beta-receptors.

Adrenergic beta-Agonists↗
PubMed1987

Influence of minor plant constituents on porcine hepatic lipid metabolism. Impact on serum lipids.

The effects of plant constituents on lipid metabolism were examined in swine that had been fed for 4 weeks a standard diet containing, in addition, (per kg diet) 3.15 g of the methanol serial solvent fraction garlic bulbs or 3.5 g of the petroleum ether solubles high-protein barley flour or 5 mg of the plant growth regulator, AMO 1618. All treatments suppressed 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and cholesterol 7 alpha-hydroxylase activities. Modest increases in serum triglycerides were associated with significantly increased hepatic lipogenic activities in response to all treatments except that of the barley extract. The methanol solubles of a second lot of garlic were fractionated by HPLC and tested in an avian hepatocyte system. One component, an isoprenoid metabolite, MW 358, suppressed HMG-CoA reductase.

Animal Feed↗
PubMed2003

Normal lipid metabolism, familial hyperlipidaemia, lipid intervention and their benefits.

Some recent developments in lipoprotein metabolism, familial hyperlipidaemias and lipid lowering therapies with reference to coronary artery disease (CAD) are reviewed. LDL-cholesterol (LDL-C) level and particle subclass are important determinants of the extent of cholesterol delivery to the peripheral tissues and thereby of atherogenesis and CAD. LDL modifications (eg, oxidation, adduct formation, desialylation, glycation, etc) enhance the above process. HDL particles bring cholesterol from peripheral tissues to liver (reverse cholesterol transport, RCT). ApoA1, LCAT enzyme, ABCA1 and cholesterol ester transfer protein are involved in RCT. Paraoxonase of HDL prevents oxidation of other lipoproteins and probably hinders atherogenesis. Lp(a) particles are like LDL except the presence of apo(a) that inhibits fibrinolysis and are epidemiologicaly linked to the development of CAD. Indians have high Lp(a), in comparison to whites. Familial hyperlipidaemias are due to altered metabolism of lipoproteins affecting plasma lipid profile. Majority of such patients are prone to atherosclerosis and CAD. LDL-C is the primary target of lipid lowering therapy. Statins inhibit HMG-CoA reductase and are mainly used alone or with other drugs for lowering blood lipids. 'National Cholesterol Education Program' now recommends a stringent LDL-C control ( < 100 mg/dl) for CAD and CAD risk equivalents. Therapeutic lifestyle changes and drug therapy are the main modalities to reduce blood lipids, aiming at total reduction of short-and long-term coronary risk for all (primary prevention), and of coronary mortality and morbidity in patients with CAD (secondary prevention).

Coronary Disease↗
PubMed1992

Evidence for an altered lipid metabolic state in circulating blood monocytes under conditions of hyperlipemia in swine and its implications in arterial lipid metabolism.

Circulating blood monocytes were isolated from normal and hypercholesterolemic swine, and the monocyte lipid compositions and lipid biosynthesis profiles were assessed. The data indicate that monocytes freshly isolated from hyperlipemic swine have increased phospholipid and cholesterol contents and have increased biosynthetic capability for synthesizing phospholipids, triglycerides, and cholesteryl esters, but not cholesterol. The profile of the stimulated lipid synthesis capability is similar to that of the swine aortic intima undergoing atherogenic change. These studies indicate that circulating blood monocytes in hyperlipemic swine, which are known to give rise to intimal foam cells in the early fatty streak lesion, can contribute to altered vessel lipid metabolism without a requirement for in situ modification by wall factors.

Animals↗
PubMed1984

Thyroid hormone action on intermediary metabolism. Part II: Lipid metabolism in hypo- and hyperthyroidism.

Despite their enhanced endogenous de novo cholesterol synthesis, hyperthyroid patients exhibit decreased total and low-density lipoprotein (LDL) cholesterol levels in the serum because of a concomitant increase in LDL catabolism, cholesterol excretion by bile and a reduced enterohepatic bile acid circulation. Hypothyroidism exhibits a reduction (1) in the synthesis of cholesterol and (2) in LDL catabolism, whereas cholesterol reabsorption is unchanged or even enhanced. In addition, obese hypothyroid patients showed an increased cholesterol synthesis which is independent of thyroid hormones and which contributes to the observed LDL cholesterolaemia. Thyroid hormones per se have only a minor influence on plasma triglyceride (TG) levels, but they induce an acceleration of TG turnover and chylomicron clearance rate. In addition, the hepatic lipogenic capacity is increased in hyperthyroidism and reduced in hypothyroidism. However, hepatic total and very low-density lipoprotein (VLDL) triglyceride output is decreased by thyroid hormones due to a reduced re-esterification and a simultaneously increased oxidation of newly synthesized fatty acids. Hypothyroid livers, by contrast, reveal an increased VLDL secretion. Despite their reduced lipogenesis, obese hypothyroidism is often accompanied by a hypertriglyceridaemia type III. The simultaneous stimulation of the synthesis of fatty acids, which are still in part converted to TG, and the degradation of TG contributes to the enhanced thermogenesis in hyperthyroid patients. The concentration and turnover of free fatty acids (FFA) are increased in hyperthyroidism, resulting from a thyroid hormone-induced increase in: (1) lipolysis, explained by an increased adipose tissue sensitivity for lipolytic hormones; and (2) oxidation of fatty acids to CO2 as well as to ketone bodies (KB).(ABSTRACT TRUNCATED AT 250 WORDS)

Cholesterol↗
PubMed1990

Changes in hepatic lipid metabolism associated with lipid accumulation and its reversal in rats given the peroxisome proliferator LY171883.

Dietary administration of 0.05, 0.1, and 0.3% LY171883 to rats for 1 day caused a dose-related increase in hepatic triglycerides. When added to rat liver mitochondria in vitro, LY171883 caused competitive inhibition of carnitine palmitoyltransferase 1 (CPT-1), the rate-limiting enzyme for mitochondrial fatty acid oxidation. This effect appears to be involved in the lipid accumulation. The hepatic triglycerides in rats given 0.1% LY171883 increased progressively through 3 months of treatment. In contrast, hepatic triglycerides in high-dose rats returned to control levels by Day 3 and remained there throughout the study. The regression of the lipid corresponded with increases in hepatic peroxisomal beta-oxidation, mitochondrial beta-oxidation, and CPT-1 activity of up to 13-, 7-, and 3.2-fold, respectively. The 0.1% dose increased these parameters modestly compared to those of high-dose rats (2-, 3-, and 1.6-fold, respectively). Addition of LY171883 to mitochondria from rats given dietary treatment for 2 weeks inhibited CPT-I by the same percentage as in control mitochondria. In mid-dose rats, the induction of CPT-I was largely negated by LY171883 in vitro. Even with the inhibition, CPT-I activity in mitochondria from high-dose rats remained 2-fold higher than that in untreated controls. The data suggest that the induction of CPT-I in high-dose rats was sufficient to overcome the inhibitory action of LY171883. The increased oxidative capacity in peroxisomes and mitochondria led to the regression of the lipid in high-dose rats. The more modest increases in fatty acid oxidation in rats given 0.1% LY171883 were not sufficient to reverse the lipid accumulation.

Acetophenones↗