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[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↗
PubMed1978

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↗
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↗
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↗
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↗
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↗
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↗
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↗