Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Lipid Metabolic Effects”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 19 recordsLinked to original sources
PubMed1992

Desogestrel-ethinylestradiol, an oral monophasic contraceptive. Clinical and lipid metabolic effects: a 5-year experience.

A comparative study of 5 years' duration using desogestrel (DSG), levonorgestrel (LN), and norethindrone (NET), combined with ethinyl estradiol (EE), was conducted. A total of 4499 cycles on DSG-EE, 3691 on LN-EE (1980 on triphasic and 1711 on monophasic schemes) and 1680 on NET-EE was evaluated. A contraceptive efficacy of 100% was obtained in all the groups. Minimal side effects were observed. In particular, body weight in those women on DSG-EE did not show noticeable changes and headaches were minimal. No alterations on blood pressure readings or on the routine laboratory tests were noticed in any of the groups. There was a significant increase in high-density lipoprotein-c (HDL-c) in women on DSG-EE. There was no change in NET-EE, and a significant decrease in women on LN-EE in both schemes. Changes in LDL-C, very low density lipoproteins, triglycerides, total lipids, total cholesterol, and glucose were not significant, although there was some increase at 60 cycles on triglycerides on those women on DSG-EE and on NET-EE. At the end of 5 years, 76% of women continued on DSG-EE. They indicated their satisfaction with this method.

Americas↗
PubMed1993

Lipid metabolism effects with desogestrel-containing oral contraceptives.

Desogestrel is a gonane progestogen that in early studies had an improved ratio between desired progestational effects and undesired androgenic effects. A review of more than 50 clinical studies suggests that desogestrel differs from progestins currently used in oral contraception in that it does not interfere with the estrogen effects on lipoprotein metabolism. This profile is attributable to the high selectivity of desogestrel.

Animals↗
PubMed1982

Does progestogen reduction in oral contraception parallel reduced lipid metabolic effects?

Twelve young fertile women participated in a cross-over design study whose purpose was to evaluate the effect on lipid metabolism induced by two sequential contraceptive preparations. Sequilarum (50 micrograms of ethinylestradiol + levonorgestrel where the levonorgestrel dose is varied from 50 micrograms during the first 11 days up to 125 micrograms during the lst 10 days of the cycle) was compared with Ovanone (50 micrograms of ethinylestradiol for 22 days with the addition of 2.5 mg lynestrenol during the last 15 days of the cycle). Serum triglycerides, phospholipids, free and total cholesterol were determined, and also was the level of these lipid components in ultracentrifugally isolated lipoprotein lipids. The relative fatty acid composition of serum lecithin and serum cholesterol ester was assessed by gas-liquid chromatography. As expected, both of these preparations are predominantly estrogenic in their effects on lipoprotein metabolism, since both raise serum and VLDL triglyceride levels. The absence of any substantial influence on HDL cholesterol should probably be interpreted as a modifying effect of the progestogen component of both preparations. As to the relative fatty acid composition of serum lecithin the shift induced in palmitic and stearic acids was the same as found in earlier studies when 17C-alkylated exogenous sex steroids were administered, i.e. an increase in the palmitic acid concomitant with a decrease in the stearic.

Adolescent↗
PubMed1993

[The clinical and lipid metabolic effects of a gestoden- and ethynyl estradiol-based monophasic contraceptive].

This is a clinical study to evaluate the efficacy, clinical side effects and in lipid metabolism of a new hormonal contraceptive preparation containing 75 mcg. of ethinyloestradiol. Thirty Mexican health women in reproductive age were studied for 12 months, giving a total of 360 cycles. The medication was highly effective for contraception, because pregnancies did not occur in this period. The clinical side effects were mild and less frequent that the ones informed with the use of other available hormonal oral contraceptives. In lipid metabolism, we did not find the adverse effects most frequently observed with the use of previous progestagens. This study, like previous ones, concludes that the combination of gestodene and ethinylestradiol is highly effective as a contraceptive with a low incidence of collateral side effects and due to its lack of interference with the metabolism of lipids is particularly suited for cases of high risk to develop pathology associated with alterations in lipid metabolism.

Adolescent↗
PubMed1993

[Effect of three antihypertensive drug groups on lipid metabolism. Effects of alpha receptor blockers, central sympatholytic drugs and vasodilators].

Basic remarks and aims: Alpha-receptor blockers, central sympathicolytic agents and vasodilators are all drugs that are often used to treat hypertension. On the basis of a study of the literature, the effects of these groups of substances on lipid metabolism are described. Main points discussed: Although the data available are few, vasodilators, in particular dihydralazine and hydralazine appear to have no unfavorable effect on serum lipids. Nor do the centrally acting alpha-receptor agonists, such as methyldopa and clonidine have any unfavorable effect, with the exception of the decrease in the HDL cholesterol observed under methyldopa. The selective alpha-1-receptor blockers, prazosin, doxazosin and urapidil, even have a positive effect of varying degree on lipid metabolism: increase in HDL cholesterol and decrease in triglycerides. Long-term studies over a number of years are, however, lacking. The effect of labetalol, reserpine and guanethidine on lipid metabolism cannot yet be definitively assessed owing to a lack of data.

Adrenergic alpha-Antagonists↗
PubMed1987

Clinical and lipid metabolic effects of unopposed oestrogen and two oestrogen-progestogen regimens in post-menopausal women.

No differences in the clinical effects on climacteric complaints of an unopposed oestrogen and two oestrogen-progestogen regimens were observed in a double-blind cross-over study. Only 4 out of 18 women with an intact uterus had withdrawal bleeding during oestradiol valerate (2 mg/day) treatment alone, but 14 out of 18 had regular bleeding during the two oestrogen-progestogen regimens (oestradiol/medroxyprogesterone acetate and oestradiol/levonorgestrel (LNG], each of which prevented the development of endometrial hyperplasia. High-density-lipoprotein cholesterol (HDL-CH) concentration remained 6% above the initial level and the atherogenic index (low-density-lipoprotein (LDL) cholesterol to HDL-CH ratio) improved significantly during the oestradiol/medroxyprogesterone acetate regimen, while the HDL-CH concentration fell by 20% in relation to the initial level and there was a deterioration in the atherogenic index during the oestradiol/LNG regimen. The data suggest that both of these oestradiol/progestogen combinations are clinically as effective and well-tolerated as oestradiol alone, but that combined oestradiol/medroxyprogesterone acetate causes fewer adverse lipid metabolic effects than the oestradiol/LNG combination.

Cholesterol↗
PubMed1993

[Lipid metabolism--effect of cardiac agents and ACE inhibitors. Effects of anti-arrhythmia agents, ACE inhibitors, positive inotropic substance and anti-angina agents].

AIM: Cardio-active substances and ACE-Inhibitors are often employed in patients with metabolic disturbances. The question as to whether they have any effect on the lipid levels therefore needs to be answered. MAJOR POINTS STUDIED: The effects of antiarrhythmics, ACE-inhibitors, positively inotropic substances and antianginal substances on lipid metabolism are discussed on the basis of a search through the literature. The wealth of data permit the conclusion that many of the drugs in these substance groups are neutral in terms of metabolism. There are, however, also individual substances that lead to an elevation of lipid levels. Via an improvement in glucose tolerance, ACE-inhibitors can contribute to a lowering of triglyceride concentrations and an increase in the HDL cholesterol levels. For a number of substance groups, the data available still do not suffice to permit a definitive conclusion to be drawn. CONCLUSION: In the case of treatment with the above-mentioned substance groups, effects on lipid metabolism should be checked wherever this is in doubt. This applies, of course, in particular to patients already suffering from hyperlipoproteinemia.

Angina Pectoris↗
PubMed1992

Characterization of 3T3-L1 storage lipid metabolism: effect of somatotropin and insulin on specific pathways.

TLC of total cellular lipids showed that 3T3-L1 cells predominantly accumulate triglycerides. GH and insulin principally regulated glucose utilization for synthesis of the fatty acid portion of 3T3-L1 triglycerides, with little effect on glucose utilization for synthesis of other lipids or triglyceride glycerol. Gas chromatographic mass spectrometry (MS) showed that 50% of 3T3-L1 triglyceride fatty acids are 16-carbon chains. However, 3T3-L1 adipocytes were unusual, in that 20% of their triglyceride fatty acids were C15 or C17 in length, observed by both MS of saponified triglycerides and electrospray MS of intact triglycerides. Gas chromatographic analysis of 14C-labeled fatty acids showed 3T3-L1 utilization of [14C]glucose for synthesis of C15 and C16 fatty acids. Insulin and GH regulated the amount of [14C]glucose incorporation into C15 and C16 fatty acids without altering their relative ratio. GH antagonized all studied insulin-regulated events. GH antagonism of insulin-stimulated 3T3-L1 glucose transport, glucose oxidation, and glucose utilization for lipid synthesis reached a plateau of 50-60% inhibition at 0.1-0.2 nM. Insulin, at 0.1 nM, suppressed 3T3-L1 generation of glycerol from lipolysis by approximately 50%. GH, between 0.04-1.0 nM, fully reversed the insulin-inhibited lipolysis, although GH did not stimulate lipolysis beyond that in untreated control cultures. The results suggest that GH regulates a very early event in the insulin signal transduction pathway, such that is affects all insulin-responsive processes to essentially the same extent.

3T3 Cells↗
PubMed2005

Different roles of liver X receptor alpha and beta in lipid metabolism: effects of an alpha-selective and a dual agonist in mice deficient in each subtype.

Liver X receptor (LXR) alpha and LXRbeta are closely related nuclear receptors that respond to elevated levels of intracellular cholesterol by enhancing transcription of genes that control cholesterol efflux and fatty acid biosynthesis. The consequences of inactivation of either LXR isoform have been thoroughly studied, as have the effects of simultaneous activation of both LXRalpha and LXRbeta by synthetic compounds. We here describe the effects of selective activation of LXRalpha or LXRbeta on lipid metabolism. This was accomplished by treating mice genetically deficient in either LXRalpha or LXRbeta with an agonist with equal potency for both isoforms (Compound B) or a synthetic agonist selective for LXRalpha (Compound A). We also determined the effect of these agonists on gene expression and cholesterol efflux in peritoneal macrophages derived from wild-type and knockout mice. Both compounds raised HDL-cholesterol and increased liver triglycerides in wild-type mice; in contrast, in mice deficient in LXRalpha, Compound B increased HDL-cholesterol but did not cause hepatic steatosis. Compound B induced ATP-binding cassette transporter (ABC) A1 expression and stimulated cholesterol efflux in macrophages from both LXRalpha and LXRbeta-deficient mice. Our data lend further experimental support to the hypothesis that LXRbeta-selective agonists may raise HDL-cholesterol and stimulate macrophage cholesterol efflux without causing liver triglyceride accumulation.

8-Bromo Cyclic Adenosine Monophosphate↗