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Results for “LIPID METABOLISM”

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PubMed1990

[Lipid metabolism and aging].

Lipids have important biochemical functions, but their excess in plasma is a risk factor for atherosclerotic disease. After puberty, the plasma total and low-density lipoprotein (LDL) cholesterol concentrations increase with age as a consequence of an increase in production and a decrease in catabolism mediated by LDL receptors. On the other hand, the plasma high-density lipoprotein (HDL) cholesterol concentrations remain constant. The correlation between serum cholesterol and coronary risk becomes weak with age but also exists in the elderly, while low levels of HDL cholesterol remain to be a risk. The rise in serum triglycerides with age results mainly from the increase in body weight and the decrease in physical activity. Dietary polyunsaturated fatty acids (PUFAs) such as linoleic acid protect against progression of atherosclerosis in part by their hypocholesterolemic effect. The proportion of linoleic acid in serum phospholipids decreases with age. This change also is a separate risk factor for cardiac and cerebral infarction. Among many prostanoids, prostaglandin I2 has antiaggregatory and vasodilatory effects and thromboxane A2 has the opposite effects. Lipid peroxides which are produced inevitably from PUFAs may damage biomembranes and might accelerate cellular aging. The questions of whether dietary manipulation can reduce the age-related changes in lipid metabolism and can improve cellular functions are of major importance.

Adolescent↗
PubMed1986

Effects of oral contraceptives on lipid metabolism.

This discussion of lipid metabolism involves lipoprotein components, the known effects of contraceptive steroids on lipoprotein metabolism and the relationships of lipid and lipoprotein parameters to cardiac risk.

Cholesterol, HDL↗
PubMed1997

Women with insulin-dependent diabetes mellitus (IDDM) complicated by eating disorders are at risk for exacerbated alterations in lipid metabolism.

OBJECTIVE: To examine lipid parameters that are affected in women with insulin-dependent diabetes mellitus (IDDM) who engaged in disordered eating behaviours. DESIGN: Randomized, unmatched. SETTING: Tertiary care. SUBJECTS: Ninety women (18-46 y) with IDDM. INTERVENTIONS: Classification of subjects based on severity of eating disorder: clinical (n = 14), subclinical (n = 13) and control (n = 63). Blood was analysed for glycosylated haemoglobin (HbA1c) and serum for triglycerides and cholesterol. Carotenoid and tocopherol concentrations were analysed by high performance liquid chromatography (HPLC). Dietary intake was assessed by the National Cancer Institute food frequency questionnaire. RESULTS: HbA1c was significantly increased im women demonstrating clinical and subclinical symptoms compared to control (10.4 +/- 2.6, 10.0 +/- 1.5 and 8.3 +/- 1.6%, respectively, P < 0.05). Triglycerides concentrations were significantly increased in women with subclinical eating disorders compared to controls. In women who intentionally omitted or reduced insulin, triglyceride cholesterol and HbA1c were significantly increased compared to controls. Women with IDDM and eating disorders who exhibited bulimic behaviours consumed significantly more energy, total fat and cholesterol compared to controls and women with eating disorders who were restrained eaters. CONCLUSION: While IDDM is known to perturb lipid metabolism, these data demonstrate that eating disorders, in combination with IDDM, results in additional alterations in lipid metabolism.

Adolescent↗
PubMed1998

[The role of estrogens in hormonal regulation of lipid metabolism in women].

In the view of lipid metabolism, adipose tissue and liver are the most important tissues for 17-beta-estradiol, the main estrogen in women's body. The lack of estrogens in women after menopause may cause coronary heart disease. It is considered, that 25 to 50% of positive effect of estrogens which are given to postmenopausal women is connected with their action on lipid metabolism. Blood plasma parameters which characterize lipid metabolism return to their physiological values during estrogens therapy. Estrogens are transferred to adipose tissue cells and liver cells by endocrine and paracrine way. They are also produced in these cells from androgens. In adipocytes 17-beta-estradiol can be stored as its esters with long-chain fatty acids. It was proved that estrogens receptors are present in adipocytes and hepatocytes but their density is much lower than in gonads. On the cellular level estrogens regulate mRNA production for particular proteins among which there are proteins involved in lipid metabolism. In adipose tissue 17-beta-estradiol has a direct effect on lipoprotein lipase (LPL) and hormone-sensitive lipase (HSL). In the case of the first enzyme its synthesis is faster, while the synthesis of the latter is slower. On the other hand, indirect action of estrogens on adipose tissue is connected with the stimulation of the releasing of other hormones which increase HSL activity. To this group of hormones there belong catecholamines, growth hormone (GH) and glucagon. In liver 17-beta-estradiol regulates the rate of synthesis of structural apolipoproteins for VLDL and HDL. 17-beta-estradiol reduces the rate of apoB-100 synthesis, while stimulates apoA-I and apoA-II synthesis. HDL fraction containing apoA-I and apoA-II is necessary for chylomicrons and VLDL degradation as well as direct and indirect cholesterol transport to liver. Moreover, in hepatocytes estrogens stimulate the synthesis of apoC-III, while they decrease the synthesis of hepatic lipase (HL). In conclusion, 17-beta-estradiol by regulating lipid metabolism in adipocytes and hepatocytes modulates the concentration of lipid substances in plasma. The lack of 17-beta-estradiol leads likely to various lipid metabolism disorders in women after menopause. Estrogens therapy in these postmenopausal women may result in the improvement of lipid metabolism.

Adipose Tissue↗
PubMed1983

[Atherogenic changes in lipid metabolism caused by alcohol].

Plasma lipid composition, and plasma and myocardial high-density lipoprotein (HDLP) content were examined in subjects who died of acute ethanol poisoning and in cases of sudden coronary death. Alcohol-induced disorders of lipid metabolism were in many respects similar to lipid metabolic disturbances associated with coronary disease (hypertriglyceridemia, hyperpre-beta- and hyper-beta-lipoproteinemia, myocardial lipoidosis). These disorders of lipid metabolism had developed in the presence of increased blood HDLP and cholesterol HDLP, which are known to produce an anti-atherogenic effect.

Alcoholic Intoxication↗
PubMed2002

[The role of lipid metabolism in Alzheimer's disease].

Lipid metabolism in the central nervous system has been focused as an important factor of Alzheimer's disease, since the apolipoprotein E gene was discovered as a genetic risk for the disease. Lipid metabolism in the brain, showing relatively closed environment, necessitates lipid reutilization. Cerebrospinal fluid contains only high-density lipoproteins composed of apoE and apoJ secreted from astrocytes and of apoA-I and apoA-II transported via the blood brain barrier. These apolipoproteins can bind to beta amyloid and possibly relate to its clearance. The aggregation of phosphorylated tau, found in neurofibrillary tangles in Alzheimer's brain, is also found in the brain with Niemann-Pick disease, suggesting that the impairment of lipid transport in neuronal cells participates in Alzheimer's disease. Mitochondrial function, lipid production, and acetylcholine production are closely related, and these alterations could be involved in cholinergic dysfunction in Alzheimer's disease. The regulation of lipid metabolism in and outside the brain could be a therapeutic and preventive target for Alzheimer's disease.

Acetyl Coenzyme A↗
PubMed1976

Lipid metabolism in Achlya: studies of lipid turnover during development.

The life cycle of Achlya involves germination of spores to form coenocytic somatic hyphae, followed by differentiation of hyphal tips into sporangia. From germination to release of new spores occupies 27-30 h. Total lipid made up 10% of dry weight in ungerminated spores. After germination, total lipid fell to 6% of dry weight in 15 h, then rose to 7.7% at the time of sporangium formation. Half of the initial loss of lipid took place within 2 h of germination. The ability of Achlya to incorporate [1-14C]acetate into lipid was maximal at the time of sporangium formation, and glycerides were the principal component of total lipid to become 14C-labelled at all stages of the life cycle. Fatty acid synthetase activity measured in cell-free extracts was low in spores and in actively elongating mycelium, but increased during idfferentiation to a level 15-fold greater than that in spores. Fatty acid oxidation, as estimated by the release of 14CO2 from 1-14C-labelled fatty acids, was also maximal at the time of sporangium formation.

Acetates↗
PubMed1995

Effects of fructose ingestion on carbohydrate and lipid metabolism during prolonged exercise in distance runners.

The effects of ingestion of fructose (F), as well as of arginine (A) and citric acid (C) on both carbohydrate metabolism and lipid metabolism during prolonged exercise in seven distance runners on treadmill running were investigated by comparing it with those of glucose + arginine + citric acid (GAC) and placebo. With the values of the plasma glucose, though FAC as well as placebo contrastively indicated almost a flat distribution, GAC increased from 30 min rest before the exercise (i.e., the time for 500 ml intake of GAC) to the beginning of the exercise. The plasma glucose for GAC showed significantly higher values (138 +/- 22 mg/dl) than that for FAC or placebo, whose values were 102 +/- 18 mg/dl and 93 +/- 8 mg/dl, respectively. The plasma glucose for GAC was likely to decrease gradually as the exercise progressed more. At the end of exercise, however, the plasma glucose for FAC indicated significantly higher values (100 +/- 12 mg/dl) than that for GAC, whose values were 89 +/- 12 mg/dl. Though the serum free fatty acid showed upward tendencies of values in all cases of FAC, placebo, and GAC as the exercise progressed, no significant difference of the values in those cases was observed (the following values were drawn at the end of the exercise; FAC:655 +/- 185 microEq/l, placebo:603 +/- 289 microEq/l, GAC:485 +/- 140 microEq/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of nicotine administration on lipid metabolism in rats.

Administration of nicotine to rats resulted in increased concentration of cholesterol, phospholipids and triglycerides in the serum and tissues. HDL cholesterol decreased while the LDL + VLDL cholesterol increased. There was increased tissue cholesterogenesis as evident from the increased activity of HMG-CoA reductase and increased incorporation into tissue unesterified cholesterol. Increased triglyceride synthesis in the tissues was evident from the increased activity of lipogenic enzymes and increased incorporation of label. Hepatic degradation of cholesterol to bile acids was decreased. The uptake of circulating triglyceride rich lipoproteins (chylomicrons and VLDL) was also decreased as revealed by the decreased activity of extrahepatic lipoprotein lipase. Plasma LCAT activity also showed a decrease in the rats given nicotine. The changes produced in the metabolism of lipids on nicotine administration were thus similar to those observed on exposure of rats to cigarette smoke, and it is felt that nicotine may therefore contribute at least partly to the risk posed by cigarette smoking in the development of atherosclerosis.

Animals↗
PubMed1991

Alpha 1 blockers: antihypertensives whose positive metabolic profile with regard to hyperinsulinaemia and lipid metabolism cannot be ignored.

The selective alpha 1-adrenoceptor-blocking agents constitute effective monotherapy in the control of essential hypertension. The failure of well-controlled trials of other antihypertensives to achieve the expected reduction in coronary heart disease has given rise to speculation that the antihypertensives used are atherogenic because of metabolic changes induced in the patient. The selective alpha 1-adrenoceptor blockers have positive effects on carbohydrate metabolism, hyperinsulinaemia and lipid metabolism. These changes, which consist of a modest reduction in total serum cholesterol, an increase in high-density-lipoprotein cholesterol, and a decrease in low-density lipoprotein, very-low-density lipoprotein and triglyceride, accompanied by a reduction in hyperglycaemia and serum insulin levels, have been observed in hypertensive patients. Experimental studies using isolated tissue culture and intact animal systems have confirmed these observations. The changes in metabolism may represent the key to prevention of coronary heart disease in the hypertensive population.

Adrenergic alpha-Antagonists↗
PubMed2006

Functions of sulfur-containing amino acids in lipid metabolism.

It is known that plasma lipid levels are controlled not only by dietary fat and carbohydrate but also by dietary protein and amino acids. Although it used to be thought that the source of protein was important, it is known that amino acid composition, amino acids themselves, and peptides from digested protein are more important than the protein source. Sulfur-containing amino acids (SAAs) are recognized to be some of the most potent modulators of lipid metabolism among amino acids. It has been demonstrated that SAAs have an increasing effect on HDL (high-density lipoprotein)-cholesterol and a decreasing effect on VLDL (very low-density lipoprotein)-cholesterol. These data lead us to propose that SAAs have some beneficial functions against atherosclerotic diseases and metabolic syndrome. Relative availability of SAAs (RASAA) as well as the amount of SAAs in dietary protein would determine lipid metabolism. Therefore, we propose RASAA as a feasible index for improvement of lipid metabolism by amino acids. Although it is not clear how SAAs influence gene expression and lipid metabolism at a molecular level, SAAs change the metabolic pathway through transcriptional stimulation and posttranslational modification of regulatory proteins.

Amino Acids, Sulfur↗
PubMed2003

Life-history evolution and the microevolution of intermediary metabolism: activities of lipid-metabolizing enzymes in life-history morphs of a wing-dimorphic cricket.

Although a considerable amount of information is available on the ecology, genetics, and physiology of life-history traits, much more limited data are available on the biochemical and genetic correlates of life-history variation within species. Specific activities of five enzymes of lipid biosynthesis and two enzymes of amino acid catabolism were compared among lines selected for flight-capable (LW[f]) versus flightless (SW) morphs of the cricket Gryllus firmus. These morphs, which exist in natural populations, differ genetically in ovarian growth (100-400% higher in SW) and aspects of flight capability including the size of wings and flight muscles, and the concentration of triglyceride flight fuel (40% greater in LW[f]). Consistently higher activity of each enzyme in LW(f) versus SW-selected lines, and strong co-segregation between morph and enzyme activity, demonstrated genetically based co-variance between wing morph and enzyme activity. Developmental profiles of enzyme activities strongly paralleled profiles of triglyceride accumulation during adulthood and previous measures of in vivo lipid biosynthesis. These data strongly imply that genetically based elevation in activities of lipogenic enzymes, and enzymes controlling the conversion of amino acids into lipids, is an important cause underlying the elevated accumulation of triglyceride in the LW(f) morph, a key biochemical component of the trade-off between elevated early fecundity and flight capability. Global changes in lipid and amino-acid metabolism appear to have resulted from microevolutionary alteration of regulators of metabolism. Finally, strong genotype x environment (diet) interactions were observed for most enzyme activities. Future progress in understanding the functional causes of life-history evolution requires a more detailed synthesis of the fields of life-history evolution and metabolic biochemistry. Wing polymorphism is a powerful experimental model in such integrative studies.

Adipose Tissue↗
PubMedDate not supplied

[Effect of physical activity on the status of lipid metabolism in pilots].

Lipid metabolism of healthy pilots was investigated and verified by the PWC170 test. Pilots with a lower physical activity showed high levels of cholesterol, triglycerides, total lipids, LDL and low levels of HDL as averaged per group. The PWC170 value and the concentration of lipid fractions in blood were found to be highly correlated, the correlation being nonlinear. The nonlinear regression data suggest that greater physical activity leads to a decrease of the lipid concentration and an increase of the content of high density lipid-protein complexes.

Adult↗
PubMed1990

Sequential changes in lipid metabolism and the fatty acid profile in liver lipids during fasting and sepsis.

The sequential changes in lipid metabolism and in the fatty acid profile of liver lipids during fasting and sepsis were studied. Liver and blood specimens were taken from normally fed rats and from nonseptically and septically fasted rats at 5, 24, and 48 hr. Sepsis was induced by injecting live Escherichia coli bacteria intraperitoneally. Sepsis attenuated the fasting-induced increase in beta-hydroxybutyrate and reduced liver and serum triglycerides at 5 hr. There was a percentage decline in the most abundant fatty acids in neutral lipids, namely oleic (18:1w9) and linoleic (18:2w6) acids. This was seen throughout fasting and septic fasting. These results indicate that 18:1w9 and 18:2w6 are used as energy substrates and are oxidized to beta-hydroxybutyrate during fasting and mainly to carbon dioxide during septic fasting. On the contrary, the most abundant fatty acids in phospholipids, stearic (18:0), arachidonic (20:4w6), and docosahexaenoic (22:6w3) acids, accumulated in neutral lipids and in phospholipids throughout fasting. However, during sepsis this accumulation was reduced in neutral lipids and reversed to a level below that in the fed and fasted state in phospholipids. These results indicate that a disturbance in membrane integrity and function induced by septic fasting may have pathophysiological consequences for lipid metabolism and liver function during sepsis.

Animals↗