Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIPID METABOLISM”

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 163 records · Page 9Linked to original sources
PubMed2003

Lipid metabolism and hemocoagulation in patients with atherosclerotic stenosis of the extracranial arteries.

Lipid metabolism, lipid peroxidation and hemocoagulation were studied in 276 patients with ischemic brain disease which developed due to atherosclerotic stenoses of the extracranial cerebral arteries (ECA). The main biochemical parameters were evaluated bearing in mind to the severity of vascular and ischemic lesion of the brain. It has been revealed as s result that the rise of the degree of arterial stenosis correlates well with the growth of the content of atherogenic lipoproteins and of the atherogenicity index. Total cholesterol (Chs) and low density lipoproteins (LDL) have a greater effect in the early disease stages whereas the high triglyceride content combined with LDL plays a relatively more important part in the late stages of vascular lesion. Both medium and high degree stenoses of the ECA are associated with a significant increase in the activity of lipid peroxidation and the build up of the number of primary products of free radical oxidation in the overwhelming majority of patients. Changes in the hemostatic system toward hyper-coagulation are associated with the high thrombotic preparedness of blood. The treatment of patients suffering from cerebral ischemia and atherosclerotic stenosfia of the EGA requires correction of the disorders in lipid metabolism, hemocoagulation and hyperreactivity of the vessel wall in different stages of disease.

Adult↗
PubMed1999

ATP-binding cassette transporter A1 (ABCA1) in macrophages: a dual function in inflammation and lipid metabolism?

Activated lipid-laden macrophages in the vascular wall are key modulators of the inflammatory processes underlying atherosclerosis. We demonstrate here that the ATP-binding cassette (ABC) transporter ABCA1 is induced during differentiation of human monocytes into macrophages. ABCA1 has been implicated in macrophage interleukin-1beta secretion and apoptosis. Moreover, ABCA1 mRNA and protein levels are strongly upregulated by uptake of modified LDL and downregulated by HDL(3)-mediated lipid efflux in macrophages. Mutation analysis in patients with the classical Tangier disease (TD), a monogenetic disorder characterized by hypersplenism, macrophage accumulation and deposition of cholesteryl esters in the reticuloendothelial system, low plasma HDL and premature atherosclerosis, revealed deleterious mutations in their ABCA1 gene. The localization pattern of the mutations within the ABCA1 protein appears to determine the tropism for either the reticuloendothelial system, as seen in the classical TD phenotype, or the artery wall, as in the case of HDL deficiency in the absence of splenomegaly. In a comprehensive analysis of the expression and regulation of all currently known human ABC transporters, we identified additional cholesterol-responsive genes that are induced during monocyte differentiation into macrophages. Our results indicate a dual regulatory function for ABCA1 in macrophage lipid metabolism and inflammation.

ATP Binding Cassette Transporter 1↗
PubMed1994

Prospective evaluation of insulin resistance and lipid metabolism in women receiving oral contraceptives.

OBJECTIVES: It has been suggested that normal women receiving oral contraceptives (OC) may develop a series of metabolic side-effects which relate to the risk of cardiovascular disease. These metabolic disturbances include changes in glucose and insulin metabolism, raised serum lipid and lipoprotein concentrations and elevated blood pressure. All these changes indicate that OC might cause insulin resistance. We have prospectively examined the effect of OC on insulin resistance and lipid metabolism including Lp(a) values. PATIENTS: The study group comprised 13 normally menstruating Chinese women. DESIGN: The study subjects were given a combined triphasic oral contraceptive which was administered on a 21-day on, 7-day off medication cyclic regimen, the first pill being administered on day 5 from the beginning of menses. The metabolic investigations were carried out during luteal phase before OC and again the third week of the third month of OC administration. MEASUREMENTS: Metabolic evaluation including insulin secretion and insulin-mediated glucose uptake were evaluated by oral glucose tolerance test and the modification of insulin suppression test. Fasting triglyceride, cholesterol, HDL-cholesterol and Lp(a) concentrations were also measured. RESULTS: The plasma glucose and insulin responses during a 75-g oral glucose challenge increased significantly (P < 0.05 and P < 0.03, respectively). The steady-state plasma glucose (SSPG) concentrations achieved during constant infusion of glucose, insulin and somatostatin increased significantly after 3 cycles of OC administration (glucose 7.5 +/- 0.8 vs 12.4 +/- 0.7 mmol/l, P < 0.001) while the steady-state plasma insulin (SSPI) concentrations were relatively similar (410 +/- 14 vs 391 +/- 7 pmol/l, NS). Plasma triglyceride levels increased significantly (0.81 +/- 0.12 vs 1.09 +/- 0.19 mmol/l, P < 0.03) following OC administration. Fasting plasma cholesterol, HDL cholesterol and calculated LDL cholesterol concentrations did not change as compared with baseline values, nor did the ratio of total cholesterol to HDL cholesterol. The Lp(a) concentrations did not change during the administration of OC (81 +/- 25 vs 71 +/- 21 mg/l, NS). CONCLUSIONS: These data indicated that intake of OC for 3 cycles induced glucose intolerance, hyperinsulinaemia and insulin resistance in normal menstruating Chinese women. These changes occurred in association with elevated plasma triglyceride concentrations and no alteration in Lp(a) or other lipid values.

Adult↗
PubMed1984

Effect of carnitine on lipid metabolism in the neonate. II. Carnitine addition to lipid infusion during prolonged total parenteral nutrition.

The effect of carnitine administration on lipid metabolism and carnitine and acylcarnitine plasma values of newborn infants, given total parenteral nutrition for the first 7 days of life, was studied during a 4-hour infusion of Intralipid. An increase in plasma concentrations of total carnitine, free carnitine, and short-chain and long-chain acylcarnitine was found, but no significant change in triglycerides, free fatty acids, glycerol, or beta-hydroxybutyrate plasma values was noted, as compared with values obtained without carnitine administration. Moreover, the low free carnitine and short-chain and long-chain acylcarnitine plasma levels found in newborn infants after 7 days of total parenteral nutrition did not seem to impair the utilization of infused lipids. The results support the concept that the relation between the carnitine pool and lipid metabolism can be influenced by intravenous glucose infusion. Low carnitine plasma concentrations do not necessarily signify a depletion of body carnitine, and sufficient tissue carnitine concentrations can probably maintain good lipid utilization for an extended period.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

[Indicators of lipid metabolism in early stages of diabetes mellitus].

The authors studied the lipid metabolism indices (total lipids, cholesterol, triglycerides, phospholipids, serum gonadotropin) in 60 patients with a latent form of diabetes mellitus, 40 persons with doubtful results of TTH, and 120 persons with a normal TTH type. In 50 patients with latent diabetes the lipid metabolism indices were determined depending on the character of treatment--diet treatment, treatment with diet and adebit, and unlimited diet. Disturbance of lipid metabolism indices was noted already at the early stages of diabetes mellitus: there was an elevation of total lipids, triglycerides, serum gonadotropin, and cholesterol. An improvement of lipid metabolism indices occurred under the action of adebit; it produced a particularly significant effect on triglycerides.

Adult↗
PubMed2006

Effects of typical and atypical antipsychotics on glucose-insulin homeostasis and lipid metabolism in first-episode schizophrenia.

RATIONALE: Glucose and lipid metabolism dysfunction is a significant side effect associated with antipsychotics. Although there are many studies about the linkages between drugs and metabolic dysfunction, most of these studies have compared the effects of two antipsychotics on only one metabolic measure: either glucose or lipid metabolism. OBJECTIVES: The present study aimed to investigate the effects of clozapine, olanzapine, risperidone, and sulpiride on glucose and lipid metabolism in first-episode schizophrenia. MATERIALS AND METHODS: One hundred twelve schizophrenics were assigned randomly to receive clozapine, olanzapine, risperidone, or sulpiride for 8 weeks. Planned assessments included body mass index (BMI), waist-to-hip ratio, fasting glucose, insulin, C-peptide, insulin resistance index (IRI), cholesterol, and triglyceride. All measures were collected at baseline and at the end of the 8-week treatment. RESULTS: After treatment, insulin, C-peptide, and IRI were significantly increased in the four groups, but not fasting glucose levels. Cholesterol and triglyceride levels were significantly increased in the clozapine and olanzapine groups. Patients treated with clozapine and olanzapine had higher fasting insulin, C-peptide, and IRI levels than those treated with risperidone and sulpiride. Among the four antipsychotics, the increases of mean BMI from high to low were as follows: clozapine, olanzapine, sulpiride, and risperidone. CONCLUSIONS: This study confirmed that the four antipsychotic drugs were associated with an increase of insulin, C-peptide, and IRI. It was found that clozapine and olanzapine were associated with an increase in cholesterol and triglyceride levels. The effects of clozapine and olanzapine on the glucose and lipid metabolism outweighed those of risperidone and sulpiride.

Adult↗
PubMed2003

Drosophila Perilipin/ADRP homologue Lsd2 regulates lipid metabolism.

Many cells store neutral lipids, as triacylglycerol and sterol esters, in droplets. PAT-domain proteins form a conserved family of proteins that are localized at the surface of neutral lipid droplets. Two mammalian members of this family, Perilipin and adipose differentiation-related protein, are involved in lipid storage and regulate lipolysis. Here, we describe the Drosophila PAT-family member Lsd2. We showed that Lsd2 is predominantly expressed in tissues engaged in high levels of lipid metabolism, the fat body and the germ line of females. Ultrastructural analysis in the germ line showed that Lsd2 localizes to the surface of lipid droplets. We have generated an Lsd2 mutant and described its phenotype. Mutant adults have a reduced level of neutral lipid content compared to wild type, showing that Lsd2 is required for normal lipid storage. In addition, ovaries from Lsd2 mutant females exhibit an abnormal pattern of accumulation of neutral lipids from mid-oogenesis, which results in reduced deposition of lipids in the egg. Consistent with its expression in the female germ line, we showed that Lsd2 is a maternal effect gene that is required for normal embryogenesis. This work demonstrates that Lsd2 has an evolutionarily conserved function in lipid metabolism and establishes Drosophila melanogaster as a new in vivo model for studies on the PAT-family of proteins.

Animals↗
PubMed1975

[The lipid metabolism of the small intestine and its correlation to the lipid and lipoprotein metabolism of the total organism].

It is attempted to discuss the intestinal lipid metabolism particularly as it relates to systemic lipid and lipoprotein metabolism. In an introductory review of recent concepts of intestinal fat absorption special reference is given to the significance of the mixed lipid micelle during the intraluminal phase of fat absorption, to special morphological and functional features of the lumen-absorptive cell interface and to the proposed role of a fatty acid binding protein in the intracellular transport of long chain fatty acids. Furthermore the metabolic fate of absorbed fatty acids within the absorptive epithelial cell is reviewed and pointed out, that certain proteins (f.i. apoprotein B) are of crucial significance for the export of intestinal lipids into lymph. Absorption of dietary fat, however, is not the only function of the intestine in lipid metabolism. Intestinal mucosa is also capable of de novo synthesis of lipids, a function which is elaborated upon in the discussion of intestinal biosynthesis of cholesterol. Since in addition biosynthesis of cholesterol in the liver has been shown to be under sensitive control of cholesterol in intestinal lymph lipoproteins and the intestine represents the only organ, in which serum cholesterol can be excreted (after conversion to bile salts in the liver), the intestine occupies the central role in cholesterol metabolism. The intensive interrelation of intestinal functions and systemic lipoprotein metabolism is underscored by the more recent finding, that the intestine also synthesizes endogenous lipoproteins, which are secreted constantly into intestinal lymph even in the fasting state, thus contributing to plasma very low density lipoproteins. The intestine is the only organ, in which extrahepatic production of endogenous lipoproteins has been demonstrated. In the special section of this paper own original work is presented, elaborating on intestinal metabolism of plasma free fatty acids (FFA) and dealing with the important question, whether plasma FFA are incorporated into intestinal lymph lipoproteins. Studies were conducted in rats initially, which were given a rapid i.v. injection of labelled fatty acids. Mucosal radioactivity of the small intestine was greatest 2 minutes after i.v. 14C-palmitate, and accounted for 1% of administered isotope. Of mucosal 14C, 42% were present in water soluble metabolites, including CO2 and ketoacids, 28% in phospholipids and only 16% in triglycerides. The specific activity of mucosal triglyceride fatty acids (TGFA) was 11 times that of serum TGFA, confirming triglyceride synthesis by intestinal mucosa. The unexpectedly low percent incorporation of 14C-palmitate into triglycerides and its preferential conversion to water soluble metabolites, reflecting oxidation, were confirmed in double label experiments (3H-palmitate intraluminally, 14C-palmitate i.v.), which showed marked differences in the metabolism of fatty acids entering mucosa simultaneously from the two sources. While i.v...

Adult↗
PubMed2006

Lipid metabolism in human endothelial cells.

Although lipids are largely involved in cardiovascular physiopathology, the lipid metabolism in endothelial cells remains largely unknown. Human umbilical vein endothelial cells (HUVECs) were used to investigate the metabolism of complex lipids. The membrane phospholipid homeostasis results from both de novo synthesis and remodelling that ensures the fine tuning of the phospholipid fatty acid composition. Using [(3)H]-glycerol and phosphoderivatives we showed the efficiency of glycerolipid synthesis from glycerol (0.9 nmol h(-1) mg proteins(-1)), but not from its phosphorylated form suggesting the requirement of a functional glycerol kinase in HUVECs. Conversely, the synthesis of triacylglycerols was very low (less than 5% of phospholipid synthesis). The incorporation rate of fatty acids into phospholipids showed that there is a specific fate for each fatty acid in respect to its chain length and saturation level. Moreover in steady state condition, increasing the long chain omega3 polyunsaturated fatty acids in the medium resulted in an increased polyunsaturated/saturated ratio in phospholipids (from 0.42 to 0.63). [(14)C]O(2) was produced form either [(14)C]-glucose or [(14)C]-palmitate indicating the functionality of the oxidation pathways, although beta-oxidation was less efficient than glucose oxidation. The endothelial cell lipid metabolism involves conventional pathways, with functional rates largely slower than in hepatocytes or in cardiomyocytes.

Cardiovascular Diseases↗
PubMed1976

Age-related changes in the lipid metabolism of Fisher 344 rats.

Lipid metabolism of male Fisher 344 rats aged 2-24 months was studied. Serum and liver cholesterol levels did not display the age-related gradual increase seen in other rat strains. An increase in the serum plus liver cholesterol pool from 2 to 6 months was followed by a plateau through 18 months and then another increase at 24 months of age. The triglyceride pool increased from 2 to 6 months and then remained unchanged through 24 months of age. Cholesterol synthesis from acetate decreased 50% between 2 and 9 months and fell only slightly through 24 months of age. Assay of 3-hydroxy-3-methyl glutaryl Coenzyme A (HMG-CoA) reductase showed a similar pattern but did not decrease further after 9 months of age. Cholesterol 7alpha hydroxylase activity was not significantly altered by age. These age- and strain-related differences present an opportunity for a comparative study of the aging process using the parameters of lipid metabolism as indicators.

Acetates↗
PubMed2005

The role of the kidney in lipid metabolism.

PURPOSE OF REVIEW: Cellular uptake of plasma lipids is to a large extent mediated by specific membrane-associated proteins that recognize lipid-protein complexes. In the kidney, the apical surface of proximal tubules has a high capacity for receptor-mediated uptake of filtered lipid-binding plasma proteins. We describe the renal receptor system and its role in lipid metabolism in health and disease, and discuss the general effect of the diseased kidney on lipid metabolism. RECENT FINDINGS: Megalin and cubilin are receptors in the proximal tubules. An accumulating number of lipid-binding and regulating proteins (e.g. albumin, apolipoprotein A-I and leptin) have been identified as ligands, suggesting that their receptors may directly take up lipids in the proximal tubules and indirectly affect plasma and tissue lipid metabolism. Recently, the amnionless protein was shown to be essential for the membrane association and trafficking of cubilin. SUMMARY: The kidney has a high capacity for uptake of lipid-binding proteins and lipid-regulating hormones via the megalin and cubilin/amnionless protein receptors. Although the glomerular filtration barrier prevents access of the large lipoprotein particles to the proximal tubules, the receptors may be exposed to lipids bound to filtered lipid-binding proteins not associated to lipoprotein particles. Renal filtration and receptor-mediated uptake of lipid-binding and lipid-regulating proteins may therefore influence overall lipid metabolism. The pathological mechanisms causing the pronounced atherosclerosis-promoting effect of uremia may involve impairment of this clearance pathway.

Glomerular Filtration Rate↗
PubMed1993

A randomized comparative open study of the effects of two oral contraceptives, Triphasil and Ortho 7/7/7, on lipid metabolism.

This study assessed serum lipid, lipoprotein and apolipoprotein changes during one year in 3 groups of nonsmoking women: 1) Triphasil(R); 2) Ortho(R) 7/7/7; 3) Controls. Both oral contraceptives contain the estrogen, ethinyl estradiol(EE), in combination with a progestin in three different ratios during each cycle. The progestin in Triphasil is d-norgestrel, as the dl-racemate norgestrel (NG), whereas that in Ortho 7/7/7 is norethindrone(NE). Total plasma triglycerides were elevated significantly from baseline (p < 0.001) with Ortho 7/7/7 at 3, 6 and 12 months, but only at 3 months with Triphasil, p = 0.047. Triglycerides were elevated in the LDL fraction with Ortho 7/7/7 at 3 months (p = 0.001), 6 months (p = 0.018) and 12 months (p = 0.010). In contrast, LDL triglycerides were not significantly elevated with Triphasil. Similarly, IDL triglycerides were elevated only in the Ortho 7/7/7 group at 6 months (p = 0.002) and 12 months (p = 0.001). Plasma cholesterol was elevated only in the Ortho 7/7/7 group at 3, 6 and 12 months with p values of 0.009, 0.005 and 0.010, respectively. Cholesterol in the LDL fraction was elevated with Ortho 7/7/7 at 12 months (p = 0.002). Plasma apolipoprotein B (apo B) increased at least 24% from baseline for both the Triphasil and Ortho 7/7/7 groups at 3 and 12 months (p < 0.001). However, at 6 months, apolipoprotein B increased only 17.7% (p = 0.008) with Triphasil compared to 29.7% (p < 0.001) with Ortho 7/7/7 at 6 months. Apo B was increased (p < 0.001) in LDL with Triphasil at 3 months only, whereas LDL apo B was increased at 3, 6 and 12 months with Ortho 7/7/7 (p < 0.001, p = 0.020 and p = 0.012, respectively). Apo B increased dramatically in the IDL fraction of both oral contraceptive user populations, with the range of increases being between 48% and 87% during the year (p < 0.001 at all times). Significant elevations in VLDL apo B ranged from 71% to 106% (p < 0.001) with Triphasil and from 42.4% (p < 0.005) to 72.6% (p < 0.001) with Ortho 7/7/7. In conclusion, norethindrone- and dl-norgestrel-formulations have divergent effects on several components of plasma lipoprotein and lipid metabolism, but both products increase plasma and IDL apo B.

Administration, Oral↗
PubMed1994

[Lipids metabolism evaluated of by vitamin E to total lipid ratio in maternal and cord sera in normal pregnancy].

Changes in plasma levels of lipids peroxide (LPO) and vitamin E(VE) are observed in pregnant women. We measured levels of VE and lipids in 80 maternal and cord sera in normal delivery and obtained the following results. 1. For each lipid and VE, the concentration gradients were preserved in maternal sera to cord sera through placentas. 2. The concentration of VE correlated with that of total lipids (TL) in both sera. 3. The VE to TL ratio (VE/TL ratio) inversely correlated with the concentration of LPO in both sera. 4. The concentration of VE correlated with the VE/TL ratio and there was a more significant correlation of the VE and VE/TL ratio than that of VE and TL in both sera. 5. The VE/TL ratio in maternal serum correlated with VE/TL ratio and the concentration of VE in cord serum. These results suggested that lipids in serum was a regulatory factor in VE and that VE and lipids maintained the gradation of the concentration according to their own placental transport systems. It seems that the fetus has a unique VE which is comparatively lowered. This may be due to the effects of the accelerated lipid metabolism in the fetus.

Female↗
PubMed2004

Weight loss and exercise: implications for muscle lipid metabolism and insulin action.

Implications for Muscle Lipid Metabolism and An accumulation of intramuscular lipid has been reported with obesity and linked with insulin resistance. The purpose of this paper is to discuss: 1) mechanisms that may be responsible for intramuscular lipid accumulation with obesity, and 2) the effects of common interventions (weight loss or exercise) for obesity on skeletal muscle lipid metabolism and intramuscular lipid content. Data suggest that the skeletal muscle of morbidly obese humans is characterized by the preferential partitioning of lipid toward storage rather than oxidation. This phenotype may, in part, contribute to increased lipid deposition in both muscle and adipose tissue, and promote the development of morbid obesity and insulin resistance. Weight loss intervention decreases intramuscular lipid content, which may contribute to improved insulin action. On the other hand, exercise training improves insulin action and increases fatty acid oxidation in the skeletal muscle of obese/morbidly obese individuals. In summary, the accumulation of intramuscular lipid appears to be detrimental in terms of inducing insulin resistance; however, the accumulation of lipid can be reversed with weight loss. The mechanism(s) by which exercise enhances insulin action remains to be determined.

Exercise↗
PubMed1992

[Dyslipoproteinemia and metabolic syndrome. Effects of insulin resistance and hyperinsulinemia on lipid metabolism].

Insulin resistance and consecutive hyperinsulinemia in individuals with the metabolic syndrome are associated with dyslipidemia. This latter is characterised by hypertriglyceridemia and a diminishment of high-density lipoprotein (HDL) cholesterol in the plasma. In severe forms of insulin resistance, low density lipoprotein (LDL) cholesterol may also be elevated. Hypertriglyceridemia is due to an increase in the rate of synthesis of very low density lipoproteins (VLDL) in the liver, and a reduction in their breakdown by the lipoprotein lipase in non-hepatic tissue. Changes in VLDL metabolism are associated with a reduction in HDL concentrations. In addition, direct effects of insulin on the lipid metabolism have been described. Changes in lipid metabolism due to insulin resistance and hyperinsulinemia may be of significance for the atherosclerosis risk in patients with the metabolic syndrome.

Cholesterol↗