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At least 19 recordsLinked to original sources
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↗
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↗
PubMed2025

Inhibition of autophagy-lysosomal function exacerbates microglial and monocyte lipid metabolism reprograming and dysfunction after brain injury.

CNS has an overall higher level of lipids than all tissues except adipose and contains up to 25% of total body cholesterol. Recent data demonstrate a complex crosstalk between lipid metabolism and inflammation, suggesting potential contribution of the lipid-rich brain environment to neuroinflammation. While recent data support the importance of brain lipid environment to inflammatory changes observed in age related chronic neurodegenerative diseases, in vivo interactions between lipid environment, lipid metabolism and neuroinflammation in acute brain disease and injury remain poorly understood. Here we utilize a mouse model of traumatic brain injury (TBI) to demonstrate that acute neurotrauma leads to widespread lipid metabolism reprograming in all microglial and brain associated and infiltrating monocyte populations. Additionally, we identify unique microglial and monocyte populations with higher degree of lipid metabolism reprograming and pronounced accumulation of neutral storage lipids, including cholesteryl esters and triglycerides. These lipids accumulate not only in lipid droplets but also in the microglial and monocyte lysosomes and are associated with lysosomal dysfunction and inhibition of autophagy after TBI. Our data indicate that lipid accumulation in these cells is the result of altered lipid handling rather than lipid synthesis and is triggered by phagocytosis of lipid-rich myelin debris generated after TBI. Finally, we use mice with autophagy defects in microglia and monocytes to demonstrate that further inhibition of autophagy leads to more pronounced lipid metabolism reprograming and exacerbated cellular lipid accumulation. Our data suggest a pathological feedback loop, where lipid phagocytosis causes inhibition of autophagy-lysosomal function, which in turn exacerbates cellular lipid retention, reprograming and inflammation.

Journal Article↗
PubMed2024

Integrated Multi-Omics Analyses Reveal Lipid Metabolic Signature in Osteoarthritis.

Osteoarthritis (OA) is the most common degenerative joint disease and the second leading cause of disability worldwide. Single-omics analyses are far from elucidating the complex mechanisms of lipid metabolic dysfunction in OA. This study identified a shared lipid metabolic signature of OA by integrating metabolomics, single-cell and bulk RNA-seq, as well as metagenomics. Compared to the normal counterparts, cartilagesin OA patients exhibited significant depletion of homeostatic chondrocytes (HomCs) (P&#xa0;=&#xa0;0.03) and showed lipid metabolic disorders in linoleic acid metabolism and glycerophospholipid metabolism which was consistent with our findings obtained from plasma metabolomics. Through high-dimensional weighted gene co-expression network analysis (hdWGCNA), weidentified PLA2G2A as a hub gene associated with lipid metabolic disorders in HomCs. And an OA-associated subtype of HomCs, namely HomC1 (marked by PLA2G2A, MT-CO1, MT-CO2, and MT-CO3) was identified, which also exhibited abnormal activation of lipid metabolic pathways. This suggests the involvement of HomC1 in OA progression through the shared lipid metabolism aberrancies, which were further validated via bulk RNA-Seq analysis. Metagenomic profiling identified specific gut microbial species significantly associated with the key lipid metabolism disorders, including Bacteroides uniformis (P&#xa0;<&#xa0;0.001, R&#xa0;=&#xa0;-0.52), Klebsiella pneumonia (P&#xa0;=&#xa0;0.003, R&#xa0;=&#xa0;0.42), Intestinibacter_bartlettii (P&#xa0;=&#xa0;0.009, R&#xa0;=&#xa0;0.38), and Streptococcus anginosus (P&#xa0;=&#xa0;0.009, R&#xa0;=&#xa0;0.38). By integrating the multi-omics features, a random forest diagnostic model with outstanding performance was developed (AUC&#xa0;=&#xa0;0.97). In summary, this study deciphered the crucial role of a integrated lipid metabolic signature in OA pathogenesis, and established a regulatory axis of gut microbiota-metabolites-cell-gene, providing new insights into the gut-joint axis and precision therapy for OA.

Humans↗
PubMed1978

Lipid metabolism in the vitamin-B12-deprived rat.

Rats were deprived of vitamin B12 in order to study the effect of this deprivation on the metabolism of lipids in the liver and the nervous system. Serum vitamin B12 concentrations of 102.7 and 78 pg/ml were found at sacrifice after 5 and 6 months, respectively. Neurological testing failed to reveal signs of neuropathy. The total liver lipids were decreased in the vitamin-B12-deprived animals, but no changes were detected in the lipid concentration or in the phospholipid composition of the nervous system. Some animals were given propionate, and in these, contrary to expectations, pentadecanoic acid and heptadecanoic acid were found in smaller amounts in the liver triglycerides of the vitamin B12-deprived rats than in the control rats. This could be due to the inhibitory effect of methylmalonyl CoA on fatty-acid synthesis, demonstrated by others in vitro.

Animals↗
PubMed1979

Effect of bran and cellulose on lipid metabolism in obese female Zucker rats.

The effects on lipid metabolism of bran and cellulose added to a low-cholesterol purified diet were studied in female obese Zucker rats. The obese Zucker rat was chosen for the experiment because of its sensitivity to dietary changes with regard to lipid metabolism. Cellulos, as well as bran, had an effect on lipid metabolism, which is expressed as an increase in the excretion of fecal bile acid and cholesterol and, in the case of bran feeding, as a decrease in liver cholesterol level and an increase of fecal fat excretion. The increased excretion rate of cholesterol and bile acids did not result in a reduction of the plasma cholesterol levels, which suggests a compensatory mechanism in the form of either an increase of hepatic cholesterol synthesis and/or changes within the body cholesterol pools. The increased excretion of fecal fat that occurred when bran was added to the diet, is not likely to influence cholesterol metabolism, since fecal fat excretion only appeared to form a small percentage of the total fat intake. Bran as well as cellulose caused a significant increase in fecal wet weight and a decrease in transit time. Though both cellulose and bran are capable of binding bile acid, cholesterol and/or fat, the intestinal transit time and the fecal bulk might also be a cause of increased steroid excretion. The fact that our results are inconsistent with those of some investigations described in the literature but in agreement with the findings of other workers, again stresses the primary need for a better chemical characterization of the various fiber sources.

Animals↗
PubMed1979

Oral contraception, mechanical contraception, and carbohydrate and lipid metabolism: a two-year study.

The carbohydrate and lipid metabolism of 100 women using an oral contraceptive (0.5 mg norgestrel + 0.05 mg ethinyl estradiol) and of 96 women using mechanical contraceptives was monitored over a 2-year period. The women had been screened for factors known to adversely affect carbohydrate and lipid metabolism. Two-hour oral glucose tolerance tests were performed at 6-month intervals during the study; serum insulin was determined at the same intervals in half the women. Triglycerides, total cholesterol, free fatty acids, and body weight were also measured. The study showed no significant differences in lipid metabolism nor in weight gain between women using oral or mechanical contraceptives. After 6 months the fasting glucose of women using oral contraceptives was significantly decreased; at 120 minutes, glucose and insulin levels were significantly increased in comparison to women using mechanical contraceptives. A greater percentage of oral contraceptive users had borderline-abnormal oral glucose tolerance tests but the abnormalities did not persist in the same individuals during the study. The incidence of a pathological oral glucose tolerance with oral contraceptives was 1%.

Body Weight↗
PubMedDate not supplied

[Biochemical aspects of lipid metabolism in multiple sclerosis].

The biochemical features of lipid metabolism in multiple sclerosis are discussed and the contribution made by work on the aetiopathogenesis of the disease is illustrated. Reference is made to diagnostic tests (E-UFA and MEM tests), whose premisses are based on lipid metabolism. A link between biochemical and immunological research in this field is put forward.

Arachidonic Acids↗
PubMed2025

Alterations in ether lipid metabolism in obesity revealed by systems genomics of multi-omics datasets.

Ratios between two metabolites are sensitive indicators of metabolic changes. Lipidomic profiling studies have revealed that plasma ether lipids, a class of glycero- and glycerophospho-lipids with reported health benefits, are negatively associated with obesity. Here, we utilized lipid ratios as surrogate markers of lipid metabolism to explore the processes underlying the inverse relationship between ether lipid metabolism and obesity. Plasma lipidomics data from two independent human cohorts (n&#x2009;=&#x2009;10,339 and n&#x2009;=&#x2009;4,492) were integrated to assess the associations between 82 lipid ratios and obesity-related markers in males and females. Results were externally validated using mouse transcriptomics data from the Hybrid Mouse Diversity Panel (n&#x2009;=&#x2009;152-227 across 74 strains). Genome-wide association studies using imputed genotypes from a population cohort (n&#x2009;=&#x2009;4,492) were performed to examine the genetic architecture of the ratios. Findings showed that waist circumference (WC), body mass index, and waist-hip ratio were inversely associated with total plasmalogens relative to total phospholipids in both sexes. Ratios comprising product-substrate pairs positioned either side of enzymes involved in plasmalogen synthesis and degradation showed positive and negative associations with WC, respectively. Branched-chain fatty acids negatively correlated with WC, while omega-6 polyunsaturated fatty acids exhibited differing associations depending on their position within the pathway. Mouse transcriptomics corroborated these results. Genomics data showed strong associations between ratios containing choline-plasmalogens and single-nucleotide polymorphisms in the transmembrane protein 229B (TMEM229B) gene region. This work demonstrates the utility of lipid ratios in understanding lipid metabolism. By applying the ratios to multi-omic datasets, we identified alterations in enzymatic activity and genetic variants likely affecting ether lipid synthesis in obesity that could not have been obtained from lipidomics data alone. Additionally, we characterized a potential role for TMEM229B, offering new perspectives on ether lipid metabolism and regulation.

Humans↗
PubMed2024

Mendelian randomization study of lipid metabolism characteristics and migraine risk.

BACKGROUND: The association between serum lipids and migraine is controversial. However, randomized controlled trials have suggested that statins may be efficacious for the prevention of migraine. In this study, we aim to investigate the relationship between lipids metabolism and migraine risk. METHODS: Single-nucleotide polymorphisms (SNPs), relating to the serum lipid traits and the effect of lipid-lowering drugs that target APOB, CETP, HMGCR, NPC1L1, and PCSK9, were extracted from genome-wide association studies (GWAS) summary data. The GWAS summary data were obtained from the Global Lipids Genetic Consortium (GLGC), the UK Biobank, and the FinnGen study, respectively. Mendelian randomization (MR) analysis was performed to evaluate the association between serum lipid traits and lipid-lowering drugs with migraine risk. RESULTS: Regarding serum lipids, it was found that SNPs related to high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol (TC), or triglycerides (TG) levels were not associated with migraine, migraine with aura (MA) or migraine without aura (MO). In addition, genotypes of HMGCR related to higher LDL-C levels were associated with increased risk of migraine (OR&#x2009;=&#x2009;1.46, p&#x2009;=&#x2009;0.035) and MA (OR&#x2009;=&#x2009;2.03, p&#x2009;=&#x2009;0.008); However, genotypes of PCSK9 related to higher LDL-C levels were associated with decreased risk of migraine (OR&#x2009;=&#x2009;0.75, p&#x2009;=&#x2009;0.001) and MA (OR&#x2009;=&#x2009;0.69, p&#x2009;=&#x2009;0.004); And genotypes of APOB related to higher LDL-C levels were associated with decreased risk of MO (OR&#x2009;=&#x2009;0.62, p&#x2009;=&#x2009;0.000). CONCLUSIONS: There is a relationship between lipid metabolism characteristics and migraine risk. SIGNIFICANCE: Based on the genome-wide association summary data, single-nucleotide polymorphisms (SNPs) related to high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), total cholesterol (TC), or triglycerides (TG) level were not associated with risk of migraine, migraine with aura (MA) or migraine without aura (MO). However, genotypes of HMGCR related to higher LDL-C levels have shown an increased risk on migraine and MA. And genotypes of APOB or PCSK9 related to higher LDL-C levels have shown a decreased risk on MO, or migraine and MA, respectively. These results suggested that there may be a relationship between lipid metabolism characteristics and the risk for migraine development.

Humans↗
PubMed2026

Subchronic benzo[a]pyrene exposure disrupts APOE4-regulated lipid metabolism to induce Tau hyperphosphorylation and cognitive deficits.

BACKGROUND: Benzo[a]pyrene (B[a]P) is both a carcinogen and a potent neurotoxic pollutant. Despite growing evidence linking B[a]P to neurological dysfunction, the responsible mechanisms have not been elucidated. METHODS: Here, we employed human apolipoprotein E4 (hAPOE4) transgenic mice and APOE knockout (APOE-KO) mice to evaluate the influence of APOE on B[a]P-mediated neurotoxicity. hAPOE4 mice overexpress the human APOE4 isoform, whereas APOE-KO mice lack APOE expression; wild-type C57BL/6&#x202f;J mice served as controls. Animals received intraperitoneal injections of B[a]P at 0, 2.5, or 6.25&#x202f;mg/kg on alternate days for 3 months. Spatial memory and learning were examined via Morris Water Maze (MWM). Neuronal morphology, including dendritic branching and spine density in the CA1 region of the hippocampus and dentate gyrus (DG), was assessed using Golgi-Cox staining. Neurofibrillary tangles were detected by silver glycine staining. Tau, phosphorylated Tau (Ser199 and Ser396), and LRP1 were evaluated using Western blot and immunohistochemical analyses. Chromatin immunoprecipitation PCR (ChIP-PCR) was undertaken to examine the regulation of APOE4 expression by the aryl hydrocarbon receptor (AHR). In addition, both untargeted metabolomics and lipidomics analyses were conducted following B[a]P exposure. RESULTS: B[a]P led to pronounced impairments in mouse spatial memory and learning, shown by greater escape latency, less time in the target quadrant, and a decreased number of platform crossings in MWM tests. Structural analyses revealed a significant reduction in dendritic branching within the hippocampal CA1 and DG regions. These neurobehavioral and morphological deficits were most severe in hAPOE4 mice, which displayed greater cognitive impairment and more extensive dendritic loss than B[a]P-treated wild-type mice, indicating that APOE4 amplifies B[a]P-induced neurotoxicity. ChIP assays demonstrated that B[a]P modulates APOE4 transcription through AHR-dependent mechanisms. Additionally, metabolomics and lipidomics analyses revealed widespread B[a]P-induced metabolic remodeling, suggesting that disrupted lipid metabolism and altered neuronal membrane integrity may contribute to the observed neurotoxicity and cognitive dysfunction. CONCLUSION: Collectively, the results indicate that B[a]P-mediated neurotoxicity may be facilitated, at least in part, by APOE4-dependent dysregulation of lipid metabolic pathways.

Animals↗
PubMedDate not supplied

[Contrast-unloading week in the complex therapy of patients with metabolic-alimentary obesity and its effect on changes in body weight and lipid metabolism indices].

The influences of the contrast-unloading week (CUW) on the changes in the anthropometric and lipid metabolism parameters was studied in 150 female patients with metabolic alimentary obesity of the II-III stages, aged from 20 to 40. On the basis of the analysis of the changes in lipid metabolism in relation to their initial level and the hyperlipoproteinemia type it is suggested that the developed CUW is mostly indicated in a combined therapy of patients with the IV type of hyperlipoproteinemia. In the II type it is recommended in combination with a dosaged physical loading. CUW can be used in out-patients, which is confirmed by the experience in the prophylactic examination of patients with metabolic alimentary obesity.

Adult↗
PubMed2026

Excess iodine induces lipid metabolic disorders by the gut microbiota SCFAs/H2S-p-AMPK&#x3b1;/PPAR&#x3b3;/SREBP-1c pathway in female rats.

With the development of living standards, the problem of excess iodine has long been overlooked. This study aimed to investigate the detrimental effects of long-term excess iodine exposure on lipid metabolism in female Sprague-Dawley rats from the gut-liver axis perspective, and to elucidate the underlying molecular mechanisms by which the gut microbiota and its metabolites mediate iodine-induced lipid metabolic disorders. The results indicated that abnormal iodine nutrition has a negative effect on the health of rats. Specifically, excess iodine not only causes thyroid disorders but also leads to liver lipid metabolism disorders, including elevated serum and hepatic total cholesterol/triglyceride levels and lipid accumulation in the liver. Further investigation revealed that excess iodine causes liver lipid metabolism disorders by altering the gut microbiota, which resulted in an increase in the relative abundance of Desulfovibrio and Lachnospiraceae NK4A136_group, and a decrease in the relative abundance of Akkermansia and Blautia in excess iodine groups. A decrease in the relative abundance of Blautia and an increase in Lachnospiraceae NK4A136_group were strongly correlated with reductions in short-chain fatty acids (acetic, propionic, and valeric acids), whereas an increase in Desulfovibrio was strongly correlated with an increase in H2S. Additionally, acetic acid was negatively correlated with H2S in serum and liver. Excess iodine reduced hepatic p-AMPK&#x3b1; expression while upregulating key regulators of lipid metabolism, including SREBP-1c, PPAR&#x3b3; and ACC1. These changes may represent one of the key mechanisms by which excess iodine induces lipid metabolism disorders through the microbiota-metabolite axis. Overall, these findings suggest that excess iodine influences lipid metabolism through the gut-liver axis. The results of this study provide scientific references and guidance for the appropriate intake of iodine and offer novel insights for early nutritional interventions targeting lipid metabolism disorders.

Journal Article↗