Nutrient metabolism in the liver and muscle of juvenile blunt snout bream (Megalobrama amblycephala) in response to dietary methionine levels

AbstractA 75-day rearing trial was designed to study the response of juvenile Megalobrama amblycephala to dietary methionine (Met) levels. Three practical diets with graded Met levels (0.40%, 0.84% and 1.28% dry matter) were prepared to feed the juvenile fish. The results showed that the 0.84% Met diet significantly improved the growth compared with 0.40% diets. Compared with 0.84% and 1.28% Met, 0.40% Met significantly increased the hepatic lipid content, while decreasing the muscular lipid and glycogen contents. 0.40% Met decreased the protein levels of phospho-Eukaryotic initiation factor 4E binding protein-1 (p-4e-bp1), 4e-bp1 and Ribosomal protein S6 kinase 1 in the liver, compared with 0.84% diet, while an increasing trend was observed in the muscle. Met supplementation tended to decrease and increase lipid synthesis in the liver and muscle, respectively, via changing mRNA levels of sterol regulatory element-binding protein 1, fatty acid synthetase and acetyl-CoA carboxylase. 1.28% dietary Met promoted fatty acid β-oxidation and lipolysis in both the liver and muscle by increasing carnitine palmitoyl transferase 1, peroxisome proliferator activated receptor alpha, lipoprotein lipase and lipase mRNA levels. Compared with 0.40% and 0.84% dietary Met, 1.28% Met enhanced the mRNA levels of hepatic gluconeogenesis related genes phosphoenolpyruvate carboxykinase (pepck), and glucose-6-phosphatase, and muscular glycolysis related genes phosphofructokinase (pfk), and pyruvate kinase (pk). The mRNA levels of hepatic pfk, pk and glucokinase were markedly downregulated by 1.28% Met compared with 0.84% level. Muscular pepck, glycogen synthase, and hepatic glucose transporters 2 mRNA levels were induced by 1.28% Met. Generally, deficient Met level decreased the growth of juvenile Megalobrama amblycephala, and the different nutrient metabolism responses to dietary Met were revealed in the liver and muscle.

Download Full-text

Tissue-specific Nutrient Metabolism in the Liver and Muscle of Juvenile Blunt Snout Bream (Megalobrama Amblycephala) in Response to Dietary Methionine Levels

10.21203/rs.3.rs-152597/v1 ◽

2021 ◽

Author(s):

Ke Ji ◽

Hualiang Liang ◽

Mingchun Ren ◽

Xianping Ge ◽

Lu Zhang ◽

...

Keyword(s):

Fatty Acid ◽

Mrna Expression ◽

Binding Protein ◽

Whole Body ◽

Megalobrama Amblycephala ◽

Mrna Levels ◽

Nutrient Metabolism ◽

Tissue Specific ◽

Expression Levels ◽

Mrna Expression Levels

Abstract BackgroundMethionine is an essential amino acid, that affects the metabolism of protein, lipid and glucose. However, the metabolic polytrophic response in the liver and muscle of juvenile Megalobrama amblycephala to dietary methionine levels is unclear.ResultsThe 0.84% methionine diet significantly improved the growth performance compared with the 0.40% diet. Dietary methionine levels had no marked effects on plasma parameters or whole body composition of juveniles. The protein levels of phospho-phosphatidylinositol 3-kinase, protein kinase B, phospho-eukaryotic initiation factor 4E binding protein-1 (p-4E-BP1), 4E-BP1 and ribosomal protein S6 kinase 1, in the liver of fish fed the 0.84% diet were higher than those in fish fed the 0.40% diet. While in muscle, these proteins showed the opposite trend. The mRNA levels of the muscular lipid synthesis associated genes: sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthetase (FAS) and acetyl-CoA carboxylase (ACC), were significantly upregulated by the 1.28% methionine diet; while hepatic SREBP1, FAS and ACC mRNA expression levels were increased by 0.40% methionine. In addition, 1.28% dietary methionine significantly induced fatty acid β-oxidation and lipolysis of the liver and muscle via increased carnitine palmitoyl transferase 1, peroxisome proliferator activated receptor alpha, lipoprotein lipase and lipase expression levels. Compared with 0.40% dietary methionine, 1.28% methionine enhanced the mRNA levels of the hepatic gluconeogenesis related genes phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase, and the muscular glycolysis related genes phosphofructokinase (PFK) and pyruvate kinase (PK). The mRNA expression levels of hepatic PFK, PK and glucokinase were markedly upregulated by the 0.84% methionine diet compared with the 1.28% diet. In addition, muscular PEPCK and glycogen synthase, and hepatic glucose transporters 2 mRNA levels were induced by 1.28% methionine. ConclusionThe study showed that optimal methionine levels could enhance the growth of juvenile Megalobrama amblycephala, and the nutrient metabolism response to dietary methionine in the liver and muscle was tissue-specific.

Download Full-text

Dietary starch types affect liver nutrient metabolism of finishing pigs

British Journal Of Nutrition ◽

10.1017/s0007114517002252 ◽

2017 ◽

Vol 118 (5) ◽

pp. 353-359 ◽

Cited By ~ 1

Author(s):

Chen Xie ◽

Yanjiao Li ◽

Jiaolong Li ◽

Lin Zhang ◽

Guanghong Zhou ◽

...

Keyword(s):

Phosphoenolpyruvate Carboxykinase ◽

Amylose Content ◽

Binding Protein ◽

Hepatic Lipase ◽

Fatty Acid Synthetase ◽

Finishing Pigs ◽

Maize Starch ◽

Nutrient Metabolism ◽

Waxy Maize ◽

Element Binding Protein

AbstractThis study aimed to evaluate the effect of different starch types on liver nutrient metabolism of finishing pigs. In all ninety barrows were randomly allocated to three diets with five replicates of six pigs, containing purified waxy maize starch (WMS), non-waxy maize starch (NMS) and pea starch (PS) (the amylose to amylopectin ratios were 0·07, 0·19 and 0·28, respectively). After 28 d of treatments, two per pen (close to the average body weight of the pen) were weighed individually, slaughtered and liver samples were collected. Compared with the WMS diet, the PS diet decreased the activities of glycogen phosphorylase, phosphoenolpyruvate carboxykinase and the expression of phosphoenolpyruvate carboxykinase 1 in liver (P<0·05). Moreover, the lipid contents, the concentrations of acetyl-CoA carboxylase, fatty acid synthetase and the expression of sterol regulatory element binding protein-1c in liver of PS and NMS diets were lower than those of WMS diet (P<0·05). However, no effect was observed in the activity of hepatic lipase, the expressions of carbohydrate-responsive element-binding protein, liver X receptor and PPARα (P>0·05). Compared with the WMS diet, the PS diet reduced the expressions of glutamate dehydrogenase and carbamoyl phosphate synthetase 1 in liver (P<0·05). PS diet decreased the expression of the insulin receptor, and increased the expressions of mammalian target of rapamycin complex 1 and ribosomal protein S6 kinase β-1 in liver compared with the WMS diet (P<0·05). These findings indicated that the diet with higher amylose content could down-regulate gluconeogenesis, and cause less fat deposition and more protein deposition by affecting the insulin/PI3K/protein kinase B signalling pathway in liver of finishing pigs.

Download Full-text

Novel Function of α-Cubebenoate Derived from Schisandra chinensis as Lipogenesis Inhibitor, Lipolysis Stimulator and Inflammasome Suppressor

Molecules ◽

10.3390/molecules25214995 ◽

2020 ◽

Vol 25 (21) ◽

pp. 4995

Author(s):

Su Ji Bae ◽

Ji Eun Kim ◽

Yun Ju Choi ◽

Su Jin Lee ◽

Jeong Eun Gong ◽

...

Keyword(s):

Fatty Acid ◽

Binding Protein ◽

Fatty Acid Synthetase ◽

Inflammasome Activation ◽

Peroxisome Proliferator ◽

Mrna Levels ◽

Schisandra Chinensis ◽

Peroxisome Proliferator Activated Receptor ◽

Fatty Acid Binding ◽

Ppar Γ

The efficacy of α-cubebenoate isolated from Schisandra chinensis has been previously studied in three disease areas, namely inflammation, sepsis, and allergy, and its role in other diseases is still being explored. To identify the novel function of α-cubebenoate on lipid metabolism and related inflammatory response, alterations in fat accumulation, lipogenesis, lipolysis, and inflammasome activation were measured in 3T3-L1 preadipocytes and primary adipocytes treated with α-cubebenoate. Lipid accumulation significantly decreased in MDI (3-isobutyl-1-methylxanthine, dexamethasone, and insulin)-stimulated 3T3-L1 adipocytes treated with α-cubebenoate without any significant cytotoxicity. The mRNA levels of peroxisome proliferator-activated receptor (PPAR)γ and CCAAT-enhancer binding protein (C/EBP) α for adipogenesis, as well as adipocyte fatty acid binding protein 2 (aP2) and fatty acid synthetase (FAS) for lipogenesis, were reduced after α-cubebenoate treatment, while cell cycle arrest at G2/M stage was restored in the same group. α-cubebenoate treatment induced glycerol release in primary adipocytes and enhanced expression of lipolytic proteins (HSL, perilipin, and ATGL) expression in MDI-stimulated 3T3-L1 adipocytes. Inflammasome activation and downstream cytokines expression were suppressed with α-cubebenoate treatment, but the expression of insulin receptor signaling factors was remarkably increased by α-cubebenoate treatment in MDI-stimulated 3T3-L1 adipocytes. These results indicate that α-cubebenoate may play a novel role as lipogenesis inhibitor, lipolysis stimulator, and inflammasome suppressor in MDI-stimulated 3T3-L1 adipocytes. Our results provide the possibility that α-cubebenoate can be considered as one of the candidates for obesity management.

Download Full-text

A novel acyl-CoA-binding protein from bovine liver. Effect on fatty acid synthesis

Biochemical Journal ◽

10.1042/bj2410189 ◽

1987 ◽

Vol 241 (1) ◽

pp. 189-192 ◽

Cited By ~ 93

Author(s):

I B Mogensen ◽

H Schulenberg ◽

H O Hansen ◽

F Spener ◽

J Knudsen

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Binding Protein ◽

Fatty Acid Synthetase ◽

Bovine Liver ◽

Acid Synthesis ◽

Fatty Acid Binding Proteins ◽

Fatty Acid Binding ◽

Medium Chain ◽

Chain Acyl

Bovine liver was shown to contain a hitherto undescribed medium-chain acyl-CoA-binding protein. The protein co-purifies with fatty-acid-binding proteins, but was, unlike these proteins, unable to bind fatty acids. The protein induced synthesis of medium-chain acyl-CoA esters on incubation with goat mammary-gland fatty acid synthetase. The possible function of the protein is discussed.

Download Full-text

PURα Promotes the Transcriptional Activation of PCK2 in Oesophageal Squamous Cell Carcinoma Cells

Genes ◽

10.3390/genes11111301 ◽

2020 ◽

Vol 11 (11) ◽

pp. 1301

Author(s):

Yan Sun ◽

Jiajia Gao ◽

Zongpan Jing ◽

Yan Zhao ◽

Yulin Sun ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Phosphoenolpyruvate Carboxykinase ◽

Rna Binding ◽

Binding Protein ◽

Luciferase Assay ◽

Pcr Analysis ◽

Mrna Levels ◽

Gastrointestinal Malignancies

Esophageal squamous cell carcinoma (ESCC) is one of the most lethal gastrointestinal malignancies due to its characteristics of local invasion and distant metastasis. Purine element binding protein α (PURα) is a DNA and RNA binding protein, and recent studies have showed that abnormal expression of PURα is associated with the progression of some tumors, but its oncogenic function, especially in ESCC progression, has not been determined. Based on the bioinformatic analysis of RNA-seq and ChIP-seq data, we found that PURα affected metabolic pathways, including oxidative phosphorylation and fatty acid metabolism, and we observed that it has binding peaks in the promoter of mitochondrial phosphoenolpyruvate carboxykinase (PCK2). Meanwhile, PURα significantly increased the activity of the PCK2 gene promoter by binding to the GGGAGGCGGA motif, as determined though luciferase assay and ChIP-PCR/qPCR. The results of Western blotting and qRT-PCR analysis showed that PURα overexpression enhances the protein and mRNA levels of PCK2 in KYSE510 cells, whereas PURα knockdown inhibits the protein and mRNA levels of PCK2 in KYSE170 cells. In addition, measurements of the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) indicated that PURα promoted the metabolism of ESCC cells. Taken together, our results help to elucidate the molecular mechanism by which PURα activates the transcription and expression of PCK2, which contributes to the development of a new therapeutic target for ESCC.

Download Full-text

Ergosterol Peroxide from the Medicinal Mushroom Ganoderma lucidum Inhibits Differentiation and Lipid Accumulation of 3T3-L1 Adipocytes

International Journal of Molecular Sciences ◽

10.3390/ijms21020460 ◽

2020 ◽

Vol 21 (2) ◽

pp. 460 ◽

Cited By ~ 5

Author(s):

Yong-Un Jeong ◽

Young-Jin Park

Keyword(s):

Transcription Factors ◽

Fatty Acid ◽

Fatty Acid Synthase ◽

Metabolic Diseases ◽

Binding Protein ◽

Regulatory Element ◽

Peroxisome Proliferator ◽

Mrna Levels ◽

Medicinal Mushrooms ◽

Ergosterol Peroxide

Ergosterol peroxide is a natural compound of the steroid family found in many fungi, and it possesses antioxidant, anti-inflammatory, anticancer and antiviral activities. The anti-obesity activity of several edible and medicinal mushrooms has been reported, but the effect of mushroom-derived ergosterol peroxide on obesity has not been studied. Therefore, we analyzed the effect of ergosterol peroxide on the inhibition of triglyceride synthesis at protein and mRNA levels and differentiation of 3T3-L1 adipocytes. Ergosterol peroxide inhibited lipid droplet synthesis of differentiated 3T3-L1 cells, expression of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAT/enhancer-binding protein alpha (C/EBPα), the major transcription factors of differentiation, and also the expression of sterol regulatory element-binding protein-1c (SREBP-1c), which promotes the activity of PPARγ, resulting in inhibition of differentiation. It further inhibited the expression of fatty acid synthase (FAS), fatty acid translocase (FAT), and acetyl-coenzyme A carboxylase (ACC), which are lipogenic factors. In addition, it inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) involved in cell proliferation and activation of early differentiation transcription factors in the mitotic clonal expansion (MCE) stage. As a result, ergosterol peroxide significantly inhibited the synthesis of triglycerides and differentiation of 3T3-L1 cells, and is, therefore, a possibile prophylactic and therapeutic agent for obesity and related metabolic diseases.

Download Full-text

Gene expression in regenerating and acute-phase rat liver

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1990.259.3.g340 ◽

1990 ◽

Vol 259 (3) ◽

pp. G340-G347 ◽

Cited By ~ 8

Author(s):

J. Milland ◽

A. Tsykin ◽

T. Thomas ◽

A. R. Aldred ◽

T. Cole ◽

...

Keyword(s):

Vitamin D ◽

Rat Liver ◽

Acute Phase ◽

Acute Phase Response ◽

Phosphoenolpyruvate Carboxykinase ◽

Binding Protein ◽

Ornithine Transcarbamylase ◽

Phase Response ◽

Mrna Levels ◽

Vitamin D Binding Protein

The integration of growth and the acute-phase response is investigated by comparing the mRNA levels in rat liver during acute inflammation with those after partial hepatectomy. Northern analysis is carried out for the mRNAs for thiostatin, alpha 2-macroglobulin, alpha 1-antitrypsin, inter-alpha-trypsin inhibitor subunit 1, haptoglobin, ceruloplasmin, transferrin, vitamin D-binding protein, alpha 1-acid glycoprotein, beta-fibrinogen, apolipoproteins A-IV and E, albumin, transthyretin, alpha 2-HS-glycoprotein, retinol-binding protein, beta-tubulin, c-myc protooncogene, glyceraldehyde-3-phosphate dehydrogenase, phosphoenolpyruvate carboxykinase, ornithine transcarbamylase, and alcohol dehydrogenase. The acute-phase response dominates during the first 18 h. Changes in mRNA levels related to growth of the liver become important thereafter, and the capacity for an acute-phase response of plasma protein synthesis becomes greatly reduced. The early increase in the level of ceruloplasmin mRNA observed during inflammation is abolished during regeneration, and that of vitamin D-binding protein mRNA is converted into a decrease. The mRNAs levels of glyceraldehyde-3-phosphate dehydrogenase increase, and those for phosphoenolpyruvate carboxykinase decrease during regeneration. Ornithine transcarbamylase mRNA levels are found to exhibit negative acute-phase regulation. The pattern of transcriptional regulation is similar during inflammation and regeneration.

Download Full-text

Reduced adiposity and improved insulin sensitivity in obese mice with antisense suppression of 4E-BP2 expression

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00350.2007 ◽

2008 ◽

Vol 294 (3) ◽

pp. E530-E539 ◽

Cited By ~ 11

Author(s):

Xing Xian Yu ◽

Sanjay K. Pandey ◽

Sheri L. Booten ◽

Susan F. Murray ◽

Brett P. Monia ◽

...

Keyword(s):

Fatty Acid ◽

Energy Homeostasis ◽

Fatty Acid Synthase ◽

Initiation Factor ◽

Synthesis Rate ◽

Mrna Levels ◽

Obese Mice ◽

Brown Adipose ◽

Hepatic Glucose ◽

Glucose Output

To investigate the possible role of eukaryotic initiation factor 4E-binding protein-2 (4E-BP2) in metabolism and energy homeostasis, high-fat diet-induced obese mice were treated with a 4E-BP2-specific antisense oligonucleotide (ASO) or a control 4E-BP2 ASO at a dose of 25 mg/kg body wt or with saline twice a week for 6 wk. 4E-BP2 ASO treatment reduced 4E-BP2 levels by >75% in liver and white (WAT) and brown adipose (BAT) tissues. Treatment did not change food intake but lowered body weight by ∼7% and body fat content by ∼18%. Treatment decreased liver triglyceride (TG) content by >50%, normalized plasma glucose and insulin levels, and reduced glucose excursion during glucose tolerance test. 4E-BP2 ASO-treated mice showed >8.5% increase in metabolic rate, >40% increase in UCP1 levels in BAT, >45% increase in β3-adrenoceptor mRNA, and 40–55% decrease in mitochondrial dicarboxylate carrier, fatty acid synthase, and diacylglycerol acyltransferase 2 mRNA levels in WAT. 4E-BP2 ASO-transfected mouse hepatocytes showed an increased fatty acid oxidation rate and a decreased TG synthesis rate. In addition, 4E-BP2 ASO-treated mice demonstrated ∼60 and 29% decreases in hepatic glucose-6-phosphatase and phospho enolpyruvate carboxykinase mRNA, respectively, implying decreased hepatic glucose output. Furthermore, increased phosphorylation of AktSer473 in both liver and fat of 4E-BP2 ASO-treated mice and increased GLUT4 levels in plasma membrane in WAT of the ASO-treated mice were observed, indicating enhanced insulin signaling and increased glucose uptake as a consequence of reduced 4E-BP2 expression. These data demonstrate for the first time that peripheral 4E-BP2 plays an important role in metabolism and energy homeostasis.

Download Full-text

Insulin induction of glucokinase and fatty acid synthase in hepatocytes: analysis of the roles of sterol-regulatory-element-binding protein-1c and liver X receptor

Biochemical Journal ◽

10.1042/bj20060811 ◽

2006 ◽

Vol 399 (2) ◽

pp. 275-283 ◽

Cited By ~ 32

Author(s):

Franck Hansmannel ◽

Sylvie Mordier ◽

Patrick B. Iynedjian

Keyword(s):

Fatty Acid ◽

Fatty Acid Synthase ◽

Glycogen Synthase ◽

Binding Protein ◽

Regulatory Element ◽

Positive Control ◽

Liver X Receptor ◽

Transcription Activator ◽

Element Binding Protein ◽

Sterol Regulatory Element

The transcription activator SREBP-1c (sterol-regulatory-element-binding protein-1c) is induced by insulin in the liver and is considered a master regulator of lipogenic genes such as FASN (fatty acid synthase). The question of whether SREBP-1c is also a mediator of insulin action on the regulatory enzyme of glucose metabolism GCK (glucokinase) is controversial. In the present paper, we induced SREBP-1c to various levels with insulin or the liver X receptor ligand T0901317 in primary hepatocytes and asked if these levels correlated with those of GCK or FASN mRNA expression, using the latter as positive control. Insulin and T0901317 triggered the accumulation of precursor and processed forms of SREBP-1c to similar levels and with comparable kinetics, and both effectors together caused synergistic increases in SREBP-1c protein levels. These effects were accompanied by commensurate elevation of FASN mRNA, notably by a synergistic response to both effectors. By contrast, GCK mRNA was unresponsive to T0901317 and was induced only by insulin. Treatment of hepatocytes with insulin and/or T0901317 resulted in the recruitment of SREBP-1c to the FASN promoter as shown by chromatin immunoprecipitation, whereas SREBP-1c did not bind to the GCK promoter. Lastly, we observed that the glycogen synthase kinase-3 inhibitor SB216763 produced a small increase in SREBP-1c protein level, which was further augmented in the presence of T0901317. The level of FASN mRNA varied in parallel with SREBP-1c, while GCK mRNA was unaffected. Collectively, these results showed that increases in SREBP-1c were neither necessary nor sufficient for GCK induction in hepatocytes, while at the same time they underscored the role of SREBP-1c as a key regulator of FASN.

Download Full-text

Dietary threonine supplementation improves hepatic lipid metabolism of Pekin ducks

Animal Production Science ◽

10.1071/an17633 ◽

2019 ◽

Vol 59 (4) ◽

pp. 673 ◽

Cited By ~ 3

Author(s):

Y. Jiang ◽

X. D. Liao ◽

M. Xie ◽

J. Tang ◽

S. Y. Qiao ◽

...

Keyword(s):

Fatty Acid ◽

Lipid Metabolism ◽

Fatty Acid Synthase ◽

Binding Protein ◽

Initiation Factor ◽

Pekin Duck ◽

Hepatic Lipid Metabolism ◽

Fatty Acid Binding ◽

Hepatic Lipid ◽

Pekin Ducks

The present study was conducted to evaluate the regulatory role of threonine (Thr) on hepatic lipid metabolism by determining the effects of dietary Thr concentration on lipid deposition and on genes related to lipid expression in the liver of Pekin duck. In total, 240 1-day-old ducklings were randomly allocated according to the average bodyweight to one of five dietary treatments with six replicate cages of eight birds per cage for each treatment. Birds were fed diets with 0.52%, 0.59%, 0.66%, 0.73% and 0.80% Thr (as-fed basis) from 1 to 21 days of age respectively. The results showed that dietary Thr supplementation increased average daily gain (P < 0.0001), average daily feed intake (P < 0.0001) and abdominal fat percentage (P < 0.04), while it decreased feed to gain ratio (P < 0.0001), the hepatic contents of total lipid (P < 0.003) and triglycerides (P < 0.003) of Pekin ducks. However, dietary Thr supplementation had no influence (P > 0.05) on the concentration of hepatic cholesterol, and plasma amino acids and biochemical parameters of Pekin ducks. Moreover, Thr-unsupplemented control diet upregulated (P < 0.05) hepatic gene expression related to lipid uptake (fatty acid-binding protein, apolipoprotein A4, lipoprotein lipase), fatty acid synthesis (sterol regulatory element-binding protein 1c, malic enzyme), fatty acid β-oxidation (peroxisome proliferator-activated receptor α, fatty acyl– coenzyme A (CoA) oxidase), ketogenesis (hydroxymethylglutaryl–CoA synthase 1, and acetyl–CoA synthetase1), responsive genes to amino acid deficiency (general control non-derepressible 2 (GCN2), GCN1, eukaryotic initiation factor 2α, impact RWD domain protein (IMPACT)), and triglyceride transport (apolipoprotein B) of Pekin ducks. In addition, dietary Thr deficiency had no effect on the expression of stearoyl CoA desaturase, fatty acid synthase, and ATP–citrate lyase in the liver of Pekin ducks. It is suggested that dietary Thr supplementation improved hepatic lipid metabolism of Pekin ducks by regulating lipid synthesis, transport and oxidation.

Download Full-text