scholarly journals Effects of Fat and Fatty Acids on the Formation of Autolysosomes in the Livers from Yellow Catfish Pelteobagrus Fulvidraco

Genes ◽  
2019 ◽  
Vol 10 (10) ◽  
pp. 751 ◽  
Author(s):  
Wu ◽  
Wei ◽  
Yang ◽  
Zhao ◽  
Luo
Keyword(s):  
Fatty Acids ◽  
Oleic Acid ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Pelteobagrus Fulvidraco ◽  
Mrna Levels ◽  
High Fat ◽  
Primary Hepatocytes ◽  
Yellow Catfish ◽  
Transcriptional Responses

The autophagy-lysosome pathway, which involves many crucial genes and proteins, plays crucial roles in the maintenance of intracellular homeostasis by the degradation of damaged components. At present, some of these genes and proteins have been identified but their specific functions are largely unknown. This study was performed to clone and characterize the full-length cDNA sequences of nine key autolysosome-related genes (vps11, vps16, vps18, vps33b, vps41, lamp1, mcoln1, ctsd1 and tfeb) from yellow catfish Pelteobagrus fulvidraco. The expression of these genes and the transcriptional responses to a high-fat diet and fatty acids (FAs) (palmitic acid (PA) and oleic acid (OA)) were investigated. The mRNAs of these genes could be detected in heart, liver, muscle, spleen, brain, mesenteric adipose tissue, intestine, kidney and ovary, but varied with the tissues. In the liver, the mRNA levels of the nine autolysosome-related genes were lower in fish fed a high-fat diet than those fed the control, indicating that a high-fat diet inhibited formation of autolysosomes. Palmitic acid (a saturated FA) significantly inhibited the formation of autolysosomes at 12 h, 24 h and 48 h incubation. In contrast, oleic acid (an unsaturated FA) significantly induced the formation of autolysosomes at 12 h, but inhibited them at 24 h. At 48 h, the effects of OA incubation on autolysosomes were OA concentration-dependent in primary hepatocytes of P. fulvidraco. The results of flow cytometry and laser confocal observations confirmed these results. PA and OA incubation also increased intracellular non-esterified fatty acid (NEFA) concentration at 12 h, 24 h and 48 h, and influenced mRNA levels of fatty acid binding protein (fabp) and fatty acid transport protein 4 (fatp4) which facilitate FA transport in primary hepatocytes of P. fulvidraco. The present study demonstrated the molecular characterization of the nine autolysosome-related genes and their transcriptional responses to fat and FAs in fish, which provides the basis for further exploring their regulatory mechanism in vertebrates.

Effect of increasing stearoyl coenzyme A desaturase mRNA concentrations using forage and concentrate diets on the fatty acid composition of ovine adipose tissue

2002 ◽  
Vol 2002 ◽  
pp. 206-206 ◽  
Author(s):  
Z.C.T.R. Daniel ◽  
R.J. Wynn ◽  
A.M. Salter ◽  
P.J. Buttery
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Oleic Acid ◽  
Fatty Acid ◽  
Stearic Acid ◽  
Acid Composition ◽  
Coenzyme A ◽  
Saturated Fatty Acids ◽  
Mrna Levels

Compared to meat from other animals lamb contains high levels of saturated fat, particularly stearic acid which comprises 18% of the total fatty acids (Enser et al, 1996). This stearic acid can be desaturated in the tissue by stearoyl coenzyme A desaturase (SCD) to produce oleic acid. In sheep SCD is produced from a single gene and the levels of SCD mRNA in the tissue correlate well with oleic acid (Ward et al, 1998, Barber et al, 2000) suggesting that an upregulation of SCD activity may increase the relative proportions of unsaturated and saturated fatty acids and so significantly improve the nutritional quality of sheep meat. Our recent studies have shown that insulin increases SCD mRNA levels and monounsaturated fatty acid synthesis in cultured ovine adipose tissue explants (Daniel et al, 2001). The present study was designed to investigate whether feeding a diet believed to manipulate SCD mRNA concentrations would significantly alter the fatty acid composition of lamb.

scholarly journals The PPARβ/δ Activator GW501516 Prevents the Down-Regulation of AMPK Caused by a High-Fat Diet in Liver and Amplifies the PGC-1α-Lipin 1-PPARα Pathway Leading to Increased Fatty Acid Oxidation

Endocrinology ◽  
2011 ◽  
Vol 152 (5) ◽  
pp. 1848-1859 ◽  
Author(s):  
Emma Barroso ◽  
Ricardo Rodríguez-Calvo ◽  
Lucía Serrano-Marco ◽  
Alma M. Astudillo ◽  
Jesús Balsinde ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
High Fat Diet ◽  
Plasma Lipoproteins ◽  
Acid Oxidation ◽  
Mrna Levels ◽  
High Fat ◽  
Hepatic Fatty Acid ◽  
Lipin 1 ◽  
Hepatic Fatty Acid Oxidation

Metabolic syndrome-associated dyslipidemia is mainly initiated by hepatic overproduction of the plasma lipoproteins carrying triglycerides. Here we examined the effects of the peroxisome proliferator-activated receptors (PPAR)-β/δ activator GW501516 on high-fat diet (HFD)-induced hypertriglyceridemia and hepatic fatty acid oxidation. Exposure to the HFD caused hypertriglyceridemia that was accompanied by reduced hepatic mRNA levels of PPAR-γ coactivator 1 (PGC-1)-α and lipin 1, and these effects were prevented by GW501516 treatment. GW501516 treatment also increased nuclear lipin 1 protein levels, leading to amplification in the PGC-1α-PPARα signaling system, as demonstrated by the increase in PPARα levels and PPARα-DNA binding activity and the increased expression of PPARα-target genes involved in fatty acid oxidation. These effects of GW501516 were accompanied by an increase in plasma β-hydroxybutyrate levels, demonstrating enhanced hepatic fatty acid oxidation. Moreover, GW501516 increased the levels of the hepatic endogenous ligand for PPARα, 16:0/18:1-phosphatidilcholine and markedly enhanced the expression of the hepatic Vldl receptor. Interestingly, GW501516 prevented the reduction in AMP-activated protein kinase (AMPK) phosphorylation and the increase in phosphorylated levels of ERK1/2 caused by HFD. In addition, our data indicate that the activation of AMPK after GW501516 treatment in mice fed HFD might be the result of an increase in the AMP to ATP ratio in hepatocytes. These findings indicate that the hypotriglyceridemic effect of GW501516 in HFD-fed mice is accompanied by an increase in phospho-AMPK levels and the amplification of the PGC-1α-lipin 1-PPARα pathway.

scholarly journals Adipocyte-specific Inactivation of Acyl-CoA Synthetase Fatty Acid Transport Protein 4 (Fatp4) in Mice Causes Adipose Hypertrophy and Alterations in Metabolism of Complex Lipids under High Fat Diet

2011 ◽  
Vol 286 (41) ◽  
pp. 35578-35587 ◽  
Author(s):  
Lena-Solveig Lenz ◽  
Jana Marx ◽  
Walee Chamulitrat ◽  
Iris Kaiser ◽  
Hermann-Josef Gröne ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
High Fat Diet ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Long Chain Fatty Acids ◽  
High Fat ◽  
Complex Lipids ◽  
Long Chain ◽  
Chain Fatty Acids

Fatp4 exhibits acyl-CoA synthetase activity and is thereby able to catalyze the activation of fatty acids for further metabolism. However, its actual function in most tissues remains unresolved, and its role in cellular fatty acid uptake is still controversial. To characterize Fatp4 functions in adipocytes in vivo, we generated a mouse line with adipocyte-specific inactivation of the Fatp4 gene (Fatp4A−/−). Under standard conditions mutant mice showed no phenotypical aberrance. Uptake of radiolabeled palmitic and lignoceric acid into adipose tissue of Fatp4A−/− mice was unchanged. When exposed to a diet enriched in long chain fatty acids, Fatp4A−/− mice gained more body weight compared with control mice, although they were not consuming more food. Pronounced obesity was accompanied by a thicker layer of subcutaneous fat and greater adipocyte circumference, although expression of genes involved in de novo lipogenesis was not changed. However, the increase in total fat mass was contrasted by a significant decrease in various phospholipids, sphingomyelin, and cholesteryl esters in adipocytes. Livers of Fatp4-deficient animals under a high fat diet exhibited a higher degree of fatty degeneration. Nonetheless, no evidence for changes in insulin sensitivity and adipose inflammation was found. In summary, the results of this study confirm that Fatp4 is not crucial for fatty acid uptake into adipocytes. Instead, under the condition of a diet enriched in long chain fatty acids, adipocyte-specific Fatp4 deficiency results in adipose hypertrophy and profound alterations in the metabolism of complex lipids.

scholarly journals Role of the stearyl-coenzyme A desaturase 1 gene in regulating palmitic acid tolerance of goose primary hepatocytes

2020 ◽  
Author(s):  
Bincheng Tang ◽  
Jia min Qiu ◽  
Shen qiang HU ◽  
Liang Li ◽  
Ji wen Wang
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Er Stress ◽  
Mrna Expression ◽  
Coenzyme A ◽  
Acid Tolerance ◽  
Mrna Levels ◽  
Primary Hepatocytes

Abstract BackgroundUnlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid tolerance of goose primary hepatocytes.MethodsTo evaluate the palmitic acid tolerance of cultured hepatocytes, MTT was examined to reflect the effect of palmitic acid on cell viability, and quantitative PCR was used to detect the mRNA expression levels of several genes related to ER stress, inflammation, and apoptosis, and the role of SCD1 in palmitic acid tolerance of goose hepatocytes was explored using RNA interfere.ResultsOur results indicated that goose hepatocytes exhibited a higher tolerant capacity to palmitic acid than human hepatic cell line (LO2 cells). Furthermore, the mRNA levels of fatty acid desaturation-related genes (SCD1 and FADS2) and fatty acid elongate enzyme-related gene (ELOVL6) were significantly upregulated in goose primary hepatocytes treated with 0.6 mM palmitic acid. However, in cultured LO2 cells, expression of ER stress-related genes (XBP, BIP and ATF6), inflammatory response-related genes (IL-6, IL-1β and IFN-γ) and apoptosis-related genes (Bax, Bcl-2, Caspase-3 and Caspase-9) was significantly enhanced by the addition of 0.6 mM palmitic acid. Additionally, siRNA-mediated downregulation of SCD1 significantly reduced the palmitic acid tolerance of goose primary hepatocytes under the treatment of 0.6 mM palmitic acid; meanwhile, the mRNA expression of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the PI3K/AKT, FoxO1, mTOR and AMPK pathways (AKT1, AKT2, FOXO1 and SIRT1), as well as the protein expression of cytochrome C and the apoptosis rate were also upregulated.ConclusionIn conclusion, our data suggested that SCD1 is involved in enhancing the palmitic acid tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.

scholarly journals Intermittent Fasting Improves High-Fat Diet-Induced Obesity Cardiomyopathy via Alleviating Lipid Deposition and Apoptosis and Decreasing m6A Methylation in the Heart

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 251
Author(s):  
Zujie Xu ◽  
Ying Qin ◽  
Binbin Lv ◽  
Zhenjun Tian ◽  
Bing Zhang
Keyword(s):  
Fatty Acid ◽  
High Fat Diet ◽  
Intermittent Fasting ◽  
Lipid Deposition ◽  
Mrna Levels ◽  
Obese Mice ◽  
High Fat ◽  
Rna Methylation ◽  
Obesity Cardiomyopathy ◽  
M6a Rna Methylation

Intermittent fasting (IF) plays an essential role in improving lipid metabolism disorders caused by metabolic cardiomyopathy. Growing evidence revealed that N6-methyladenosine (m6A) RNA methylation is related to obesity and lipid metabolic. Our study aimed to assess the beneficial effects of IF on lipid deposition, apoptosis, and m6A methylation in high-fat diet (HFD)-induced obesity cardiomyopathy. Male C57BL/6J mice were fed a normal diet (ND) or HFD ad libitum for 13 weeks, after which time a subgroup of HFD mice were subjected to IF for 24 h and fed HFD in the other day for 8 weeks. We found that IF intervention significantly improved cardiac functional and structural impairment and serum lipid metabolic disorder induced by HFD. Furthermore, IF intervention decreased the mRNA levels of the fatty acid uptake genes of FABP1, FATP1, and CD36 and the fatty acid synthesis genes of SREBF1, FAS, and ACCα and increased the mRNA levels of the fatty acid catabolism genes of ATGL, HSL, LAL, and LPL in cardiac tissueof HFD-induced obese mice. TUNEL-positive cells, Bax/Bcl-2 ratio, and Cleaved Caspase-3 protein expression in HFD-induced obese mice hearts was down-regulated by IF intervention. In addition, IF intervention decreased the m6A methylation levels and METTL3 expression and increased FTO expression in HFD-induced obesity cardiomyopathy. In conclusion, our findings demonstrate that IF attenuated cardiac lipid deposition and apoptosis, as well as improved cardiac functional and structural impairment in HFD-induced obesity cardiomyopathy, by a mechanism associated with decreased m6A RNA methylation levels.

scholarly journals A Trans Fatty Acid Substitute Aggravates Nonalcoholic Steatohepatitis Induced in Mice by Feeding a Choline-Deficient, Methionine-Lowered, L-Amino Acid-Defined, High-Fat Diet

2020 ◽  
Author(s):  
Noriko Suzuki-Kemuriyama ◽  
Akari Abe ◽  
Kinuko Uno ◽  
Shuji Ogawa ◽  
Atsushi Watanabe ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Amino Acid ◽  
Nonalcoholic Steatohepatitis ◽  
High Fat Diet ◽  
Saturated Fatty Acids ◽  
Elevated Serum ◽  
High Fat ◽  
Hepatocellular Apoptosis ◽  
Liver Changes

Abstract Background: Nonalcoholic steatohepatitis (NASH) is a form of liver disease characterized by steatosis, necroinflammation, and fibrosis, resulting in cirrhosis and cancer. Trans fatty acid (TFA) is hazardous for human health and a risk factor of NASH; thus, efforts have focused on reducing its intake. However, the health benefits of reducing dietary TFA are not fully elucidated. We investigated effects of TFA and its substitute on NASH induced in mice by feeding a choline-deficient, methionine-lowered, L-amino acid-defined, high-fat diet (CDAA-HF). Methods: Mice were fed CDAA-HF containing shortening with TFA (CDAA-HF-T(+)), CDAA-HF containing shortening with a TFA substitute (CDAA-HF-T(−)), or a control chow for 13/26 weeks. Results: CDAA-HF-T(+) contained TFA, whereas CDAA-HF-T(−) contained no TFA and much saturated fatty acids. CDAA-HF-T(+) and CDAA-HF-T(−) induced NASH in mice, evidenced by elevated serum transaminase activity and liver changes, including steatosis, inflammation, and fibrosis. CDAA-HF-T(−) induced more hepatocellular apoptosis and proliferative (preneoplastic and non-neoplastic) nodular lesions than CDAA-HF-T(+). Conclusions: Thus, replacement of dietary TFA with its substitute does not prevent but aggravates nutritionally induced NASH in mice, at least under the present conditions. Attention should be paid regarding future TFA substitute use in humans, and a fatty acid balance is likely more important than the particular types of fatty acids.

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