Effects of dietary carbohydrate sources on lipid metabolism and SUMOylation modification in the liver tissues of yellow catfish

AbstractDysregulation in hepatic lipid synthesis by excess dietary carbohydrate intake is often relevant with the occurrence of fatty liver; therefore, the thorough understanding of the regulation of lipid deposition and metabolism seems crucial to search for potential regulatory targets. In the present study, we examined TAG accumulation, lipid metabolism-related gene expression, the enzyme activities of lipogenesis-related enzymes, the protein levels of transcription factors or genes involving lipogenesis in the livers of yellow catfish fed five dietary carbohydrate sources, such as glucose, maize starch, sucrose, potato starch and dextrin, respectively. Generally speaking, compared with other carbohydrate sources, dietary glucose promoted TAG accumulation, up-regulated lipogenic enzyme activities and gene expressions, and down-regulated mRNA expression of genes involved in lipolysis and small ubiquitin-related modifier (SUMO) modification pathways. Further studies found that sterol regulatory element binding protein 1 (SREBP1), a key transcriptional factor relevant to lipogenic regulation, was modified by SUMO1. Mutational analyses found two important sites for SUMOylation modification (K254R and K264R) in SREBP1. Mutant SREBP lacking lysine 264 up-regulated the transactivation capacity on an SREBP-responsive promoter. Glucose reduced the SUMOylation level of SREBP1 and promoted the protein expression of SREBP1 and its target gene stearoyl-CoA desaturase 1 (SCD1), indicating that SUMOylation of SREBP1 mediated glucose-induced hepatic lipid metabolism. Our study elucidated the molecular mechanism of dietary glucose increasing hepatic lipid deposition and found that the SREBP-dependent transactivation was regulated by SUMO1 modification, which served as a new target for the transcriptional programmes governing lipid metabolism.

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Dietary Fenofibrate Reduces Hepatic Lipid Deposition by Regulating Lipid Metabolism in Yellow Catfish Pelteobagrus fulvidraco Exposed to Waterborne Zn

Lipids ◽

10.1007/s11745-015-3999-7 ◽

2015 ◽

Vol 50 (4) ◽

pp. 417-426 ◽

Cited By ~ 10

Author(s):

Jia-Lang Zheng ◽

Zhi Luo ◽

Wei Hu ◽

Ya-Xiong Pan ◽

Mei-Qing Zhuo

Keyword(s):

Lipid Metabolism ◽

Pelteobagrus Fulvidraco ◽

Lipid Deposition ◽

Yellow Catfish ◽

Hepatic Lipid

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Differential effects of acute and chronic zinc (Zn) exposure on hepatic lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco

Aquatic Toxicology ◽

10.1016/j.aquatox.2013.02.002 ◽

2013 ◽

Vol 132-133 ◽

pp. 173-181 ◽

Cited By ~ 67

Author(s):

Jia-Lang Zheng ◽

Zhi Luo ◽

Cai-Xia Liu ◽

Qi-Liang Chen ◽

Xiao-Ying Tan ◽

...

Keyword(s):

Pelteobagrus Fulvidraco ◽

Lipid Deposition ◽

Yellow Catfish ◽

Hepatic Lipid ◽

Differential Effects

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Dietary Glucose Increases Glucose Absorption and Lipid Deposition via SGLT1/2 Signaling and Acetylated ChREBP in the Intestine and Isolated Intestinal Epithelial Cells of Yellow Catfish

Journal of Nutrition ◽

10.1093/jn/nxaa125 ◽

2020 ◽

Vol 150 (7) ◽

pp. 1790-1798 ◽

Cited By ~ 1

Author(s):

Tao Zhao ◽

Shui-Bo Yang ◽

Guang-Hui Chen ◽

Yi-Huan Xu ◽

Yi-Chuang Xu ◽

...

Keyword(s):

Gene Expression ◽

Lipid Metabolism ◽

Epithelial Cells ◽

Fatty Acid Synthase ◽

Intestinal Epithelial Cells ◽

Glucose Absorption ◽

Lipid Deposition ◽

Intestinal Epithelial ◽

Yellow Catfish ◽

Induced Changes

ABSTRACT Background Dietary carbohydrate affects intestinal glucose absorption and lipid deposition, but the underlying mechanisms are unknown. Objectives We used yellow catfish and their isolated intestinal epithelial cells (IECs) to test the hypothesis that sodium/glucose cotransporters (SGLTs) 1/2 and acetylated carbohydrate response element binding protein (ChREBP) mediated glucose-induced changes in glucose absorption and lipid metabolism. Methods Yellow catfish (mean ± SEM weight: 4.68 ± 0.02 g, 3 mo old, mixed sex) were fed diets containing 250 g carbohydrates/kg from glucose (G, control), corn starch (CS), sucrose (S), potato starch (PS), or dextrin (D) for 10 wk. IECs were isolated from different yellow catfish and incubated for 24 h in a control or glucose (15 mM) solution with or without a 2-h pretreatment with an inhibitor [sotagliflozin (LX-4211) or tubastatin A (TBSA)]. Human embryonic kidney cells (HEK293T cells) were transfected with a Flag-ChREBP plasmid to explore ChREBP acetylation. Triglyceride (TG) and glucose concentrations and enzymatic activities were measured in the intestine and IECs of yellow catfish. They also were subjected to immunofluorescence, immunoprecipitation, qPCR, and immunoblotting. Immunoblotting and immunoprecipitation were performed with HEK293T cells. Results The G group had greater intestine TGs (0.99- to 2.30-fold); activities of glucose 6-phospate dehydrogenase, 6-phosphogluconate dehydrogenase, and isocitrate dehydrogenase (0.12- to 2.10-fold); and expression of lipogenic genes (0.32- to 2.34-fold) than the CS, PS, and D groups. The G group had greater intestine sglt1/2 mRNA and protein expression than the CS, S and D groups (0.35- to 1.12-fold and 0.40- to 4.67-fold, respectively), but lower mRNA amounts of lipolytic genes (48.6%–65.8%) than the CS and PS groups. LX-4211 alleviated the glucose-induced increase in sglt1/2 mRNA (38.2%–47.4%) and SGLT1 protein (48.0%) expression, TGs (29.3%), and lipogenic enzyme activities (27.7%–42.1%) and gene expression (38.0%–55.5%) in the IECs. TBSA promoted the glucose-induced increase in TGs (11.3%), fatty acid synthase activity (32.6%), and lipogenic gene expression (21.6%–34.4%) in the IECs and acetylated ChREBP (10.5%) in HEK293T cells. Conclusions SGLT1/2 signaling and acetylated ChREBP mediated glucose-induced changes in glucose absorption and lipid metabolism in the intestine and IECs of yellow catfish.

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PP271 LIPID COMPOSITION OF PARENTERAL NUTRITION ACUTELY AFFECTS HEPATIC LIPID DEPOSITION AND LIPID METABOLISM IN PRETERM PIGS

Clinical Nutrition Supplements ◽

10.1016/s1744-1161(10)70346-x ◽

2010 ◽

Vol 5 (2) ◽

pp. 128-129

Author(s):

A. Vegge ◽

L. Lauritzen ◽

T. Thymann ◽

P.T. Sangild

Keyword(s):

Lipid Metabolism ◽

Parenteral Nutrition ◽

Lipid Composition ◽

Lipid Deposition ◽

Hepatic Lipid

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miR-101b Regulates Lipid Deposition and Metabolism of Primary Hepatocytes in Teleost Yellow Catfish Pelteobagrus fulvidraco

Genes ◽

10.3390/genes11080861 ◽

2020 ◽

Vol 11 (8) ◽

pp. 861

Author(s):

Guang-Hui Chen ◽

Tao Zhao ◽

Xiao-Lei Wei ◽

Dian-Guang Zhang ◽

Mei-Qin Zhuo ◽

...

Keyword(s):

Lipid Metabolism ◽

Underlying Mechanism ◽

Pelteobagrus Fulvidraco ◽

Transcriptional Level ◽

Lipid Deposition ◽

Fat Intake ◽

Primary Hepatocytes ◽

Yellow Catfish ◽

Fatty Livers ◽

Insight Into

Excessive fat deposition in the hepatocytes, associated with excess dietary fat intake, was related to the occurrence of fatty livers in fish. miR-101b plays the important roles in controlling lipid metabolism, but the underlying mechanism at the post-transcriptional level remains unclear. The purpose of this study is to explore the roles and mechanism of miR-101b-mediating lipid deposition and metabolism in yellow catfish Pelteobagrus fulvidraco. We found that miR-101b directly targeted fatty acid translocase (cd36), caspase9 (casp9) and autophagy-related gene 4A (atg4a). Furthermore, using palmitic acid (PA) or oleic acid (OA) to incubate the primary hepatocytes of yellow catfish, we demonstrated that miR-101b inversely regulated cd36, casp9, and atg4a expression at the transcriptional level; the inhibition of miR-101b aggravated fatty acids (FAs, PA or OA)-induced lipid accumulation, indicating that miR-101b mediated FAs-induced variations of lipid metabolism in yellow catfish. Taken together, our study gave novel insight into the regulatory mechanism of lipid deposition and metabolism and might provide potential targets for the prevention and treatment of fatty livers in fish.

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Growth Performance, Lipid Deposition and Hepatic Lipid Metabolism Related Gene Expression in Schizothorax prenanti fed with Dietary Acidolysis-Oxidized Konjac Glucomannan Supplementation

Journal of Aquaculture Research & Development ◽

10.4172/2155-9546.1000519 ◽

2017 ◽

Vol 09 (01) ◽

Author(s):

Mingrui Chen ◽

Yinglong Wu ◽

Qiuping Yan ◽

Zhenzhen Lv ◽

Mei He ◽

...

Keyword(s):

Gene Expression ◽

Lipid Metabolism ◽

Growth Performance ◽

Konjac Glucomannan ◽

Lipid Deposition ◽

Related Gene ◽

Schizothorax Prenanti ◽

Hepatic Lipid Metabolism ◽

Hepatic Lipid ◽

Oxidized Konjac Glucomannan

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Effects of dietary curcumin on growth, antioxidant capacity, fatty acid composition and expression of lipid metabolism-related genes of large yellow croaker fed a high-fat diet

British Journal Of Nutrition ◽

10.1017/s0007114520004171 ◽

2020 ◽

pp. 1-10

Author(s):

Renlei Ji ◽

Xiaojun Xiang ◽

Xueshan Li ◽

Kangsen Mai ◽

Qinghui Ai

Keyword(s):

Fatty Acid Composition ◽

Fatty Acid ◽

Lipid Metabolism ◽

Antioxidant Capacity ◽

High Fat Diet ◽

Control Group ◽

Large Yellow Croaker ◽

Lipid Deposition ◽

High Fat ◽

Hepatic Lipid

Abstract A 10-week feeding trial was conducted to investigate the effect of dietary curcumin (CC) on growth antioxidant responses, fatty acid composition, and expression of lipid metabolism-related genes of large yellow croaker fed a high-fat diet (HFD). Four diets (lipid level at 18 %) were formulated with different levels of curcumin (0, 0·02, 0·04 and 0·06 %). The best growth performance was found in the 0·04 % curcumin group, with the body and hepatic lipid levels lower than the control group (0 % CC). The content of TAG, total cholesterol and LDL-cholesterol was the least in the 0·06 % curcumin group. The lowest malondialdehyde and the highest superoxide dismutase, catalase and total antioxidant capacity were observed in the 0·04 % curcumin group. The 0·04 % curcumin group had higher expression of Δ6fad, elovl5 and elovl4 and showed higher hepatic n-6 and n-3 PUFA. Expression of ppara, cpt1, and aco was significantly increased, while expression of srebp1 and fas was dramatically decreased in curcumin groups compared with the control group. Overall, 0·04 % curcumin supplementation could mitigate the negative effects caused by HFD and promote growth via reducing hepatic lipid deposition, improving antioxidant activity and increasing PUFA of large yellow croaker. To conclude, abnormal hepatic lipid deposition was probably due to increased fatty acid oxidation and reduced de novo synthesis of fatty acids.

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