PARPs in lipid metabolism and related diseases

Szántó, Magdolna; Gupte, Rebecca; Kraus, W. Lee; Pacher, Pál; Bai, Péter

doi:10.1016/j.plipres.2021.101117

Cited by 58 publications

(22 citation statements)

References 388 publications

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“…The PARP family of 17 proteins is involved in a wide range of biological processes [ 43 , 44 ], and many of the 17 PARPs are involved in lipid metabolism, including PARP2 and PARP7 [ 43 ]. In our RNA-Seq data, four PARP genes were significantly up-regulated ( PARP9 , PARP10 , PARP12 , and PARP14 ; Supplementary Table S2 ).…”

Section: Discussionmentioning

confidence: 99%

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Ran

Yang

Luo

et al. 2022

Cells

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The positive regulatory role of lncFAM200B in differentiation and lipid deposition in yak intramuscular preadipocytes has been demonstrated in our previous study. However, the regulatory mechanisms remain unclear. In this study, we aimed to produce complete mRNA and microRNA (miRNA) profiles after adenovirus-mediated lncFAM200B overexpression in yak preadipocytes using high-throughput sequencing. We constructed a competing endogenous RNA (ceRNA) network with lncFAM200B as the core and identified the functions of the selected target miRNA during cell proliferation and differentiation. We obtained 118 differentially expressed genes (DEGs) after lncFAM200B overexpression, 76 of which were up-regulated, including Notch signaling members NOTCH3, DTX3L, and HES4, and 42 DEGs were down-regulated, including genes related to the cell cycle (CCNA2, BUB1, CDC20, TOP2A, and KIF20A). Additionally, many ubiquitin-mediated proteolysis pathway members were also significantly up-regulated (BUA7, PML, TRIM21, and TRIM25). MiRNA sequencing showed that 13 miRNAs were significantly up-regulated, and 12 miRNAs were down-regulated. Among them, 29 targets of 10 differentially expressed miRNAs (DEMs) were differentially expressed, including miR-152-FBXO33, miR-6529a-TRIM21, miR-148c-NOTCH3, and the miR-6529b-HES4 axis. We further verified that overexpression and inhibition of miR-6529a can inhibit and promote, respectively, the proliferation and differentiation of preadipocytes. Taken together, our study not only revealed the regulatory network of lncFAM200B during yak preadipocytes differentiation but also laid a foundation for elucidating the cause for lower intramuscular fat content in yaks at the molecular level.

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Section: Discussionmentioning

confidence: 99%

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Ran

Yang

Luo

et al. 2022

Cells

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“…As for lipid localization/transport pathways, we focused on Abca1 , Hdlbp , Osbpl9 , and Pitpnc1 . Abca1 is a transporter central to the synthesis of HDL by mediating the efflux of cholesterol and phospholipids to lipoproteins [ 23 ], and low expression levels of Abca1 reduce cholesterol flux into bile, as well as toward LDL [ 24 ]. Hdlbp affects the metabolism of major lipoproteins and specifically binds HDL molecules, which may function in the removal of excess cellular cholesterol [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Maternal Protein Restriction and Post-Weaning High-Fat Feeding Alter Plasma Amino Acid Profiles and Hepatic Gene Expression in Mice Offspring

Miyoshi

Saito

Jia

et al. 2022

Foods

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Maternal undernutrition during pregnancy is closely associated with epigenetic changes in the child, and it affects the development of obesity throughout the child’s life. Here, we investigate the effect of fetal low protein exposure and post-weaning high-fat consumption on plasma amino acid profiles and hepatic gene expression. Mother C57BL/6J mice were fed a 20% (CN) or 9% (LP) casein diet during pregnancy. After birth, the male offspring of both these groups were fed a high-fat diet (HF) from 6 to 32 weeks. At 32 weeks, the final body weight between the two groups remained unchanged, but the LP-HF group showed markedly higher white fat weight and plasma leptin levels. The LP-HF group exhibited a significant increase in the concentrations of isoleucine, leucine, histidine, phenylalanine, serine, and tyrosine. However, no differences were observed in the lipid content in the liver. According to the hepatic gene expression analysis, the LP-HF group significantly upregulated genes involved in the chromatin modification/organization pathways. Thus, maternal low protein and a post-weaning high-fat environment contributed to severe obesity states and changes in gene expression related to hepatic chromatin modification in offspring. These findings provide novel insights for the prevention of lifestyle-related diseases at the early life stage.

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“…Hepatic FAs oxidation (FAO), commonly induced by low-circulating glucose concentrations, occurs mainly in the mitochondria to provide energy, which is controlled by PPARα [75]. FAs are transported into the mitochondria via CPT1 situated in the outer mitochondrial membrane and preferably metabolized via peroxisomal β-oxidation.…”

Section: Hepatic Fas Oxidationmentioning

confidence: 99%

Hepatic Lipid Homeostasis in NAFLD

Zhang¹,

Jia²,

Yang³

et al. 2023

Non-Alcoholic Fatty Liver Disease - New Insight and Glance Into Disease Pathogenesis

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Non-alcoholic fatty liver disease (NAFLD) is currently the most common liver disease, affecting 25% of world population. Hepatic steatosis has 60–90% prevalence among obese patients. It is also associated with multitude of detrimental effects and increased mortality. This narrative chapter investigates hepatic lipid homeostasis in NAFLD, focusing on the four molecular pathways of hepatic steatosis to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition pathways exceeding lipid disposal pathways. In NAFLD, hepatic uptake of fatty acids and de novo lipogenesis surpass fatty acid oxidation and lipid export. The imbalance of the hepatic lipid may promote cellular damage by inducing oxidative stress in peroxisomes and cytochromes, especially with compromised mitochondrial function. Lipid export may even decrease with disease progression, sustaining the accumulation of lipids. NAFLD has a complex molecular mechanism regulating hepatic lipid homeostasis. Thus, as well as inter-individual differences, any intervention targeting one or more pathway is likely to have consequences on multiple cellular signaling pathways. We should be taken into careful consideration when developing future treatment options for NAFLD.

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PARPs in lipid metabolism and related diseases

Cited by 58 publications

References 388 publications

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Molecular Regulation of Yak Preadipocyte Differentiation and Proliferation by LncFAM200B and ceRNA Regulatory Network Analysis

Maternal Protein Restriction and Post-Weaning High-Fat Feeding Alter Plasma Amino Acid Profiles and Hepatic Gene Expression in Mice Offspring

Hepatic Lipid Homeostasis in NAFLD

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