scholarly journals Genome-wide identification and characterization of perirenal adipose tissue microRNAs in rabbits fed a high-fat diet

2021 ◽  
Author(s):  
Jie Wang ◽  
Jiahao Shao ◽  
Yanhong Li ◽  
Mauricio A Elzo ◽  
Xianbo Jia ◽  
...  
Keyword(s):  
Intermediate Filament ◽  
High Fat Diet ◽  
Metabolic Regulation ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Normal Diet ◽  
Pathway Enrichment Analysis ◽  
High Fat ◽  
Cytoskeleton Organization ◽  
Kegg Pathways

MicroRNAs (miRNAs) are a class of endogenous single-stranded RNA molecules that play an important role in gene regulation in animals by pairing with target gene mRNA. Extensive evidence shows that miRNAs are key players in metabolic regulation and the development of obesity. However, the systemic understanding of miRNAs in the adipogenesis of obese rabbit need further investigate. Here, seven small RNA libraries from rabbits fed either a standard normal diet (SND; n = 3) or high-fat diet (HFD; n = 4) were constructed and sequenced. Differentially expressed (DE) miRNAs were identified using the edgeR data analysis package from R. Software miRanda and RNAhybrid were used to predict the target genes of miRNAs. To further explore the functions of DE miRNAs, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. A total of 81,449,996 clean reads were obtained from the seven libraries, of which, 52 known DE miRNAs (24 up-regulated, 28 down-regulated) and 31 novel DE miRNAs (14 up-regulated, 17 down-regulated) were identified. GO enrichment analysis revealed that the DE miRNAs target genes were involved in intermediate filament cytoskeleton organization, intermediate filament-based process, and alpha-tubulin binding. DE miRNAs were involved in p53 signaling, linoleic acid metabolism, and other adipogenesis-related KEGG pathways. Our study further elucidates the possible functions of DE miRNAs in rabbit adipogenesis, contributing to the understanding of rabbit obesity.

scholarly journals Genome-wide Identification and Characterization of Perirenal Adipose Tissue MiRNAs in Rabbits Fed With a High-fat Diet

2020 ◽  
Author(s):  
Jie Wang ◽  
Jiahao Shao ◽  
Yanhong Li ◽  
Mauricio A. Elzo ◽  
Xianbo Jia ◽  
...  
Keyword(s):  
Intermediate Filament ◽  
High Fat Diet ◽  
Target Genes ◽  
Enrichment Analysis ◽  
Normal Diet ◽  
Pathway Enrichment Analysis ◽  
High Fat ◽  
Alpha Tubulin ◽  
Cytoskeleton Organization ◽  
Kegg Pathways

Abstract Background MicroRNAs (miRNAs) are a class of endogenous single-stranded RNA molecules that play an important role in gene regulation in animals by pairing with target gene mRNAs. However, the functions of miRNAs in the adipogenesis of obese rabbits are poorly understood. Methods Six small RNA libraries from rabbits under a standard normal diet (SND; n = 3) and a high-fat diet (HFD; n = 3) were constructed and sequenced. Differentially expressed (DE) miRNAs were identified using the edgeR data analysis package from R. Software miRanda and RNAhybrid were used to predict the target genes of miRNAs. To further explore the functions of DE miRNAs, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed. Results A total of 69577441 clean reads were obtained from the six libraries, of which, 52 known DE miRNAs (24 up-regulated, 28 down-regulated) and 31 novel DE miRNAs (14 up-regulated, 17 down-regulated) were identified. GO enrichment analysis revealed that the DE miRNAs target genes were involved in intermediate filament cytoskeleton organization, intermediate filament-based process, and alpha-tubulin binding. DE miRNAs were involved in p53 signaling, linoleic acid metabolism, and other adipogenesis-related KEGG pathways. Conclusions Our study further elucidates the possible functions of DE miRNAs in rabbit adipogenesis, contributing to the understanding of rabbit obesity.

scholarly journals Proteomics Analysis of Testis of Rats Fed a High-Fat Diet

2018 ◽  
Vol 47 (1) ◽  
pp. 378-389 ◽  
Author(s):  
Xiu-Yan Yang ◽  
Yu-jie Gu ◽  
Tian An ◽  
Jia-Xian Liu ◽  
Yan-Yun Pan ◽  
...  
Keyword(s):  
Gene Ontology ◽  
Metabolic Pathways ◽  
High Fat Diet ◽  
Male Fertility ◽  
Enrichment Analysis ◽  
Normal Diet ◽  
Differentially Expressed ◽  
High Fat ◽  
Non Coding Rnas ◽  
Reproductive Processes

Background/Aims: The adverse effects of obesity on male fertility have been widely reported. In recent years, the relationship between the differential expression of proteins and long non-coding RNAs with male reproductive disease has been reported. However, the exact mechanism in underlying obesity-induced decreased male fertility remains unclear. Methods: We used isobaric tags for relative and absolute quantification to identify differential protein expression patterns in the testis of rats fed a high-fat diet and normal diet. A microarray-based gene expression analysis protocol was used to compare the differences in long non-coding RNAs in high-fat diet-fed and normal diet-fed rats. Five obviously upregulated or downregulated proteins were examined using western blot to verify the accuracy of their expression. Then, we carried out functional enrichment analysis of the differentially expressed proteins using gene ontology and pathway analysis. Finally, the metabolic Gene Ontology terms and pathways involved in the differential metabolites were analyzed using the MetaboAnalyst 2.0 software to explore the co-expression relationship between long non-coding RNAs and proteins. Results: We found 107 proteins and 263 long non-coding RNAs differentially expressed between rats fed a high-fat diet and normal diet. The Gene Ontology term enrichment analysis showed that the protein function most highly enriched was related to negative regulation of reproductive processes. We also found five Gene Ontology terms and two metabolic pathways upregulated or downregulated for both proteins and long non-coding RNAs. Conclusion: The study revealed different expression levels for both proteins and long non-coding RNAs and showed that the function and metabolic pathways of differently expressed proteins were related to reproductive processes. The Gene Ontology terms and metabolic pathways upregulated or downregulated in both proteins and long non-coding RNAs may provide new candidates to explore the mechanisms of obesity-induced male infertility for both protein and epigenetic pathways.

scholarly journals Cardiac Transcriptome Analysis Reveals Nr4a1 Mediated Glucose Metabolism Dysregulation in Response to High-Fat Diet

Genes ◽  
2020 ◽  
Vol 11 (7) ◽  
pp. 720
Author(s):  
Lihui Men ◽  
Wenting Hui ◽  
Xin Guan ◽  
Tongtong Song ◽  
Xuan Wang ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Transcriptome Analysis ◽  
High Fat Diet ◽  
Critical Role ◽  
Enrichment Analysis ◽  
Pathway Enrichment Analysis ◽  
High Fat ◽  
Altered Expression ◽  
Increased Risk ◽  
H9c2 Cardiomyocytes

Obesity is associated with an increased risk of developing cardiovascular disease (CVD), with limited alterations in cardiac genomic characteristics known. Cardiac transcriptome analysis was conducted to profile gene signatures in high-fat diet (HFD)-induced obese mice. A total of 184 differentially expressed genes (DEGs) were identified between groups. Based on the gene ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of DEGs, the critical role of closely interlocked glucose metabolism was determined in HFD-induced cardiac remodeling DEGs, including Nr4a1, Fgf21, Slc2a3, Pck1, Gck, Hmgcs2, and Bpgm. Subsequently, the expression levels of these DEGs were evaluated in both the myocardium and palmitic acid (PA)-stimulated H9c2 cardiomyocytes using qPCR. Nr4a1 was highlighted according to its overexpression resulting from the HFD. Additionally, inhibition of Nr4a1 by siRNA reversed the PA-induced altered expression of glucose metabolism-related DEGs and hexokinase 2 (HK2), the rate-limiting enzyme in glycolysis, thus indicating that Nr4a1 could modulate glucose metabolism homeostasis by regulating the expression of key enzymes in glycolysis, which may subsequently influence cardiac function in obesity. Overall, we provide a comprehensive understanding of the myocardium transcript molecular framework influenced by HFD and propose Nr4a1 as a key glucose metabolism target in obesity-induced CVD.

scholarly journals Unveil the transcriptome alteration of POMC neuron in diet-induced obesity

2019 ◽  
Author(s):  
Peng Lyu ◽  
Zhishun Huang ◽  
Qingjun Feng ◽  
Yongfu Su ◽  
Mengying Zheng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
High Fat Diet ◽  
Arcuate Nucleus ◽  
Enrichment Analysis ◽  
Sphingolipid Metabolism ◽  
Pathway Enrichment Analysis ◽  
High Fat ◽  
Transcriptomic Profiling ◽  
Diet Induced Obesity ◽  
Underlying Mechanisms

Abstract Background: Loss of neuron homeostasis in the Arcuate nucleus (ARC) is suggested to be responsible for the development diet-induced-obesity (DIO). We previously reported that loss of Rb1 gene compromised the homeostasis of anorexigenic POMC neurons in ARC and induced obesity in mice.Method: To shed light on how DIO develops, we propose to analyze the transcriptomic alteration of POMC neurons in mice following high fat die (HFD) feeding. We isolated the POMC neurons from established DIO mice and performed transcriptomic profiling on them by RNA-seq.Results: A total of 1,066 genes (628 up-regulated and 438 down-regulated) were identified as differentially expressed genes (DEGs). Pathway enrichment analysis with these DEGs further revealed that ‘cell cycle’, ‘apoptosis’, ‘chemokine signalling’ and ‘sphingolipid metabolism’ pathways were correlated with the development of DIO. Moreover, we validated that the pRb protein, key regulator of ‘cell cycle pathway’, was inactivated by phosphorylation in POMC neurons with HFD feeding. Importantly, reversal of deregulated cell cycle by stereotaxic delivering of the unphosphorylated pRb∆P in ARC significantly meliorated the DIO. Together, our study provides insights into the mechanisms related to the loss of homeostasis of POMC neurons in DIO, and suggests pRb phosphorylation as a potential intervention target to treat DIO. Conclusion: The Arcuate nucleus is the material basis that controlled energy balance and glucose metabolism, which is vulnerable to high-fat-diet (HFD) in diet-induced-obesity (DIO). In this study, we conducted transcriptomic profiling in anorexigenic POMC neurons of ARC with HFD to disclose the underlying mechanisms related with the homeostasis maintenance and the development of DIO. Importantly, we suggest that DIO could be prevented of treated by reversal of the deregulated cell cycle in POMC neurons through targeting pRb phosphorylation. Keywords: High-Fat-Diet (HFD); Diet-Induced Obesity (DIO); POMC neuron; Neuron homeostasis; pRb phosphorylation

scholarly journals N-glycoproteomic analysis of Ginsenoside Rb1 on a hyperlipidemia rat model

2021 ◽  
Author(s):  
Yixin Ma ◽  
Shunyu Ning ◽  
Nan Song ◽  
Si Chen ◽  
Xue Leng ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Protein Modification ◽  
Ion Homeostasis ◽  
Enrichment Analysis ◽  
Control Group ◽  
Pathway Enrichment Analysis ◽  
Hypolipidemic Effect ◽  
Ginsenoside Rb1 ◽  
High Fat ◽  
Glycosylation Sites

Abstract Background: Ginsenoside Rb1, known as Renshen in traditional Chinese medicine, is one of the major bioactive saponins isolated from Panax ginseng C.A.Mey. N-glycosylation is the most common type of post-translational modification in cells. The widespread localization of N-glycosylated proteins (N-glycoproteins) between extracellular spaces and on the cell surfaces give them unique advantages as disease biomarkers and drug targets. Previous study found that Ginsenoside Rb1 could potentially play a preventive role in hyperlipidemia. This study aims to reveal the hypolipidemic effect at the protein modification level. Methods: 24 male SD rats were randomly devided into 3 groups: control group (CON), high fat diet group (HFD) and Ginsenoside Rb1 group (Rb1). Both HFD and Rb1 groups were fed with high-fat diet for 12 weeks. The Rb1 group started intragastric administering Ginsenoside Rb1 200 mg·kg -1 ·d -1 at 5th week for 8 weeks, while the CON and HFD group the same amount of normal saline for the same amount of time. Lipid levels and liver histology were assayed to evaluate the effects of Ginsenoside Rb1 intake on hyperlipidemia rats. Furthermore, the workflow by combination of isotope TMT labeling, HILIC enrichment, and high-resolution LC-MS/MS analysis were employed to exploring the mechanisms of regulation role in hyperlipidemia rats.Results: The histopathologic characteristics and biochemical data shows that Ginsenoside Rb1 exhibited regulative effects on hyperlipidemia rats. After being analyzed by N-glycoproteomic, 98 differential N-glycosylation sites on 53 glycoproteins between 2 comparison groups (HFD: CON, Rb1: HFD) were identified. Analyses of N-glycosylation sites distribution found that albumin (Alb) and Serpinc1 were most heavily modified with 6 N-glycosylation sites changed in this work. GO enrichment analysis showed that differential modified glycoproteins were involved in inflammatory response, cellular iron ion homeostasis and positive regulation of cholesterol efflux etc. biosynthetic process. Complement and coagulation cascades was the most significant enriched in the KEGG pathway enrichment analysis. Conclusions: This study presents a comprehensive analysis of a new set of N-glycoproteins which are altered by Ginsenoside Rb1 and offers some valuable clues for novel mechanistic insights into the ragulative mechanism of Ginsenoside Rb1. Results from N-glycoproteomic suggest that to suppress hyperlipidemia, Rb1 may regulates N-glycosylation of Alb, Serpinc1, PON1, Lrp1, Cp and THBS1, as well as differentially modified glycoproteins in complement and coagulation cascades, which in turn improve the imbalance of lipid homeostasis.

scholarly journals Resveratrol on the Metabolic Reprogramming in Liver: Implications for Advanced Atherosclerosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Ying Ma ◽  
Dongliang Li ◽  
Wenfeng Liu ◽  
Xiaoxiao Liu ◽  
Yingqi Xu ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Unsaturated Fatty Acids ◽  
Enrichment Analysis ◽  
Normal Diet ◽  
Metabolic Reprogramming ◽  
High Fat ◽  
Beneficial Effects ◽  
Highly Correlated ◽  
Iga Production ◽  
Oil Red O Staining

Background/Aims: Atherosclerosis (AS) is one of the major leading causes of death globally, which is highly correlated with metabolic abnormalities. Resveratrol (REV) exerts beneficial effects on atherosclerosis. Our aim is to clarify the involvement of liver metabolic reprogramming and the atheroprotective effects of REV.Methods: ApoE-deficient mice were administered with normal diet (N), high-fat diet (H), or HFD with REV (HR). Twenty-four weeks after treatment, Oil Red O staining was used to assess the severity of AS. Non-targeted metabolomics was employed to obtain metabolic signatures of the liver from different groups.Results: High-fat diet–induced AS was alleviated by REV, with less lipid accumulation in the lesions. The metabolic profiles of liver tissues from N, H, and HR groups were analyzed. A total of 1,146 and 765 differentially expressed features were identified between N and H groups, and H and HR groups, respectively. KEGG enrichment analysis uncovered several metabolism-related pathways, which are potential pathogenesis mechanisms and therapeutic targets including “primary bile acid biosynthesis,” “phenylalanine metabolism,” and “glycerophospholipid metabolism.” We further conducted trend analysis using 555 metabolites with one-way ANOVA, where p < 0.05 and PLS-DA VIP >1. We found that REV could reverse the detrimental effect of high-fat diet–induced atherosclerosis. These metabolites were enriched in pathways including “biosynthesis of unsaturated fatty acids” and “intestinal immune network for IgA production.” The metabolites involved in these pathways could be the potential biomarkers for AS-related liver metabolic reprogramming and the mechanism of REV treatment.Conclusions: REV exerted atheroprotective effects partially by modulating the liver metabolism.

scholarly journals Genome-Wide DNA Methylation Changes of Perirenal Adipose Tissue in Rabbits Fed a High-Fat Diet

Animals ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 2213
Author(s):  
Jiahao Shao ◽  
Xue Bai ◽  
Ting Pan ◽  
Yanhong Li ◽  
Xianbo Jia ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Enrichment Analysis ◽  
Epigenetic Mechanism ◽  
Pathway Enrichment Analysis ◽  
High Fat ◽  
Perirenal Adipose Tissue ◽  
Pathway Enrichment ◽  
Genome Wide

DNA methylation is an epigenetic mechanism that plays an important role in gene regulation without an altered DNA sequence. Previous studies have demonstrated that diet affects obesity by partially mediating DNA methylation. Our study investigated the genome-wide DNA methylation of perirenal adipose tissue in rabbits to identify the epigenetic changes of high-fat diet-mediated obesity. Two libraries were constructed pooling DNA of rabbits fed a standard normal diet (SND) and DNA of rabbits fed a high-fat diet (HFD). Differentially methylated regions (DMRs) were identified using the option of the sliding window method, and online software DAVID Bioinformatics Resources 6.7 was used to perform Gene Ontology (GO) terms and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis of DMRs-associated genes. A total of 12,230 DMRs were obtained, of which 2305 (1207 up-regulated, 1098 down-regulated) and 601 (368 up-regulated, 233 down-regulated) of identified DMRs were observed in the gene body and promoter regions, respectively. GO analysis revealed that the DMRs-associated genes were involved in developmental process (GO:0032502), cell differentiation (GO:0030154), and lipid binding (GO:0008289), and KEGG pathway enrichment analysis revealed the DMRs-associated genes were enriched in linoleic acid metabolism (KO00591), DNA replication (KO03030), and MAPK signaling pathway (KO04010). Our study further elucidates the possible functions of DMRs-associated genes in rabbit adipogenesis, contributing to the understanding of HFD-mediated obesity.

scholarly journals Proto-oncoprotein Zbtb7c and SIRT1 repression: implications in high-fat diet-induced and age-dependent obesity

2021 ◽  
Author(s):  
Won-Il Choi ◽  
Jae-Hyun Yoon ◽  
Seo-Hyun Choi ◽  
Bu-Nam Jeon ◽  
Hail Kim ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
High Fat Diet ◽  
Target Genes ◽  
Proximal Promoter ◽  
High Fat ◽  
Tissue Mass ◽  
Adipose Tissues ◽  
Adipose Tissue Mass ◽  
Age Dependent ◽  
Treatment Of Diabetes

AbstractZbtb7c is a proto-oncoprotein that controls the cell cycle and glucose, glutamate, and lipid metabolism. Zbtb7c expression is increased in the liver and white adipose tissues of aging or high-fat diet-fed mice. Knockout or knockdown of Zbtb7c gene expression inhibits the adipocyte differentiation of 3T3-L1 cells and decreases adipose tissue mass in aging mice. We found that Zbtb7c was a potent transcriptional repressor of SIRT1 and that SIRT1 was derepressed in various tissues of Zbtb7c-KO mice. Mechanistically, Zbtb7c interacted with p53 and bound to the proximal promoter p53RE1 and p53RE2 to repress the SIRT1 gene, in which p53RE2 was particularly critical. Zbtb7c induced p53 to interact with the corepressor mSin3A-HADC1 complex at p53RE. By repressing the SIRT1 gene, Zbtb7c increased the acetylation of Pgc-1α and Pparγ, which resulted in repression or activation of Pgc-1α or Pparγ target genes involved in lipid metabolism. Our study provides a molecular target that can overexpress SIRT1 protein in the liver, pancreas, and adipose tissues, which can be beneficial in the treatment of diabetes, obesity, longevity, etc.

scholarly journals Aberrant expression of HDL-bound microRNA induced by a high-fat diet in a pig model: implications in the pathogenesis of dyslipidaemia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Guoyuan Sui ◽  
Lianqun Jia ◽  
Nan Song ◽  
Dongyu Min ◽  
Si Chen ◽  
...  
Keyword(s):  
Real Time ◽  
Real Time Pcr ◽  
High Fat Diet ◽  
Enrichment Analysis ◽  
Diet Group ◽  
High Fat ◽  
Positive Regulation ◽  
Aberrant Expression ◽  
Balanced Diet ◽  
Mirna Sequencing

Abstract Background A high-fat diet can affect lipid metabolism and trigger cardiovascular diseases. A growing body of studies has revealed the HDL-bound miRNA profiles in familial hypercholesterolaemia; in sharp contrast, relevant studies on high-fat diet-induced dyslipidaemia are lacking. In the current study, HDL-bound miRNAs altered by a high-fat diet were explored to offer some clues for elucidating their effects on the pathogenesis of dyslipidaemia. Methods Six pigs were randomly divided into two groups of three pigs each, namely, the high-fat diet and the balanced diet groups, which were fed a high-fat diet and balanced diet separately for six months. HDL was separated from plasma, which was followed by dissociation of the miRNA bound to HDL. miRNA sequencing of the isolated miRNA was performed to identify the differential expression profiles between the two groups, which was validated by real-time PCR. TargetScan, miRDB, and miRWalk were used for the prediction of genes targeted by the differential miRNAs. Results Compared with the balanced diet group, the high-fat diet group had significantly higher levels of TG, TC, LDL-C and HDL-C at six months. miRNA sequencing revealed 6 upregulated and 14 downregulated HDL-bound miRNAs in the high-fat diet group compared to the balanced diet group, which was validated by real-time PCR. GO enrichment analysis showed that dysregulated miRNAs in the high-fat diet group were associated with the positive regulation of lipid metabolic processes, positive regulation of lipid biosynthetic processes, and positive regulation of Ras protein signal transduction. Insulin resistance and the Ras signalling pathway were enriched in the KEGG pathway enrichment analysis. Conclusions Twenty HDL-bound miRNAs are significantly dysregulated in high-fat diet-induced dyslipidaemia. This study presents an analysis of a new set of HDL-bound miRNAs that are altered by a high-fat diet and offers some valuable clues for novel mechanistic insights into high-fat diet-induced dyslipidaemia. Further functional verification study using a larger sample size will be required.

Hyperbaric oxygen therapy attenuates D-galactose-induced-age-related cardiac dysfunction through mitigating cardiac mitochondrial dysfunction in pre-diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bo-Htay ◽  
T Shwe ◽  
S Palee ◽  
T Pattarasakulchai ◽  
K Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Lv Function ◽  
High Fat ◽  
Insulin Resistant ◽  
Lv Dysfunction ◽  
Age Related ◽  
Mitochondrial Functions

Abstract Background D-galactose (D-gal) induced ageing has been shown to exacerbate left ventricular (LV) dysfunction via worsening of apoptosis and mitochondrial dysfunction in the heart of obese rats. Hyperbaric oxygen therapy (HBOT) has been demonstrated to exert anti-inflammatory and anti-apoptotic effects in multiple neurological disorders. However, the cardioprotective effect of HBOT on inflammation, apoptosis, LV and mitochondrial functions in D-gal induced ageing rats in the presence of obese-insulin resistant condition has never been investigated. Purpose We sought to determine the effect of HBOT on inflammation, apoptosis, mitochondrial functions and LV function in pre-diabetic rats with D-gal induced ageing. We hypothesized that HBOT attenuates D-gal induced cardiac mitochondrial dysfunctions and reduces inflammation and apoptosis, leading to improved LV function in pre-diabetic rats. Methods Forty-eight male Wistar rats were fed with either normal diet or high-fat diet for 12 weeks. Then, rats were treated with either vehicle groups (0.9% NSS, subcutaneous injection (SC)) or D-gal groups (150 mg/kg/day, SC) for 8 weeks. At week 21, rats in each group were equally divided into 6 sub-groups: normal diet fed rats treated with vehicle (NDV) sham, normal diet fed rats treated with D-gal (NDDg) sham, high fat diet fed rats treated with D-gal (HFDg) sham, high fat diet fed rats treated with vehicle (HFV) + HBOT, NDDg + HBOT and HFDg + HBOT. Sham treated rats were given normal concentration of O2 (flow rate of 80 L/min, 1 ATA for 60 minutes), whereas HBOT treated rats were subjected to 100% O2 (flow rate of 250 L/min, 2 ATA for 60 minutes), given once daily for 2 weeks. Results Under obese-insulin resistant condition, D-gal-induced ageing aggravated LV dysfunction (Fig 1A) and impaired cardiac mitochondrial function, increased cardiac inflammatory and apoptotic markers (Fig 1B). HBOT markedly reduced cardiac TNF-α level and TUNEL positive apoptotic cells, and improved cardiac mitochondrial function as indicated by decreased mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, resulting in the restoration of the normal LV function in HFV and NDDg rats, compared to sham NDDg rats. In addition, in HFDg treated rats, HBOT attenuated cardiac TNF-α level, TUNEL positive apoptotic cells and cardiac mitochondrial dysfunction, compared to sham HFDg rats, leading to improved cardiac function as indicated by increased %LV ejection fraction (LVEF) (Figure 1). Conclusion HBOT efficiently alleviates D-gal-induced-age-related LV dysfunction through mitigating inflammation, apoptosis and mitochondrial dysfunction in pre-diabetic rats. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): 1. The National Science and Technology Development Agency Thailand, 2. Thailand Research Fund Grants

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