Backfat thickness (BT) and intramuscular fat (IMF) content are closely appertained to meat production and quality in pig production. Deposition in subcutaneous adipose (SA) and IMF concerns different genes and regulatory mechanisms. And larger studies with rigorous design should be carried to explore the molecular regulation of fat deposition in different tissues. The purpose of this study is to gain a better understanding of the molecular mechanisms underlying differences in fat deposition among different tissues and identify tissue-specific genes involved in regulating fat deposition. The SA-associated datasets (GSE122349 and GSE145956) and IMF-associated datasets (GSE165613 and GSE207279) were downloaded from the Gene Expression Omnibus (GEO) as the BT and IMF group, respectively. Subsequently, the Robust Rank Aggregation (RRA) algorithm identified 27 down- and 29 up-regulated differentially expressed genes (DEGs) in the BT group. Based on bioinformatics and three machine learning algorithms, four SA deposition-related potential biomarkers, namely , , , and were selected. was evaluated as the most valuable biomarker for the SA mechanism. The 18 down- and 34 up-regulated DEGs in the IMF group were identified, and and were screened as the IMF deposition-related candidate core genes, especially the may play the critical role in IMF deposition regulation. Moreover, based on the constructed ceRNA network, we postulated that the role of predicted ceRNA interaction network of XIST, NEAT1/miR-15a-5p, miR-16-5p, miR-424-5p, miR-497-5p/ were vital in the SA metabolism, XIST, NEAT1/miR-27a/b-3p, 181a/c-5p/ might contribute to the regulation to IMF metabolism, which all gave suggestions in molecular mechanism for regulation of fat deposition. These findings may facilitate advancements in porcine quality at the genetic and molecular levels and assist with human obesity-associated diseases.
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http://dx.doi.org/10.1016/j.heliyon.2024.e31311 | DOI Listing |
Exp Cell Res
January 2025
Department of Internal Medicine, Hebei Medical University, Shijiazhuang 050017, Hebei, China; Department of Cardiology, Hebei General Hospital, Shijiazhuang 050051, Hebei, China. Electronic address:
SRY-Box Transcription Factor-11 (SOX11) is a transcriptional regulatory factor that plays a crucial role in inflammatory responses. However, its involvement in atherosclerosis (AS), a cardiovascular disease driven by endothelial cell inflammation, remains unknown. This study aims to elucidate the role of SOX11 in AS.
View Article and Find Full Text PDFWhile fructose is a key dietary component, concerns have been raised about its potential risks to the liver. This study aimed to assess quercetin's protective effects against fructose-induced mouse hepatic steatosis. Thirty-two male C57BL/6J mice were randomly allocated into four groups: control, high fructose diet (HFrD), HFrD supplemented with low-dose quercetin (HFrD+LQ), and HFrD supplemented with high-dose quercetin (HFrD+HQ).
View Article and Find Full Text PDFFood Sci Nutr
January 2025
Laboratory of Biotechnology and Natural Resources Valorization, Faculty of Sciences Ibn Zohr University Agadir Morocco.
Hepatic steatosis/non-alcoholic fatty liver disease is a major public health delinquent caused by the excess deposition of lipid into lipid droplets (LDs) as well as metabolic dysregulation. Hepatic cells buildup with more fat molecules when a person takes high fat diet that is excessive than the body can handle. At present, millions of people in the world are affected by this problem.
View Article and Find Full Text PDFDiabetes Metab Syndr Obes
January 2025
Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.
Purpose: Mitochondrial dysfunction mediated by c-Jun N-terminal kinase (JNK) plays an important role in lipotoxic liver injury in nonalcoholic steatohepatitis (NASH). This study aims to investigate the pharmacological mechanism of Jiangzhi Granule (JZG), a Chinese herbal formula against NASH, with a focus on its regulation of JNK signaling-mediated mitochondrial function.
Methods: Hepatocytes were induced by palmitic acid (PA) for 24 h to establish an in vitro lipotoxic model, which was simultaneously treated with either JZG or vehicle control.
Nat Commun
January 2025
Department of Cardiology, Tangdu Hospital, Airforce Medical University, Xi'an, China.
Physical exercise is a cornerstone for preventing diet-induced obesity, while it is unclear whether physical exercise could offset high-fat, high-calories diet (HFCD)-induced cardiac dysfunction. Here, mice were fed with HFCD and simultaneously subjected to physical exercise. As expected, physical exercise prevented HFCD-induced whole-body fat deposition.
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