Effects of Nutritionally Induced Obesity on Metabolic Pathways of Zebrafish.
Xixi LiGuodong GeGuili SongQing LiZongbin CuiPublished in: International journal of molecular sciences (2023)
Human obesity has become a global epidemic that can lead to many metabolic diseases, including insulin resistance, type 2 diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver. The development of obesity is closely associated with excess food intake and energy imbalance, family history, lifestyle, psychology and other factors, but molecular mechanisms underlying the induction and development of obesity remain to be intensively studied under a variety of internal and external pathogenesis conditions. In this study, we generated two obesity models of zebrafish that were treated with a high-fat diet (HFD) or an overfeeding diet (DIO). Both HFD and DIO zebrafish exhibited higher levels of lipid accumulation, fat distribution, microvascular steatosis and ectopic accumulation of lipid droplets in liver and muscle than normal diet (NOD) fish. The comparison of transcriptome sequencing data for the livers of HFD, DIO and NOD groups identified common and specific genes and signaling pathways that are potentially associated with zebrafish obesity induced by HFD and/or DIO. These findings provide clues for further understanding the mechanisms of obesity development and preventing nutritionally induced obesity through targeting the common signaling pathways and biological processes.
Keyphrases
- insulin resistance
- high fat diet
- type diabetes
- metabolic syndrome
- weight loss
- high fat diet induced
- adipose tissue
- skeletal muscle
- polycystic ovary syndrome
- weight gain
- physical activity
- high glucose
- signaling pathway
- artificial intelligence
- endothelial cells
- diabetic rats
- single cell
- drug delivery
- fatty acid
- genome wide
- epithelial mesenchymal transition
- drug induced
- oxidative stress
- cell proliferation
- innate immune