Knockdown of CPT1A Induce Chicken Adipocyte Differentiation to Form Lipid Droplets

Abstract

Lipid metabolism dysfunction is closely related to obesity, inflammation, diabetes, lipodystrophy, cardiovascular disease. Along with having a positive effect on energy homeostasis during fasting or prolonged exercise through mitochondrial fatty acid oxidation (FAO), more than two dozen enzymes and transport proteins are involved in the activation and transport of fatty acids into the mitochondrial, providing insights into their critical roles in metabolism. CPT1A has been reported to be expressed ubiquitously in the body and associated with dire consequences affecting fat deposition as the key rate-limiting enzyme of FAO. However, there is a dearth of data on the specific role of CPT1A on adipogenic differentiation and adipocyte lipolysis on chicken. This study assessed CPT1A's function in adipocyte differentiation andadipocyte lipolysis, and the mechanisms were investigated. We found that CPT1A knockdown (KD) promotes the differentiation of chicken preadipocytes into mature adipocytes. CPT1A KD increased PPARγ protein expression level. Expression levels of lipid synthesis-related genes were increased, and lipolysis genes were reduced.Also, CPT1A KD can encourage the formation of lipid droplets. So our results confirmed that knockdown of CPT1A induced the lipid differentiation and inhibited the β-oxidation process to promote the formation of lipid droplets. These findings may deepen our understanding on CPT1A function, especially its regulatory role in adipocyte biology.

Fat deposition, fatty acid profiles, antioxidant capacity and differentially expressed genes in subcutaneous fat of Tibetan sheep fed wheat‐based diets with and without xylanase supplementation

“…As the pivotal rate‐limiting enzyme of fatty acid oxidation, CPT1A regulates the oxidation of fatty acids in mammals (Lin et al, 2021). Knockdown of CPT1A contributed to the differentiation of preadipocytes to mature adipocytes in chicken via up‐regulation of PPARγ expression (Gao et al, 2023; Li et al, 2022). In response to a high‐fat diet, the expression of CPT1A and sterol o‐acyltransferase1 (SOAT1) were enhanced and contributed to the development of hepatocellular carcinoma by disruption of lipid homoeostasis (Ren et al, 2021).…”