GRK6棕榈酰化修饰在炎症导致的猪肝脏糖脂代谢紊乱中的作用及其机制

炎症常会导致猪肝脏代谢紊乱，但其机制如何目前仍不清楚。G蛋白偶联受体激酶6（G protein-coupled receptor kinases，GRK6）是催化诱导G蛋白偶联受体（GPCRs）失去生物功能的重要激酶，它通过调控GPCRs介导的多条通路，广泛地参与机体的代谢过程。棕榈酰化修饰是蛋白质的脂质修饰形式，能够增加蛋白质的疏水性，对蛋白质的转运、细胞器定位和功能具有重要的作用。GRK6转位到细胞膜是其调控GPCRs信号的先决条件。炎症状态下猪肝脏GRK6如何通过棕榈酰化修饰转位到细胞膜上，其调控机制是什么？棕榈酰化修饰的GRK6对炎症状态下肝脏糖脂代谢有何具体作用？本研究拟通过体内外的实验，探索炎症感染后猪肝脏GRK6棕榈酰化修饰的变化，阐明其发生机制以及对肝脏糖脂代谢的影响。研究结果为进一步改善炎症感染下的动物肝脏代谢失衡，促进动物健康养殖提供新的靶点和治疗方案。

Inflammation can cause metabolic disorders in pig livers, but the mechanism is still unclear. G protein-coupled receptor kinases (GRK6) is an important kinase that catalyzed G protein-coupled receptor (GPCR) to lose its biological function. It is widely involved in metabolic processes by regulating multiple pathways mediated by GPCRs, and it is a hot spot in the current signal transduction research. Palmitoylation is a reversible lipid modification of proteins, which can increase the hydrophobicity of proteins and play an important role in protein transport, organelle localization and function. GRK6 translocation to the cell membrane is a prerequisite for its regulation of GPCRs signaling. In the inflammatory state, whether GRK6 is translocated to the cell membrane by palmitoylation modification, and what is its regulatory mechanism? Which glycolipid metabolism-related GPCRs of liver cells are mainly affected by activated GRK6? It's unclear until now. The purpose of this study was to explore the changes of palmitoylation of GRK6 in pig liver after inflammatory infection through in vivo and in vitro experiments, and to elucidate its specific mechanism of action and its effect on glucose and lipid metabolism in liver. The results of this study will provide a new target and treatment for further improving the metabolic imbalance of animals under inflammatory and promoting the healthy breeding of animals.