Key Lab of Chinese Medicine Resources Conservation, State Administration of Traditional Chinese Medicine of the People's Republic of China, Engineering Research Center of Chinese Medicine Resource, Ministry of Education, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China.
Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Comp Biochem Physiol B Biochem Mol Biol. 2024 Oct-Dec;274:110999. doi: 10.1016/j.cbpb.2024.110999. Epub 2024 Jun 7.
Non-blood-feeding leeches, Whitmania pigra, have evolved unique digestive structures and physiological mechanisms to cope with fasting. However, the metabolic changes and molecular mechanisms induced by fasting remain unclear. Therefore, this study recorded the weights of leeches during the fasting process. The weight changes were divided into two stages: a rapid decline period (1-9 weeks) and a fluctuating decline period (9-24 weeks). Leeches fasted for 4 (H4), 11 (H11), and 24 (H24) weeks were selected for transcriptome sequencing. Compared to the control group (H0), 436, 1157, and 337 differentially expressed genes (DEGs) were identified, which were mainly related to glycolysis/gluconeogenesis, amino acid metabolism, and the lipid metabolism pathway. The 6-phosphofructokinase (Pfk), pyruvate kinase (PK), and phosphoenolpyruvate carboxykinase (Pck) transcription levels revealed glycolysis/gluconeogenesis activation during the early stage of fasting and peaked at 11 weeks. Decreased expression of the rate-limiting enzyme acetyl-CoA carboxylase (ACC) in fatty acid synthesis during fasting may impede fatty acid synthesis. These results indicated that the nutrient storage and energy-supplying pathways in W. pigra were modified to improve fasting resistance. The findings of this study provided guidance for exploring the mechanism underlying fasting metabolism and laid a foundation for artificial breeding to improve the resistance of leeches.
非吸血类蚂蟥,宽体金线蛭,进化出了独特的消化结构和生理机制以应对饥饿。然而,饥饿诱导的代谢变化和分子机制仍不清楚。因此,本研究记录了蚂蟥在禁食过程中的体重变化。体重变化分为两个阶段:快速下降期(1-9 周)和波动下降期(9-24 周)。选择禁食 4(H4)、11(H11)和 24(H24)周的蚂蟥进行转录组测序。与对照组(H0)相比,鉴定出 436、1157 和 337 个差异表达基因(DEGs),主要与糖酵解/糖异生、氨基酸代谢和脂质代谢途径有关。6-磷酸果糖激酶(Pfk)、丙酮酸激酶(PK)和磷酸烯醇丙酮酸羧激酶(Pck)的转录水平显示,糖酵解/糖异生在禁食早期被激活,并在 11 周时达到峰值。脂肪酸合成中限速酶乙酰辅酶 A 羧化酶(ACC)的表达减少可能会阻碍脂肪酸的合成。这些结果表明,W. pigra 的营养物质储存和能量供应途径发生了改变,以提高其对饥饿的抵抗力。本研究的结果为探索禁食代谢机制提供了指导,并为人工养殖提高蚂蟥的抵抗力奠定了基础。