Antistarvation Strategies of E. Sinensis: Regulatory Networks under Hepatopancreas Consumption

Abstract

Crustaceans have a more persistent starvation tolerance than mammals, birds, reptiles, and even fish. This study is aimed at assessing the survival strategy and regulatory mechanism of crustaceans in response to starvation through an animal model using Eriocheir sinensis. In the 42-day starvation experiment, the hepatopancreas was found to become the target organ, which was characterized by atrophy of the thin wall in the hepatic tubules and expansion of the lumen. During short-term starvation, E. sinensis activates lipid and glycogen metabolism in the hepatopancreas with lipid metabolism dominating. In lipid metabolism, there was a significant decline in triglyceride, whereas cholesterol did not change significantly. Meanwhile, the fatty acid metabolism pathway was inhibited, but autophagy increased in the hepatopancreas, which may be the selective pathway for the decomposition of intracellular substances. However, under long-term starvation, the stored energy in the hepatopancreas was depleted, and E. sinensis selects to consume hepatopancreatic cells and maintain energy metabolism through apoptosis, which was triggered by both the death receptor pathway and the mitochondrial pathway. In addition, cell proliferation was blocked to reduce unnecessary energy consumption.

Vital Carbohydrate and Lipid Metabolites in Serum Involved in Energy Metabolism during Pubertal Molt of Mud Crab (Scylla paramamosain)

“…In crustaceans, the hepatopancreas is the central organ for lipid metabolism, including the digestion, storage, catabolism, and anabolism of lipids [34]. When fasting occurs in molting, crustaceans activate lipid and glycogen metabolism in the hepatopancreas, with lipid metabolism dominating [35,36]. In the present study, 16 glycerophosphocholines were identified in serum during the pubertal molting, including 9 significantly changed glycerophosphocholines (Tables S1 and 1, Figure 3).…”

Aberrant serum and tissue levels of Beclin1 and mechanistic target of rapamycin (mTOR) proteins in epithelial ovarian cancer

“…[31] We also discovered that Beclin1 and mTOR proteins might interact with MAPKAP1, PIK3C3, FKBP1A, RICTOR, AKTI, ATG14, PPP2CA, PRTOR, RRAGC, RPS6KB1, MLST8, RRAGD, RHEB, RRAGA, RRAGB, and LAMTOR1-5, which are involved in the cellular response to stress, [32] the cell cycle, [33] cell division, [34] autophagy, [35] cellular nutrition, [36] and receptor decomposition. [37] In high Beclin1-expressing ovarian cancer, patient survival is better, [38] but knockdown of Beclin1 expression resulted in the development of resistance to platinum drugs by ovarian adenocarcinoma Skov3 cells. [39] Additionally, the PI3K/AKT/mTOR pathway promotes tumor cell proliferation and chemotherapy resistance, which are frequently present in ovarian cancer.…”

Long-Term Ammonia Toxicity in the Hepatopancreas of Swimming Crab Portunus trituberculatus: Cellular Stress Response and Tissue Damage

“…The sections (5-6 µm) were prepared with a microtome, stained with hematoxylin-eosin (HE), and observed under a light microscope (Olympus, Tokyo, Japan). After observation, the relative area of the tubule (%) and relative area of the lumen (%) (4-5 fields for each individual, and three individuals for each treatment) were quantified according to the previous study (Huang et al, 2020) and using the CaseViewer 2.0 software.…”