Restrição alimentar e realimentação na tilápia do Nilo (Oreochromis niloticus): efeitos sobre o tecido hepático, parâmetros fisiológicos e bioquímicos do sangue

Abstract

Throughout evolution, organisms developed mechanisms to monitor and respond to fluctuations in nutrient supply. In vertebrates, during fasting, changes in the use of energyfuels mark metabolic adaptations that involve the main pathways of intermediary metabolism, particularly in the liver. At the cellular level, a redirection of metabolism to increased catabolism and decreased anabolism through phosphorylation of key proteins in several cellular pathways, including lipid homeostasis, glycolysis/glycogenolysis and autophagy operates to maintain ATP levels for basal metabolism. In this study, a multiparametric approach was used that included the assessment of morphological biomarkers (condition factor and hepatosomatic index), plasma metabolites (glucose, triglycerides, cholesterol, total proteins, alanine transaminase and aspartate transaminase), autophagy and apoptosis, histology and liver ultrastructure, to assess the response of Nile tilapia (Oreochromis niloticus) to the condition of total food restriction at different times (7, 14, 21 and 28 days) and refeeding (food restriction and refeeding cycles). The results of morphometric biomarkers indicated a decrease in the hepatosomatic index for the total food restriction group and complete recovery for the refeeding groups. Starvation also caused an early drop and decrease in glucose, triglyceride, and cholesterol plasma levels. In the groups refeeding, a quick and complete recovery of blood glucose, but triglycerides and cholesterol have not returned to the levelsof the control group within 7 days of refeeding. A histopathological analysis showed an occurrence of steatosis limited to small areas after 7 days, progressively increasing until reaching a large part of the liver at 28 days of starvation. Inflammatory infiltrate and necrosis were also observed at 14 days, becoming the more frequent change at 28 days. Hepatic glycogen levels were depleted at the beginning of starvation but returned to similar values to the control group after refeeding. Lipoperoxidation increased with a progression of starvation, probably being partially responsible for liver damage. Autophagy proteins (beclin1 and LC3­ II) reveal a drop in autophagy at 21 and 28 days of starvation. The hepatic dynamics of apoptotic death pointed to an increase in apoptosis in the starvation groups, particularly at times 21 and 28 days of total food restriction. Ultrastructural analysis evidenced the occurrence of autophagic structures in addition to glycogen depletion, occurrence of steatosis and other cellular degenerations, especially in the group submitted to 28 days of starvation. Thus, dietary restriction can lead to progressive liver damage in Nile tilapia after 7 days of starvation. However, two refeeding cycles can recover most of the depleted energy stocks in addition to mitigating the deleterious effects of extended period of starvation.