Hepatic lipidosis is a common lesion in chelonians and may be related with vitellogenesis, hyperparathyroidism, follicular stasis, fatty diets or lacking nutrients, sedentary life and obesity, bacterial toxins in live...Hepatic lipidosis is a common lesion in chelonians and may be related with vitellogenesis, hyperparathyroidism, follicular stasis, fatty diets or lacking nutrients, sedentary life and obesity, bacterial toxins in liver and starvation. Clinical signs are unspecific. Routine biochemical tests don＇t have specificity and it is better defined through biopsy. The objective was evaluated the biochemical hepatic profile of red footed tortoises （Chelonoidis carbonaria） with the histopathological findings of lipidosis by laparoscopic biopsy. Samples of blood were collected for biochemistry of thirty-six animals from two different groups, twenty animals from a zoo and sixteen from a breeder. The animals were submitted to liver biopsy by videolaparoscopy. Three fragments were collected, two of them were processed by histology and one went to electron microscopy. Nineteen tortoises from the zoo had lipidosis in laparoscopy and macrovesicular degeneration. Fifteen tortoises from the breeder had microvesicular degeneration. The diagnosis of steatosis was confirmed by electron microscopy. There was no statistical difference of aspartate aminotransferase levels between the two groups; however there was significant difference of triglycerides levels. The enzymatic activity of transaminases is not related to the histological grading of lipidosis in tortoises, however triglycerides levels are higher in animals with more severe gradation.展开更多
Nonalcoholic fatty liver disease(NAFLD)encompasses a spectrum of pathologies,ranging from steatosis to nonalcoholic steatohepatitis(NASH).The factors promoting the progression of steatosis to NASH are still unclear.Re...Nonalcoholic fatty liver disease(NAFLD)encompasses a spectrum of pathologies,ranging from steatosis to nonalcoholic steatohepatitis(NASH).The factors promoting the progression of steatosis to NASH are still unclear.Recent studies suggest that mitochondrial lipid composition is critical in NASH develop-ment.Here,we showed that CDP-DAG synthase 2(Cds2)was downregulated in genetic or diet-induced NAFLD mouse models.Liver-specific deficiency of Cds2 provoked hepatic steatosis,inflammation and fibrosis in five-week-old mice.CDS2 is enriched in mitochondria-associated membranes(MAMs),and hepatic Cds2 deficiency impaired mitochondrial function and decreased mitochondrial PE levels.Overexpression of phosphatidylserine decarboxylase(PISD)alleviated the NASH-like phenotype in Cds2^(f/f);AlbCre mice and abnormal mitochondrial morphology and function caused by CDS2 deficiency in hepatocytes.Additionally,dietary supplementation with an agonist of peroxisome proliferator-activated receptor alpha(PPARa)attenuated mitochondrial defects and ameliorated the NASH-like phe-notype in Cds2^(f/f);AlbCre mice.Finally,Cds2 overexpression protected against high-fat diet-induced hepatic steatosis and obesity.Thus,Cds2 modulates mitochondrial function and NASH development.展开更多
文摘Hepatic lipidosis is a common lesion in chelonians and may be related with vitellogenesis, hyperparathyroidism, follicular stasis, fatty diets or lacking nutrients, sedentary life and obesity, bacterial toxins in liver and starvation. Clinical signs are unspecific. Routine biochemical tests don＇t have specificity and it is better defined through biopsy. The objective was evaluated the biochemical hepatic profile of red footed tortoises （Chelonoidis carbonaria） with the histopathological findings of lipidosis by laparoscopic biopsy. Samples of blood were collected for biochemistry of thirty-six animals from two different groups, twenty animals from a zoo and sixteen from a breeder. The animals were submitted to liver biopsy by videolaparoscopy. Three fragments were collected, two of them were processed by histology and one went to electron microscopy. Nineteen tortoises from the zoo had lipidosis in laparoscopy and macrovesicular degeneration. Fifteen tortoises from the breeder had microvesicular degeneration. The diagnosis of steatosis was confirmed by electron microscopy. There was no statistical difference of aspartate aminotransferase levels between the two groups; however there was significant difference of triglycerides levels. The enzymatic activity of transaminases is not related to the histological grading of lipidosis in tortoises, however triglycerides levels are higher in animals with more severe gradation.
基金the Ministry of Science and Technology of China(2018YFA0506902,2016YFA0500100,and 2018YFA081104)the National Natural Science Foundation of China(9195420001,31771305,and 31630019)Chinese Academy of Sciences(XDPB17)。
文摘Nonalcoholic fatty liver disease(NAFLD)encompasses a spectrum of pathologies,ranging from steatosis to nonalcoholic steatohepatitis(NASH).The factors promoting the progression of steatosis to NASH are still unclear.Recent studies suggest that mitochondrial lipid composition is critical in NASH develop-ment.Here,we showed that CDP-DAG synthase 2(Cds2)was downregulated in genetic or diet-induced NAFLD mouse models.Liver-specific deficiency of Cds2 provoked hepatic steatosis,inflammation and fibrosis in five-week-old mice.CDS2 is enriched in mitochondria-associated membranes(MAMs),and hepatic Cds2 deficiency impaired mitochondrial function and decreased mitochondrial PE levels.Overexpression of phosphatidylserine decarboxylase(PISD)alleviated the NASH-like phenotype in Cds2^(f/f);AlbCre mice and abnormal mitochondrial morphology and function caused by CDS2 deficiency in hepatocytes.Additionally,dietary supplementation with an agonist of peroxisome proliferator-activated receptor alpha(PPARa)attenuated mitochondrial defects and ameliorated the NASH-like phe-notype in Cds2^(f/f);AlbCre mice.Finally,Cds2 overexpression protected against high-fat diet-induced hepatic steatosis and obesity.Thus,Cds2 modulates mitochondrial function and NASH development.
