The Isolation, Culture, and Propagation of Murine Intestinal Enteroids for the Study of Dietary Lipid Metabolism

2017 ◽  
pp. 195-204 ◽  
Author(s):  
Diana Li ◽  
Hongli Dong ◽  
Alison B. Kohan

2021 ◽  
Author(s):  
Ningning Su ◽  
Minglei Xu ◽  
Yuanyuan Zhou ◽  
Huaqun Ye ◽  
Kangsen Mai ◽  
...  


1978 ◽  
Vol 61 (10) ◽  
pp. 1400-1406 ◽  
Author(s):  
Y.T. Yang ◽  
J.M. Rohde ◽  
R.L. Baldwin






2020 ◽  
Vol 58 (2) ◽  
pp. 97-104
Author(s):  
Takahiro NAGATAKE ◽  
Jun KUNISAWA


2019 ◽  
Vol 50 (11) ◽  
pp. 3369-3381 ◽  
Author(s):  
Nina Gou ◽  
Zhiguang Chang ◽  
Wei Deng ◽  
Hong Ji ◽  
Jishu Zhou


2018 ◽  
Vol 115 (40) ◽  
pp. E9499-E9506 ◽  
Author(s):  
Zhiguang Huang ◽  
Menglu Zhang ◽  
Abigail A. Plec ◽  
Sandi Jo Estill ◽  
Ling Cai ◽  
...  

Acetyl-CoA synthetase 2 (ACSS2) is a conserved nucleocytosolic enzyme that converts acetate to acetyl-CoA. Adult mice lacking ACSS2 appear phenotypically normal but exhibit reduced tumor burdens in mouse models of liver cancer. The normal physiological functions of this alternate pathway of acetyl-CoA synthesis remain unclear, however. Here, we reveal that mice lacking ACSS2 exhibit a significant reduction in body weight and hepatic steatosis in a diet-induced obesity model. ACSS2 deficiency reduces dietary lipid absorption by the intestine and also perturbs repartitioning and utilization of triglycerides from adipose tissue to the liver due to lowered expression of lipid transporters and fatty acid oxidation genes. In this manner, ACSS2 promotes the systemic storage or metabolism of fat according to the fed or fasted state through the selective regulation of genes involved in lipid metabolism. Thus, targeting ACSS2 may offer a therapeutic benefit for the treatment of fatty liver disease.



2019 ◽  
Vol 123 (2) ◽  
pp. 149-160 ◽  
Author(s):  
Peng Sun ◽  
Min Jin ◽  
Lefei Jiao ◽  
Óscar Monroig ◽  
Juan Carlos Navarro ◽  
...  

AbstractThe regulation of lipogenesis and lipolysis mechanisms related to consumption of lipid has not been studied in swimming crab. The aims of the present study were to evaluate the effects of dietary lipid levels on growth, enzymes activities and expression of genes of lipid metabolism in hepatopancreas of juvenile swimming crab. Three isonitrogenous diets were formulated to contain crude lipid levels at 5·8, 9·9 and 15·1 %. Crabs fed the diet containing 15·1 % lipid had significantly lower growth performance and feed utilisation than those fed the 5·8 and 9·9 % lipid diets. Crabs fed 5·8 % lipid had lower malondialdehyde concentrations in the haemolymph and hepatopancreas than those fed the other diets. Highest glutathione peroxidase in haemolymph and superoxide dismutase in hepatopancreas were observed in crabs fed 5·8 % lipid. The lowest fatty acid synthase and glucose 6-phosphate dehydrogenase activities in hepatopancreas were observed in crabs fed 15·1 % lipid, whereas crabs fed 5·8 % lipid had lower carnitine palmitoyltransferase-1 activity than those fed the other diets. Crabs fed 15·1 % lipid showed lower hepatopancreas expression of genes involved in long-chain-PUFA biosynthesis, lipoprotein clearance, fatty acid uptake, fatty acid oxidation, lipid anabolism and lipid catabolism than those fed the other diets, whereas expression of some genes of lipoprotein assembly and fatty acid oxidation was up-regulated compared with crabs fed 5·8 % lipid. Overall, high dietary lipid level can inhibit growth, reduce antioxidant enzyme activities and influence lipid metabolic pathways to regulate lipid deposition in crab.



2019 ◽  
Vol 6 ◽  
Author(s):  
Azusa Saika ◽  
Takahiro Nagatake ◽  
Jun Kunisawa


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