High fat diet liver steatosis

By | February 13, 2021

high fat diet liver steatosis

Non-alcoholic fatty liver disease NAFLD, which includes steatosis and its progression to non-alcoholic steatohepatitis, is a liver disorder of increasing clinical significance. Here we characterize a murine model of high fat diet-induced NAFLD with progression from liver steatosis to histological features compatible with steatohepatitis and more advanced stages of NAFLD in humans, including chronic portal inflammation, pericellular and bridging fibrosis, Mallory body formation, and bile ductular reaction. Chronic changes induced by the prolonged consumption of a high-fat diet alone culminate in the development of primary liver dysplasias. Importantly, we extend these studies to demonstrate that even the early stages of uncomplicated steatosis provide a permissive microenvironment for the growth of colon cancer cells that are metastatic to the liver. High fat diet-induced steatosis, coupled with a splenic injection model of experimental liver metastasis using syngeneic MC38 colon cancer cells, resulted in an increased number of secondary tumor nodules and metastatic burden in steatotic livers. Metastatic nodules were associated with focal peritumoral areas of infiltrating inflammatory cells and associated apoptotic cell populations. These results suggest that the modulation of specific host factors in the steatotic liver contributes to tumor progression in the microenvironment of NAFLD.

Hepatic steatosis is the most common phenomenon of lipid metabolism disorder in farmed fish, but its molecular mechanism is poorly understood. Therefore, the present study was aimed to investigate hepatic steatosis induced by high-fat diet HFD and explore underlying mechanism in tilapia. The fish were fed on control diet or HFD for 90 days. The blood and liver tissues were collected to determine biochemical parameter, gene expression and protein level after 30, 60, and 90 days, and analyzed lipid accumulation, endoplasmic reticulum ER stress and autophagy. Further, with increasing lipid accumulation, ER stress was induced, which worsened hepatic steatosis via activating IRE1 signaling pathway in liver of HFD group after 90 days. Our results demonstrated that HFD feeding induced extensive lipid deposition, promoted ER stress, suppressed autophagy in tilapia liver. Interestingly, these pathological features were positively correlated with the duration of HFD feeding. Steatosis is the most common phenomenon of lipid metabolism disorder in liver of cultured fish, which results in reduction of growth, feed utilization rate, immunity, stress tolerance, etc. Dai et al. Various predisposing factors for hepatic steatosis have been reported, such as nutritional imbalance, environmental stress and physiological dysfunction Du, Among them, excessive lipid intake is a primary factor in the majority of cultured fish Cao et al. Lipid, as a non-protein energy substitute, is essential for aquatic animal, and therefore, high-fat diet HFD has been frequently fed to farmed fish to provide more energy or replace partial protein Watanabe, ; Boujard et al.

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These data indicated that HFD induced dysregulation of cholesterol metabolism in liver. Synergistic interaction of dietary cholesterol and dietary fat in inducing experimental steatohepatitis. Animal models of steatosis. Toxicol Appl Pharmacol. Here, we evaluated, in the early steps of NAFLD, the iron-status parameters and activity and expression of the proteins which have critical functions in iron metabolism. EMBO J — Address reprint requests to D. Importantly, it has been suggested that tumor cells may actually commandeer inflammatory cell mediators such as chemokines and growth factors for their own growth advantage. Therefore, the majority of studies opted to end the experiment during the late middle stage of obesity.

Not steatosis high liver fat diet you have correctlyNon-alcoholic fatty liver disease NAFLD, which includes steatosis and its progression to non-alcoholic steatohepatitis, is a liver disorder of increasing clinical significance. Here we characterize a murine model of high fat diet-induced NAFLD with progression from liver steatosis to histological features compatible with steatohepatitis and more advanced stages of NAFLD in humans, including chronic portal inflammation, pericellular and bridging fibrosis, Mallory body formation, and bile ductular reaction. Chronic changes induced by the prolonged consumption of a high-fat diet alone culminate in the development of primary liver dysplasias. Importantly, we extend these studies to demonstrate that even the early stages of uncomplicated steatosis provide a permissive microenvironment for the growth of colon cancer cells that are metastatic to the liver.
Opinion diet high steatosis fat liver think thatStudies are initially distinguished into researches in which mice received lipids by oral gavage and studies in which lipid was added to the diet, and each of these designs has peculiarities that must be considered. Oral gavage can be stressful for animals and needs trained handlers but allows accurate control of the dose administered. The addition of oils to the diet can prevent stress caused to mice by gavage, but possible changes in the consistency, taste, and smell of the diet should be considered.
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