Western or fast food style diets fed to induce NASH with metabolic syndrome contain 40 – 45% kcal from milkfat (a fat source high in palmitate) with added cholesterol (0.15 – 2%) and are high in sucrose (>30%). Dietary palmitate and cholesterol have both previously been associated with the progression from simple steatosis to NASH.
導致肥胖、代謝綜合征和輕度 NAFLD/NASH 的飲食
用于誘發患有代謝綜合征的 NASH 的西式或快餐式飲食含有 40 – 45% 來自乳脂(棕櫚酸酯含量高的脂肪來源)的 kcal,并添加了膽固醇(0.15 – 2%),并且蔗糖含量高(>30%)。 膳食棕櫚酸酯和膽固醇以前都與從簡單脂肪變性到 NASH 的進展有關。
Examples:
- TD.88137 Adjusted Calories Diet (42% from fat)
- TD.96121 21% MF, 1.25% Chol. Diet
- TD.120528 42% Kcal/Fat Diet (Incr. Sucrose, 1.25% Chol.)
Western and Fast Food diets with milkfat and cholesterol
Research use:
These diets can induce obesity, metabolic syndrome, and simple steatosis within nine weeks of feeding. Increased hepatic inflammation has been observed after 12 weeks of feeding. NASH typically requires longer feeding with fibrosis developing within nine months and late stage fibrosis including hepatic ballooning occurring after 14 – 20 months of feeding. Increasing dietary sucrose (~41%) and cholesterol (~1.25%) accelerates the NASH phenotype with steatosis, inflammation and hepatocyte ballooning observed within 12 weeks. In addition to feeding a high fat diet, providing a glucose/fructose mixture in the drinking water may further promote NASH development.
研究用途:
這些飲食會在喂食后的九周內誘發肥胖、代謝綜合征和單純性脂肪變性。 喂養 12 周后觀察到肝臟炎癥增加。 NASH 通常需要更長的喂養時間,在 9 個月內出現纖維化,在 14-20 個月的喂養后出現包括肝氣球樣變在內的晚期纖維化。 增加膳食蔗糖 (~41%) 和膽固醇 (~1.25%) 會加速 NASH 表型,在 12 周內觀察到脂肪變性、炎癥和肝細胞膨脹。 除了喂食高脂肪飲食外,在飲用水中提供葡萄糖/果糖混合物可能會進一步促進 NASH 的發展。
Select References:? 參考文獻
Charlton, M., et al., Fast food diet mouse: novel small animal model of NASH with ballooning, progressive fibrosis, and high physiological fidelity to the human condition. Am J Physiol Gastrointest Liver Physiol, 2011. 301(5): p. G825-34. www.ncbi.nlm.nih.gov/pubmed/21836057
Gores, G., Charlton M, Krishnan A, Viker K, Sanderson S, Cazanave S, McConico A, Masuoko H. Am J Physiol Gastrointest Liver Physiol, 2015. 308: p. G159. ajpgi.physiology.org/content/308/2/G159
Li, Z.Z., et al., Hepatic lipid partitioning and liver damage in nonalcoholic fatty liver disease: role of stearoyl-CoA desaturase. J Biol Chem, 2009. 284(9): p. 5637-44. www.ncbi.nlm.nih.gov/pubmed/19119140
Ioannou, G.N., et al., Hepatic cholesterol crystals and crown-like structures distinguish NASH from simple steatosis. J Lipid Res, 2009. 54(5): p. 1326-34. www.ncbi.nlm.nih.gov/pubmed/23417738
Alkhouri, N., et al., Adipocyte apoptosis, a link between obesity, insulin resistance, and hepatic steatosis. J Biol Chem, 2010. 285(5): p. 3428-38. www.ncbi.nlm.nih.gov/pubmed/19940134
Dixon, L.J., et al., Caspase-1 as a central regulator of high fat diet-induced non-alcoholic steatohepatitis. PLoS One, 2013. 8(2): p. e56100. www.ncbi.nlm.nih.gov/pubmed/23409132
DeLeve, L.D., et al., Prevention of hepatic fibrosis in a murine model of metabolic syndrome with nonalcoholic steatohepatitis. Am J Pathol, 2008. 173(4): p. 993-1001. www.ncbi.nlm.nih.gov/pubmed/18772330
VanSaun, M.N., et al., High fat diet induced hepatic steatosis establishes a permissive microenvironment for colorectal metastases and promotes primary dysplasia in a murine model. Am J Pathol, 2009. 175(1): p. 355-64. www.ncbi.nlm.nih.gov/pubmed/19541928
Asgharpour, A., et al., A diet-induced animal model of non-alcoholic fatty liver disease and hepatocellular cancer. J Hepatol, 2016. 65(3): p. 579-88. www.ncbi.nlm.nih.gov/pubmed/27261415
Tetri, L.H., et al., Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent. Am J Physiol Gastrointest Liver Physiol, 2008. 295(5): p. G987-95. www.ncbi.nlm.nih.gov/pubmed/18772365
Tsuchida, T., et al., A simple diet-and chemical-induced murine NASH model with rapid progression of steatohepatitis, fibrosis and liver cancer. Journal of hepatology, 2018. 69(2):385-395. www.ncbi.nlm.nih.gov/pubmed/29572095