Saturated fat and cholesterol are critical to inducing murine metabolic syndrome with robust nonalcoholic steatohepatitis.

@article{Mells2015SaturatedFA,
  title={Saturated fat and cholesterol are critical to inducing murine metabolic syndrome with robust nonalcoholic steatohepatitis.},
  author={Jamie Eugene Mells and Ping P. Fu and Pradeep Kumar and Tekla D Smith and Saul J. Karpen and Frank A Anania},
  journal={The Journal of nutritional biochemistry},
  year={2015},
  volume={26 3},
  pages={
          285-92
        }
}
UNLABELLED Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome (MetS). Up to a third of NAFLD subjects are at risk for developing nonalcoholic steatohepatitis (NASH). Many rodent models fail to replicate both MetS and NASH. The purpose of this study was to develop a reliable mouse model of NASH and MetS using a diet containing cholesterol, saturated fat and carbohydrate that is reflective of Western diets of North Americans. EXPERIMENTAL DESIGN We… 
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References

SHOWING 1-10 OF 56 REFERENCES
Synergistic interaction of dietary cholesterol and dietary fat in inducing experimental steatohepatitis
TLDR
Dietary fat and dietary cholesterol interact synergistically to induce the metabolic and hepatic features of NASH, whereas neither factor alone is sufficient to cause NASH in mice.
Severe NAFLD with hepatic necroinflammatory changes in mice fed trans fats and a high-fructose corn syrup equivalent.
TLDR
It was established that trans fats played a major role in promoting hepatic steatosis and injury, whereas inclusion of HFCS promoted food consumption, obesity, and impaired insulin sensitivity, and their role in the epidemic of NASH needs further evaluation.
Good fat/bad fat
TLDR
A more complex model of steatosis was used, employing db/db mice fed a methionine-restricted, choline-deficient (MCD) diet, and there was some optimism that blocking DGAT2, which catalyzes the final step in hepatic triglyceride production, may be beneficial in NAFLD/NASH.
The role of fatty acids in the development and progression of nonalcoholic fatty liver disease.
TLDR
Data suggest that saturated fatty acids may represent an intrinsic second hit to the liver that hastens the development of NASH.
Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS‐55
TLDR
Examination of the effects of HFCS‐55 on hepatocyte lipogenesis, insulin signaling, and cellular function, in vitro and in vivo, indicates a potential mechanism by which HFCs‐55 may contribute to the pathogenesis of NAFLD.
Fructose consumption as a risk factor for non-alcoholic fatty liver disease.
TLDR
The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption, and fructose resulted in dose-dependent increase in KHK protein and activity.
Dietary cholesterol, rather than liver steatosis, leads to hepatic inflammation in hyperlipidemic mouse models of nonalcoholic steatohepatitis
TLDR
Findings indicate that dietary cholesterol, possibly in the form of modified plasma lipoproteins, is an important risk factor for the progression to hepatic inflammation in diet‐induced NASH.
Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin.
TLDR
The hypothesis that high fructose consumption may not only lead to liver damage through overfeeding but also may be directly pro-inflammatory by increasing intestinal translocation of endotoxin is supported.
Nonalcoholic fatty liver disease: an overview of current insights in pathogenesis, diagnosis and treatment.
TLDR
Taking all together, NAFLD has become the third most important indication for liver transplantation and training programmes in internal medicine, gastroenterology and hepatology should stress the importance of diagnosing and treating properly those at risk for developing complications of portal hypertension and concomitant cardiovascular disease.
Dysfunctional very‐low‐density lipoprotein synthesis and release is a key factor in nonalcoholic steatohepatitis pathogenesis
TLDR
A growing body of literature suggests that a deterioration in fatty acid oxidation and V LDL secretion from the liver, caused by the impediment of VLDL synthesis, might induce serious lipid oxidation and DNA oxidative damage, impacting the degree of liver injury and thereby contributing to the progression of NASH.
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