Temporal development of dyslipidemia and nonalcoholic fatty liver disease (Nafld) in syrian hamsters fed a high‐fat, high‐fructose, high‐cholesterol diet
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Temporal development of dyslipidemia and nonalcoholic fatty liver disease (Nafld) in syrian hamsters fed a high‐fat, high‐fructose, high‐cholesterol diet. / Jensen, Victoria Svop; Fledelius, Christian; Wulff, Erik Max; Lykkesfeldt, Jens; Hvid, Henning.
In: Nutrients, Vol. 13, No. 2, 604, 2021, p. 1-18.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Temporal development of dyslipidemia and nonalcoholic fatty liver disease (Nafld) in syrian hamsters fed a high‐fat, high‐fructose, high‐cholesterol diet
AU - Jensen, Victoria Svop
AU - Fledelius, Christian
AU - Wulff, Erik Max
AU - Lykkesfeldt, Jens
AU - Hvid, Henning
PY - 2021
Y1 - 2021
N2 - The use of translationally relevant animal models is essential, also within the field of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Compared to frequently used mouse and rat models, the hamster may provide a higher degree of physiological similarity to humans in terms of lipid profile and lipoprotein metabolism. However, the effects in hamsters after long‐term exposure to a NASH diet are not known. Male Syrian hamsters were fed either a high‐fat, high‐fructose, high‐cholesterol diet (NASH diet) or control diets for up to 12 months. Plasma parameters were assessed at two weeks, one, four, eight and 12 months and liver histopathology and biochemistry was characterized after four, eight and 12 months on the experimental diets. After two weeks, hamsters on NASH diet had developed marked dyslipidemia, which persisted for the remainder of the study. Hepatic steatosis was present in NASH‐fed hamsters after four months, and hepatic stellate cell activation and fibrosis was observed within four to eight months, respectively, in agreement with progression towards NASH. In summary, we demonstrate that hamsters rapidly develop dyslipidemia when fed a high‐fat, high‐fructose, high‐cholesterol diet. Moreover, within four to eight months, the NASH‐diet induced hepatic changes with resemblance to human NAFLD.
AB - The use of translationally relevant animal models is essential, also within the field of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Compared to frequently used mouse and rat models, the hamster may provide a higher degree of physiological similarity to humans in terms of lipid profile and lipoprotein metabolism. However, the effects in hamsters after long‐term exposure to a NASH diet are not known. Male Syrian hamsters were fed either a high‐fat, high‐fructose, high‐cholesterol diet (NASH diet) or control diets for up to 12 months. Plasma parameters were assessed at two weeks, one, four, eight and 12 months and liver histopathology and biochemistry was characterized after four, eight and 12 months on the experimental diets. After two weeks, hamsters on NASH diet had developed marked dyslipidemia, which persisted for the remainder of the study. Hepatic steatosis was present in NASH‐fed hamsters after four months, and hepatic stellate cell activation and fibrosis was observed within four to eight months, respectively, in agreement with progression towards NASH. In summary, we demonstrate that hamsters rapidly develop dyslipidemia when fed a high‐fat, high‐fructose, high‐cholesterol diet. Moreover, within four to eight months, the NASH‐diet induced hepatic changes with resemblance to human NAFLD.
KW - Animal models
KW - Dyslipidemia
KW - Hamster
KW - Nonalcoholic fatty liver disease
KW - Nonalcoholic steatohepatitis
U2 - 10.3390/nu13020604
DO - 10.3390/nu13020604
M3 - Journal article
C2 - 33673227
AN - SCOPUS:85100659867
VL - 13
SP - 1
EP - 18
JO - Nutrients
JF - Nutrients
SN - 2072-6643
IS - 2
M1 - 604
ER -
ID: 257875579