Characterization of liver changes in ZSF1 rats, an animal model of metabolic syndrome
2017
Background: The non-alcoholic fatty liver disease is the
hepatic counterpart of the metabolic syndrome. ZSF1 rats are a
metabolic syndrome animal model in which liver changes have not
been described yet.
Aim: The characterization of liver histological and innate immunity
changes in ZSF1 rats.
Methods: Five groups of rats were included (n = 7 each group):
healthy Wistar-Kyoto control rats (Ctrl), hypertensive ZSF1 lean
(Ln), ZSF1 obese rats with a normal diet (Ob), ZSF1 obese rates
with a high-fat diet (Ob-HFD), and ZSF1 obese rats with low-intensity
exercise training (Ob-Ex). The animals were sacrificed at 20
weeks of age, their livers were collected for: a) measurements of
the area of steatosis, fibrosis and inflammation (histomorphological
analysis); and b) innate immunity (toll-like receptor [TLR] 2, TLR4,
peroxisome proliferator-activated receptor γ [PPARγ], toll interacting
protein [TOLLIP]) and inflammatory marker (tumor necrosis
factor-alpha [TNFvs], interleukin 1 [IL-1]) expression analysis by
real-time PCR.
Results: Ob, Ob-HFD and Ob-Ex were significantly heavier
than Ln and Ctrl animals. Ob, Ob-HFD and Ob-Ex animals had
impaired glucose tolerance and insulin resistance. ZSF1 Ob, ObHFD
and Ob-Ex presented a higher degree of steatosis (3,5x; p <
0.05) than Ctrl or ZSF1 Ln rats. Steatohepatitis and fibrosis were
not observed in any of the groups. No differences in expression
were observed between Ctrl, Ln and Ob animals (except for the
significantly higher expression of TOLLIP observed in the Ob vs Ln
comparison). Ob-HFD and Ob-Ex rats showed increased expression
of PPARγ and TOLLIP as compared to other groups. However,
both groups also showed increased expression of TLR2 and TLR4.
Nevertheless, this did not translate into a differential expression of
TNFα or IL-1 in any of the groups.
Conclusion: The ZSF1 model is associated with liver steatosis
but not with steatohepatitis or a significantly increased expression
of innate immunity or inflammation markers.
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