Liver dysfunction

Biology

Endocrinology

Fructose

Biochemistry

Fatty liver

Food science

Nonalcoholic fatty liver disease

Internal medicine

Medicine

Disease

Diabetes

The FATZO mouse is a polygenic model with an intact leptin system and was developed by cross breeding of C57BL6/J (C57) with AKR/J. FATZO mice have been used in many dysmetabolic studies. The epidemic health issue of nonalcoholic fatty liver disease (NAFLD, including NASH) is the organ dysmetabolic manifestation. This study was to investigate a high fat/fructose diet (HFFD) on liver function in FATZO mice. The body weights of FATZO (n=30) at age of 9 to 10 weeks were significantly heavier than those of age-matched C57 (n=19) mice (39±0.4g vs. 23±0.2g, p&amp;lt;0.001). The serum glucose levels in FATZO were higher than those in C57 (212±5mg/dL vs. 131±7mg/dL). The body weights were gradually increased during 5-month feeding with HFFD or 5C08 (Figure 1). FATZO+HFFD mice significantly elevated serum AST, ALT and ALP, compared with FATZO+5C08, C57+HFFD and C57+5C08 mice. These elevations in FATZO+HFFD mice reached peak in 3-month feeding and then maintained at the high levels (Figure 1). Serum TC, HDL and LDL (except TG) were also significantly elevated in FATZO+HFFD mice. Interestingly, serum glucose and HbA1c levels were significantly reduced in FATZO+HFFD mice (from 216±7mg/dL and 6.2±0.1% at the baseline to 169±5mg/dL and 4.3±0.1% after 5-month feeding, respectively). Our data demonstrate that the HFFD progressively caused liver dysfunction in FATZO, but not C57. FATZO + the HFFD could thus be a very valuable model for NAFLD/NASH research. Disclosure X. Wang: None. W. Ye: None. Y. Chen: None. X. Zhang: None. Y. Wang: None. Y. Xiao: Employee; Self; Crown Bioscience Inc.

1998-P: Progressive Liver Dysfunction Resulted from a High-Fat, High-Fructose Diet in Fatzo Mice