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Chronic Postnatal Overnutrition Aggravates the Development of Diet-induced Steatohepatitis during Adulthood

Author: ZhangZuoJuan
Tutor: LiJiBin
School: Chongqing Medical University
Course: Nutrition and Food Hygiene
Keywords: Chronic postnatal overnutrition IR NASH inflammation
CLC: R151.2
Type: Master's thesis
Year: 2013
Downloads: 29
Quote: 0
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Background: Chronic postnatal overnutrition (CPO) contributes toobesity and insulin resistance among adults. IR is considered to be theinitial and central risk factor increasing the development of non-alcoholicfatty liver disease (NAFLD). NAFLD is an inclusive term for liver diseaseincluding simple steatosis, nonalcoholic steatohepatitis (NASH), cirrhosisand hepatocellular carcinoma. The “two-hit hypothesis” is widely used forexplaining the mechanism of NAFLD development. IR is thought to be thefirst hit for the livers. However, the specific mechanism remains to beelucidated. In the present study, we used a well-characterized mouse modelto investigate whether overnutrition in early life increases susceptibility tothe development of non-alcoholic steatohepatitis (NASH) after methionineand choline deficient (MCD) diet feeding.Methods: CPO was induced by adjusting litters to3pups per dam incontrast to10pups per dam as control (CTR), and then weaned ontostandard chow at3-weeks of age. At11wks, mice were fed with standard chow diet (S) or MCD diet for4wks. Therefore CTR and MCD wererandomly set into four subgroups: CTR-S, CTR-MCD, CPO-S andCPO-MCD. The mice were sacrificed at3-wks and15-wks of age. For3-wks old mice, the ultra-structure change of hepatocyte was observed bytransmission electron microscope; Interested gene expressions wereanalyzed by real-time quantitative PCR; Protein levels of carnitinepalmitoyltransferase-1(CPT-1) and cytochrome C (Cyt-C)were analysedby western blot. For15-wks old mice, H&E, oil-red O, picrosirius redstaining and F4/80, ɑ-SMA immunohistochemistry staining wereperformed to identify macrophages in liver tissue, lipid droplets, the degreeof inflammation and fibrosis; Serum biochemical assays were performedusing automatic biochemistry equipment; Interested genes expression weredetermined with real-time quantitative PCR and Western blot analysis wasperformed to determine the protein level of sterol regulatory elementbinding protein-1c (SREBP-1c).Results:Compared with CTR, mice from CPO group showed higherbody weight gain from2-wks age on, and more profound glucoseintolerance during adulthood. SREBP-1c and FAS mRNA expressions inliver were also up-regulated in CPO mice at3-wks age. Typicalmitochondrial swelling in hepatocytes was observed. At the same time,CPT-1mRNA and protein levels, Cyt-C protein level were down-regulated.MCD diets induced typical changes of NASH, which was more significant in CPO-MCD mice, characterized by obvious lipids accumulation,macrovesicular steatosis, ballooned hepatocytes, inflammatory cellsinfiltration, up-regulated TNF-α mRNA expression in liver and increasedserum ALT and AST levels. However,there were no significant differencesfor the degree of liver fibrosis and TGF-β1mRNA level in all groups. Weidentified decreased expressions of liver SREBP-1c, FAS, ACC-1, SCD,MTTP, FABP1, ABCA1and ABCA2in CPO mice fed with MCD diets.Conclusion: Ove-rnutrition during early life may bring long-termadverse effects on the metabolic function and promote the progression ofNASH during adulthood, which is possibly the result of impaired lipidssecretion from hepatocytes and aggravated hepatic inflammation. Early lifeovernutrition may be one of the most important risk factors for NASHdevelopment.

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CLC: > Medicine, health > Preventive Medicine,Health > Nutrition, hygiene,food hygiene > Nutrition > Nutritional Biochemistry
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