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Dietary salmon milt extracts attenuate hepatosteatosis and liver dysfunction in diet‐induced fatty liver model
Author(s) -
Sakurai Toshihiro,
Hayasaka Takahiro,
Sekiguchi Hirotaka,
Satoh Hiroshi,
Chen Zhen,
Chiba Hitoshi,
Hui ShuPing
Publication year - 2018
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.9352
Subject(s) - medicine , endocrinology , carnitine o palmitoyltransferase , steatosis , fatty liver , liver function , peroxisome , carnitine , biology , peroxisome proliferator activated receptor , receptor , beta oxidation , metabolism , disease
BACKGROUND Dietary nucleotides have several reported beneficial effects. Here, we report on a proteomic analysis of the effect of dietary nucleotides‐rich salmon milt extract (SME) on the liver in a diet‐induced fatty liver model. RESULTS Young male normal ddY mice were fed a normal chow diet, high carbohydrate diet (HCD), HCD containing 1% SME, or HCD containing 10% SME for 5 days following by a 2‐day fast. Increased serum alanine transferase and aspartate transferase activities were observed in the HCD group and were significantly attenuated in the SME groups ( P < 0.05). Hepatic steatosis was observed in all the HCD groups. Hepatic expression of Tnfα was significantly suppressed in the 10% SME group ( P < 0.05). Comprehensive proteomic analysis of the liver in the SME groups revealed an increase in the levels of major proteins involved in mitochondrial bioenergetics, including peroxisome proliferator‐activated receptor gamma co‐activator 1 alpha, mitochondrial thioredoxin, cardiolipin synthase, peroxisome proliferator‐activated receptor alpha, and carnitine palmitoyltransferase I. CONCLUSION Dietary SME improved liver function in the diet‐induced fatty liver model. Activation of mitochondrial biogenetic function might be involved in this process. © 2018 Society of Chemical Industry