Dietary salmon milt extracts attenuate hepatosteatosis and liver dysfunction in diet‐induced fatty liver model

Abstract

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.

Evaluation of the efficacy and safety of chum salmon milt deoxyribonucleic acid for improvement of hepatic functions: a placebo-controlled, randomised, double-blind, and parallel-group, pilot clinical trial

“…The study provided insights into the potential of SM DNA for developing functional foods with therapeutic effects against liver dysfunction. 11 Several other studies have also reported the efficacy of salmon milt extracts in improving alcohol-induced liver cirrhosis 12 and diet-induced fatty liver and liver dysfunction in mice 13 and increasing the activity of superoxide dismutase in the liver in an aging-accelerated mouse model. 14 In addition, in human clinical trials, administration of nucleic acid-supplemented drinks promoted alcohol metabolism and reduced blood acetaldehyde levels.…”

A mouse model of short‐term, diet‐induced fatty liver with abnormal cardiolipin remodeling via downregulated Tafazzin gene expression

“…We also reported that mitochondrial dysfunction could be caused by the low levels of several proteins involved in mitochondrial biogenesis, such as peroxisome proliferator‐activated receptor gamma co‐activator 1 alpha, mitochondrial thioredoxin, cardiolipin synthase, peroxisome proliferator‐activated receptor alpha, 11 indicating that reduction in CL level and mitochondrial dysfunction could be directly related. Cardiolipin is localized only in the mitochondrial cristae, and is strongly associated with regulating mitochondrial function 19 .…”

“…All animal experimental protocols were approved by the animal care committee of Hokkaido University (approval protocol number: 15–0174) as explained in a previous study 11 . In this study, we used the same liver samples as those reported in a previous study 11 .…”

“…All animal experimental protocols were approved by the animal care committee of Hokkaido University (approval protocol number: 15–0174) as explained in a previous study 11 . In this study, we used the same liver samples as those reported in a previous study 11 . Briefly, nine male ddY mice (age: 7 week) were obtained from Sankyo Labo Service Corporation, Inc. (Sapporo, Japan) and housed individually with ad libitum access to solid‐type food and water.…”

“…Furthermore, a reduction in mitochondrial activation has been reported in patients with fatty liver 9 . In our recent study, we reported that hepatosteatosis, liver dysfunction, and abnormalities in the expression of primary proteins involved in mitochondrial function and lipogenesis were observed in overeating mice fed a high carbohydrate diet (HCD) for 5 days (short term) after 2 days of fasting 11 . Although the relationship between a carbohydrate‐rich diet and changes in CL composition was determined in rats fed high amounts of sucrose for a long‐term period (24 weeks), 12 similar studies on the effect of such a diet for a short term have not been performed yet.…”