TY - JOUR
T1 - Unacylated ghrelin does not alter mitochondrial function, redox state and triglyceride content in rat liver in vivo
AU - Gortan Cappellari, Gianluca
AU - Zanetti, Michela
AU - Semolic, Annamaria
AU - Vinci, Pierandrea
AU - Ruozi, Giulia
AU - De Nardo, Margherita
AU - Filigheddu, Nicoletta
AU - Guarnieri, Gianfranco
AU - Giacca, Mauro
AU - Graziani, Andrea
AU - Barazzoni, Rocco
N1 - Publisher Copyright:
© 2015
PY - 2015/12/1
Y1 - 2015/12/1
N2 - Changes in liver mitochondrial function with more oxidized redox state and enhanced inflammation may contribute to the onset of obesity- and insulin resistance-associated hepatic complications, including non-alcoholic fatty liver disease and steato-hepatitis. Unacylated ghrelin (UnAG) is a gastric hormone reported to be associated with lower oxidative stress in different cell types, but its potential effects on liver mitochondrial function, redox state and inflammation in vivo remains undetermined. We investigated the impact of chronic UnAG overexpression (Tg Myh6/Ghrl) leading to systemic upregulation of circulating hormone on mitochondrial ATP production, redox state (oxidized-to-total glutathione) and inflammation markers in lean mice. Compared to wild-type animals (wt), Tg Myh6/Ghrl had superimposable liver weight, triglyceride content and plasma lipid profile. Liver mitochondrial enzyme activities and ATP production as well as oxidized-to-total glutathione were also similar in the two groups. In addition, no differences were observed in tissue inflammation marker TNF-alpha between wild-type and Tg Myh6/Ghrl animals. Thus, chronic systemic UnAG upregulation does not alter liver triglyceride content, mitochondrial function, redox state and inflammation markers in lean mice. These findings do not support a major role of UnAG as a physiological modulator of in vivo liver oxidative-lipid metabolism and inflammation.
AB - Changes in liver mitochondrial function with more oxidized redox state and enhanced inflammation may contribute to the onset of obesity- and insulin resistance-associated hepatic complications, including non-alcoholic fatty liver disease and steato-hepatitis. Unacylated ghrelin (UnAG) is a gastric hormone reported to be associated with lower oxidative stress in different cell types, but its potential effects on liver mitochondrial function, redox state and inflammation in vivo remains undetermined. We investigated the impact of chronic UnAG overexpression (Tg Myh6/Ghrl) leading to systemic upregulation of circulating hormone on mitochondrial ATP production, redox state (oxidized-to-total glutathione) and inflammation markers in lean mice. Compared to wild-type animals (wt), Tg Myh6/Ghrl had superimposable liver weight, triglyceride content and plasma lipid profile. Liver mitochondrial enzyme activities and ATP production as well as oxidized-to-total glutathione were also similar in the two groups. In addition, no differences were observed in tissue inflammation marker TNF-alpha between wild-type and Tg Myh6/Ghrl animals. Thus, chronic systemic UnAG upregulation does not alter liver triglyceride content, mitochondrial function, redox state and inflammation markers in lean mice. These findings do not support a major role of UnAG as a physiological modulator of in vivo liver oxidative-lipid metabolism and inflammation.
KW - Ghrelin
KW - Liver
KW - Mitochondria
UR - http://www.scopus.com/inward/record.url?scp=84983490216&partnerID=8YFLogxK
U2 - 10.1016/j.yclnex.2015.10.001
DO - 10.1016/j.yclnex.2015.10.001
M3 - Article
SN - 2352-9393
VL - 4
SP - 1
EP - 7
JO - Clinical Nutrition Experimental
JF - Clinical Nutrition Experimental
ER -
