Influence of nicotine on choline-deficient, L-amino acid-defined diet-induced non-alcoholic steatohepatitis in rats

• Published in: PloS one Vol. 12; no. 6; p. e0180475
• Main Authors: Kanamori, Hiroyuki, Nakade, Yukiomi, Yamauchi, Taeko, Sakamoto, Kazumasa, Inoue, Tadahisa, Yamamoto, Takaya, Kobayashi, Yuji, Ishii, Norimitsu, Ohashi, Tomohiko, Ito, Kiyoaki, Sumida, Yoshio, Nakao, Haruhisa, Fukuzawa, Yoshitaka, Yoneda, Masashi
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 29-06-2017; Public Library of Science (PLoS)
• Subjects: Amino acids; Amino Acids - metabolism; Animal models; Animals; Apoptosis; Attenuation; Biology and Life Sciences; Body weight; Body weight gain; Causes of; Choline; Choline Deficiency - metabolism; Cigarette smoke; Development and progression; Diet; Fatty acids; Fatty liver; Fibrosis; Food; Food intake; Gastroenterology; Gene expression; Genes; Hepatitis; Hepatology; Inflammation; Inhibition; Internal medicine; Laboratory animals; Liver diseases; Male; Mammals; Medicine; Medicine and Health Sciences; Metabolism; Nicotine; Nicotine - pharmacology; Non-alcoholic Fatty Liver Disease - metabolism; Obesity; Physiological aspects; Rats; Rats, Wistar; Rodents; Smoke; Steatosis; vagotomy; Vagus nerve; Japan
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0180475

Nicotine, a major compound in cigarette smoke, decreases food intake and body weight gain in mammals; however, the influence of nicotine on the progression of non-alcoholic steatohepatitis (NASH) remains controversial. This study aimed to investigate the effect of nicotine on NASH in rat models. Male Wistar rats were fed choline-deficient, l-amino acid-defined (CDAA) diet and treated with nicotine or saline. Food intake, body weight gain, presence of hepatic steatosis, inflammation, and fibrosis were assessed 6 weeks after the rats were fed CDAA diet. Hepatic branch vagotomy was performed to elucidate the mechanism through which nicotine affected steatohepatitis. CDAA diet induced hepatic steatosis, inflammation, and fibrosis, as well as increased the expression of inflammation-related genes. Conversely, nicotine significantly attenuated food intake, body weight gain, and inhibited the CDAA-diet-induced hepatic steatosis, inflammation, and fibrosis, together with increased expression of inflammation-related genes. Hepatic branch vagotomy by itself decreased food intake, body weight gain, and attenuated the CDAA-diet-induced hepatic steatosis, but not inflammation. However, nicotine did not change the food intake, body weight gain, and CDAA diet-induced hepatic steatosis and inflammation in vagotomized rats. These results suggest that nicotine attenuates the CDAA-diet-induced hepatic steatosis and inflammation through the hepatic branch of the vagus nerve in rats.