Maternal nicotine exposure aggravates metabolic associated fatty liver disease via PI3K/Akt signaling in adult offspring mice

• DOI: 10.1111/liv.14902
• Publication Date: 2021-04-24T17:35:41Z
• Authors: Shu‐Jing Huang; Shu‐qiang Chen; Yan Lin; Hong‐Yi Yang; Jing Ran; Fang‐Fang Yan; Mei Huang; Xian‐Lan Liu; Long‐Cheng Hong; Xiao‐Dong Zhang; Guo‐Rong Lyu; Zhan‐Xiang Wang; Yi‐Ming Su
• Keywords: 2. Zero hunger; Nicotine; 0303 health sciences; Diet, High-Fat; Lipid Metabolism; 3. Good health; Fatty Liver; Mice; Phosphatidylinositol 3-Kinases; 03 medical and health sciences; Liver; Pregnancy; Prenatal Exposure Delayed Effects; Animals; Female; Insulin Resistance; Proto-Oncogene Proteins c-akt

The aim of this study is to investigate the effect maternal nicotine exposure (MNE) on development metabolic associated fatty liver disease (MAFLD) in adulthood offspring and underlying mechanism.Pregnant mice (n = 22) were subcutaneously injected with either saline vehicle 11) or twice a day gestational days 11-21. Offspring 176) from both groups weaned at postnatal 21, for 6 months after 96 fed standard chow diet 48) high-fat 48). Serum lipid indicators, function insulin, mitochondrial respiration analyzed. expression levels fibrosis-related proteins, phosphorylated PI3K, Akt, sterol regulatory element-binding transcription factor 1 (SREBP1c), peroxisome proliferator-activated receptor alpha (PPAR-α) detected by immunohistochemistry Western blotting.MNE significantly decreased weight (~30%) inhibited organ growth (P < .05). MNE also increased serum total bile acid, triglycerides, cholesterol, glucose, alanine aminotransferase, aspartate low-density lipoprotein, insulin while decreasing high-density lipoprotein activity normal (all P These effects metabolism resistance mediated via PI3K Akt phosphorylation down-regulation SREBP1c PPAR-α.Our data indicate induces disorder promote MAFLD progression adult through activation PI3K/Akt signaling suppression PPARα protein expression.