Zinc oxide nanoparticles attenuate hepatic steatosis development in high-fat-diet fed mice through activated AMPK signaling axis. Nanomedicine 2019 Apr;17:210-222
Date
02/02/2019Pubmed ID
30708053DOI
10.1016/j.nano.2019.01.013Scopus ID
2-s2.0-85062392120 (requires institutional sign-in at Scopus site) 57 CitationsAbstract
Insulin resistance is thought to be a common link between obesity and Non-Alcoholic Fatty Liver Disease (NAFLD). NAFLD has now reached epidemic status worldwide and identification of molecules or pathways as newer therapeutic strategies either to prevent or overcome insulin resistance seems critical. Dysregulated hepatic lipogenesis (DNL) is a hallmark of NAFLD in humans and rodents. Therefore, reducing DNL accretion may be critical in the development of therapeutics of NAFLD. In our in vivo model (high-fat-diet fed [HFD] obese mice) we found Zinc oxide nanoparticles (ZnO NPs) significantly decreased HFD-induced hepatic steatosis and peripheral insulin resistance. This protective mechanism of ZnO NPs was signaled through hepatic SIRT1-LKB1-AMPK which restricted SREBP-1c within the cytosol limiting its transcriptional ability and thereby ameliorating HFD mediated DNL. These observations indicate that ZnO NP can serve as a therapeutic strategy to improve the physiological homeostasis during obesity and its associated metabolic abnormalities.
Author List
Dogra S, Kar AK, Girdhar K, Daniel PV, Chatterjee S, Choubey A, Ghosh S, Patnaik S, Ghosh D, Mondal PAuthor
Khyati Girdhar PhD Assistant Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AMP-Activated Protein KinasesAnimals
Diet, High-Fat
Enzyme Activators
Hep G2 Cells
Humans
Insulin Resistance
Liver
Mice, Inbred C57BL
Nanoparticles
Non-alcoholic Fatty Liver Disease
Signal Transduction
Zinc Oxide
