Lipogenic Diet-induced Alteration Of MicroRNAs In Hepatic Stress Signaling: Implications For Hepatic Lipoprotein Metabolism And Insulin Resistance | 36239
ISSN: 2165-7904

Journal of Obesity & Weight Loss Therapy
Open Access

Our Group organises 3000+ Global Conferenceseries Events every year across USA, Europe & Asia with support from 1000 more scientific Societies and Publishes 700+ Open Access Journals which contains over 50000 eminent personalities, reputed scientists as editorial board members.

Open Access Journals gaining more Readers and Citations
700 Journals and 15,000,000 Readers Each Journal is getting 25,000+ Readers

This Readership is 10 times more when compared to other Subscription Journals (Source: Google Analytics)
Google scholar citation report
Citations : 1407

Journal of Obesity & Weight Loss Therapy received 1407 citations as per google scholar report

Journal of Obesity & Weight Loss Therapy peer review process verified at publons
Indexed In
  • Index Copernicus
  • Google Scholar
  • Open J Gate
  • Genamics JournalSeek
  • Centre for Agriculture and Biosciences International (CABI)
  • RefSeek
  • Hamdard University
  • OCLC- WorldCat
  • SWB online catalog
  • CABI full text
  • Cab direct
  • Publons
  • Geneva Foundation for Medical Education and Research
  • Euro Pub
  • University of Bristol
Share This Page

Lipogenic diet-induced alteration of microRNAs in hepatic stress signaling: Implications for hepatic lipoprotein metabolism and insulin resistance

3rd International Conference and Exhibition on Obesity & Weight Management

Qiaozhu Su

University of Nebraska-Lincoln, USA

ScientificTracks Abstracts-Workshop: J Obes Weight Loss Ther

DOI: 10.4172/2165-7904.C1.020

Emerging evidence has demonstrated the important role of microRNAs in energy metabolism and their participation in excessive caloric intake-induced metabolic syndrome. The consequences of the altered microRNAs, however, have not been well explored. The present study sought to advance our understanding of the potential association between reduced expression of microRNAs induced by high-fructose diet in the initiation of cellular stress signaling and their contribution to the onset of dyslipidemia and hepatic insulin resistance. By applying nutrition manipulated animal models, the high-fructose fed-rat and hamster models, and human apolipoprotein B100 (apoB100) transgenic mice, we were able to demonstrate that high-fructose diet significantly reduced expression of 13 hepatic microRNAs that are associated with genes involved in inflammatory cell differentiation and lipid signaling, including microRNA-15 and microRNA-378/378*. These phenotypes were closely associated with disruption of mitochondrial membrane integrity, induction of oxidative stress and activation of mitochondrial unfolding protein response (UPR). In vitro, delivering the microRNAs isolated from the livers of fructose fedhamsters into McA-7777 cells, a rat hepatoma cell line, induced activation of mitochondrial UPR. Further investigating the lipid and lipoprotein metabolic profiles of the fructose-fed rats, we noticed that the reduced microRNA expression was associated with overproduction of hepatic apoB100, increased secretion of hepatic VLDL-apoB, and the development of hepatic steatosis and insulin resistance. Our finding unveils a novel role for microRNAs in maintaining metabolic homeostasis of intracellular stress-responding machinery (e.g. mitochondria). It also provides evidence for exploring microRNAs as pharmaceutical targets for the prevention and treatment of metabolic syndrome derived from nutrient–surplus.

Qiaozhu Su received her PhD from McGill University in 2007 and completed her post-doctoral fellowship at the University of Toronto, Canada. She is an assistant professor in the Department of Nutrition and Health Sciences at the University of Nebraska-Lincoln. Qiaozhu has published more than 20 papers in reputed journals and served as an editorial board member for several professional journals. Her research interests include lipid and lipoprotein metabolism, mechanism of metabolic syndrome, with a particular emphasis on the role of microRNAs, ER and mitochondrial stress in obesity, fatty liver disease and insulin resistance.

Email: [email protected]