search for




 

Lactobacillus acidophilus NS1 Reduces Phosphoenolpyruvate Carboxylase Expression by Regulating HNF4α Transcriptional Activity
Korean J. Food Sci. An. 2017;37:529-534
Published online August 31, 2017
© 2017 Korean Society for Food Science of Animal Resources

Sung-Soo Park, Garam Yang, and Eungseok Kim*

Department of Biological Sciences, College of Science, Chonnam National University, Gwangju 61186, Korea
Correspondence to: Eungseok Kim
Department of Biological Sciences, College of Science, Chonnam National University, Gwangju 61186, Korea
Tel: +82-62-530-3402 Fax: +82- E-mail: ekim@jnu.ac.kr
Received June 1, 2017; Revised July 12, 2017; Accepted July 12, 2017.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Probiotics have been known to reduce high-fat diet (HFD)-induced metabolic diseases, such as obesity, insulin resistance, and type 2 diabetes. We recently observed that Lactobacillus acidophilus NS1 (LNS1), distinctly suppresses increase of blood glucose levels and insulin resistance in HFD-fed mice. In the present study, we demonstrated that oral administration of LNS1 with HFD feeding to mice significantly reduces hepatic expression of phosphoenolpyruvate carboxykinase (PEPCK), a key enzyme in gluconeogenesis which is highly increased by HFD feeding. This suppressive effect of LNS1 on hepatic expression of PEPCK was further confirmed in HepG2 cells by treatment of LNS1 conditioned media (LNS1-CM). LNS1-CM strongly and specifically inhibited HNF4α-induced PEPCK promoter activity in HepG2 cells without change of HNF4α mRNA levels. Together, these data demonstrate that LNS1 suppresses PEPCK expression in the liver by regulating HNF4α transcriptional activity, implicating its role as a preventive or therapeutic approach for metabolic diseases.
Keywords : Lactobacillus acidophilus NS1, HNF4α, PEPCK, gluconeogenesis


October 2017, 37 (5)