HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: M800418-JLR200v1 50/8/1521    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Collison, K. S. Articles by Al-Mohanna, F. A. Search for Related Content PubMed PubMed Citation Articles by Collison, K. S. Articles by Al-Mohanna, F. A. Social Bookmarking                      What's this?

Journal of Lipid Research, Vol. 50, 1521-1537, August 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Effect of dietary monosodium glutamate on trans fat-induced nonalcoholic fatty liver disease

Kate S. Collison¹, Zakia Maqbool, Soad M. Saleh, Angela Inglis, Nadine J. Makhoul, Razan Bakheet, Mohammed Al-Johi, Rana Al-Rabiah, Marya Z. Zaidi and Futwan A. Al-Mohanna

Cell Biology and Diabetes Research Unit, Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia

¹ To whom correspondence should be addressed. e-mail: kate{at}kfshrc.edu.sa

The effects of dietary monosodium glutamate (MSG) on trans-fatty acid (TFA)-induced nonalcoholic fatty liver disease (NAFLD) are addressed in an animal model. We used Affymetrix microarray analysis to investigate hepatic gene expression and the contribution of visceral white adipose tissue (WAT) to diet-induced NAFLD. Trans-fat feeding increased serum leptin, FFA, HDL-cholesterol (HDL-C), and total cholesterol (T-CHOL) levels, while robustly elevating the expression of genes involved in hepatic lipogenesis, including the transcription factor sterol-regulatory element binding protein 1c. Histological examination revealed hepatic macrosteatosis in TFA-fed animals. Conversely, dietary MSG at doses similar to human average daily intake caused hepatic microsteatosis and the expression of β-oxidative genes. Serum triglyceride, FFA, and insulin levels were elevated in MSG-treated animals. The abdominal cavities of TFA- or MSG-treated animals had increased WAT deposition compared with controls. Microarray analysis of WAT gene expression revealed increased lipid biosynthetic gene expression, together with a 50% decrease in the key transcription factor Ppargc1a. A combination of TFA+MSG resulted in the highest levels of serum HDL-C, T-CHOL, and leptin. Microarray analysis of TFA+MSG-treated livers showed elevated expression of markers of hepatic inflammation, lipid storage, cell damage, and cell cycle impairment. TFA+MSG mice also had a high degree of WAT deposition and lipogenic gene expression. Levels of Ppargc1a were further reduced to 25% by TFA+MSG treatment. MSG exacerbates TFA-induced NAFLD.

Supplementary key words trans-fatty acid • triglycerides • free fatty acids • mitochondria • peroxisomes • microsomes

Abbreviations: AA, arachidonic acid; Acly, ATP citrate lyase; Ahr, aryl hydrocarbon receptor; bw, body weight; CYP7A1, cholesterol 7 -hydroxylase; Cyp, Cytochrome P450; Fasn, fatty acid synthase; HDL-C, high density lipoprotein cholesterol; Fmo2, flavin-containing monooxygenase 2; HE, hematoxin-eosin; Hsd3b, 3-hydroxy-3-methylglytaryl-CoA synthase; MSG, monosodium glutamate; MTTP, microsomal triglyceride transfer protein; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic hepatic steatosis; qRT-PCR, quantitative reverse transcription polymerase chain reaction; RBP4, Retinol Binding Protein 4; REDOX, reduction/oxidation reaction; SREBP1c, sterol-regulatory element binding protein 1c; T-CHOL, total cholesterol; TFA, trans-fatty acid; TG, triglyceride; WAT, white adipose tissue

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?