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

Journal of Lipid Research

Zakia Maqbool¹  Marya Z. Zaidi²  Futwan A. Al-Mohanna²  Razan Bakheet²  Rana Al-Rabiah²  Soad M. Saleh²  Angela Inglis²  Nadine J. Makhoul²  Mohammed Al-Johi²  Kate S. Collison³ 

[1] Cell Biology and Diabetes Research Unit, Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia;Cell Biology and Diabetes Research Unit, Department of Biological and Medical Research, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia;To whom correspondence should be addressed.;

关键词: trans-fatty acid;    triglycerides;    free fatty acids;    mitochondria;    peroxisomes;    microsomes;   

DOI  :  

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown