718 Dietary Monosodium Glutamate Exacerbates Trans Fat-Induced Nonalcoholic Fatty Liver Disease

Nutrigenomics of hepatic steatosis in a feline model: effect of monosodium glutamate, fructose, and Trans-fat feeding

“…In humans, obesity is strongly associated with fatty liver disease that has been extensively studied in various rodent models of dietinduced NAFLD (Collison et al 2009a(Collison et al , 2010. Simple fatty liver disease is usually a benign condition; however, some individuals develop a progressively severe pathology involving fibrosis, inflammation, and cirrhosis, and the reason for this is not fully understood (Wouters et al Anstee and Goldin 2006;Ogasawara et al 2011).…”

“…Several dietary macronutrients have been proposed to play a role in the development of hepatic steatosis (Lê and Bortolotti 2008), in particular a diet enriched with Trans-fat and a high fructose corn syrup (HFCS) equivalent was shown to promote severe NAFLD and hepatic necroinflammatory changes in rodents (Tetri et al 2008). Additionally, we have shown that Trans-fat (Collison et al 2009a) and HFCS (Collison et al 2010) alter rodent hepatic and white adipose tissue gene expression, promoting upregulation of lipogenic gene transcription and the deposition of hepatic TAG. The majority of research into the etiology and pathophysiology of hepatic steatosis has been performed using small animal models; however, rodent models of progressive diet-induced liver disease have been disappointing for a number of reasons (Larter and Yeh 2008;Anstee and Goldin 2006;Ogasawara et al 2011), and there is still a need for additional models that may contribute to our knowledge of the factors associated with the development of hepatic fibrosis and more severe associated pathology.…”

“…Levels of hepatic TAG were quantified from snap-frozen tissue using the Triglyceride Determination Kit TRO100 with appropriate triacylglycerol standards (Sigma Aldrich, MO, USA) as described previously (Collison et al 2009a(Collison et al , 2010.…”

“…Preliminary real-time RT-PCR experiments were performed with each primer pair to determine the annealing temperature that yielded the greatest amount of specific product with melting temperature (Tm) separable from primer dimer Tm. Standard curves were prepared for each run using known quantities of cDNA as described previously (Collison et al 2009a(Collison et al , 2010. Relative quantitation measurements were taken using external standard curves for both target and b-actin housekeeping gene.…”

“…Our goal therefore was to compared the effects of four isocaloric diets on feline hepatic histology and gene expression, using a combination of partially hydrogenated vegetable shortening (PHVS) and HFCS to generate a Trans-fat (9%), HFCS (24%) diet. The effect of this diet was compared to an isocaloric standard chow, either in the presence or absence of dietary MSG (1.125%), in a model that we have previously established in rodents (Collison et al 2009a(Collison et al , 2010, and more recently in cats (Collison et al 2011). We bred our study animals from female cats who were previously established on these separate diets for 3 weeks prior to mating, since some of the effects of MSG are believed to occur only during the neonatal period (Alponti et al 2011;Roman-Ramos et al 2011;Hirata et al 1997;Diniz et al 2005;Matyšková 2008;Nemeroff et al 1978;Yu et al 1997), and because developmental programming of the metabolic syndrome may be affected by maternal nutritional balance (Armitage et al 2004;De Campos et al 2007).…”