Effect oftrans-fat, fructose and monosodium glutamate feeding on feline weight gain, adiposity, insulin sensitivity, adipokine and lipid profile

Abstract

The incidence of obesity and type 2 diabetes mellitus (T2DM) is increasing, and new experimental models are required to investigate the diverse aspects of these polygenic diseases, which are intimately linked in terms of aetiology. Feline T2DM has been shown to closely resemble human T2DM in terms of its clinical, pathological and physiological features. Our aim was to develop a feline model of diet-induced weight gain, adiposity and metabolic deregulation, and to examine correlates of weight and body fat change, insulin homeostasis, lipid profile, adipokines and clinical chemistry, in order to study associations which may shed light on the mechanism of diet-induced metabolic dysregulation. We used a combination of partially hydrogenated vegetable shortening and high-fructose corn syrup to generate a high-fat-high-fructose diet. The effects of this diet were compared with an isoenergetic standard chow, either in the presence or absence of 1.125 % dietary monosodium glutamate (MSG). Dual-energy X-ray absorptiometry body imaging and a glucose tolerance test were performed. The present results indicate that dietary MSG increased weight gain and adiposity, and reduced insulin sensitivity (P < 0.05), whereas high-fat-high-fructose feeding resulted in elevated cortisol and markers of liver dysfunction (P < 0.01). The combination of all three dietary constituents resulted in lower insulin levels and elevated serum β-hydroxybutyrate and cortisol (P < 0.05). This combination also resulted in a lower first-phase insulin release during glucose tolerance testing (P < 0.001). In conclusion, markers of insulin deregulation and metabolic dysfunction associated with adiposity and T2DM can be induced by dietary factors in a feline model.

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

“…Given the fact that maternal oral administration of MSG can result in detectable levels of glutamic acid accumulation in the fetal brain (Hermanussen and Tresguerres 2003;Nemeroff et al 1978), and that in rodents, the hepatotoxic effects of MSG may also be apparent even when administered orally (Yu et al 1997), it would be of interest to ascertain the effects of neonatal administration of dietary MSG in a higher animal model. It has previously been shown that intravenous injections of MSG promote the development of hypothalamic lesions in young cats (Tanaka et al 1983); and we have previously shown that whereas neonatal exposure to MSG promotes a phenotype of increased feline adiposity and reduced insulin sensitivity, Trans-fat and HFCS feeding results in an apparent elevation in cortisol and markers of liver dysfunction (Collison et al 2011). The present study seeks to further investigate the effect of Trans-fat, HFCS, and/or MSG on feline hepatic steatosis and gene expression.…”

“…A total of 8 female domestic cats were used to breed the 18 male subjects used in this study, as previously described (Collison et al 2011). Briefly, heating and cooling were electronically controlled and were set to maintain the room in a temperature range from 18 to 25°C.…”

“…Average MSG consumption as part of the diet A and C was 201.4 ± 18.65 mg/Kg body weight. A preliminary diet acceptability study was performed on the breeder animals over a period of 1 week, to ascertain that the diets were palatable, as previously described (Collison et al 2011). Food consumption was monitored at every feed, and body weight was recorded at the beginning and end of the acceptability study.…”

“…The male offspring from these four diet groups continued to consume their respective diets throughout the length of the study. Percentage body fat in the study subjects was assessed at 9 months of age by dual energy X-ray absorptiometry (DEXA) using the Lunar DPX-IQ densitometer (http:// www.gehealthcare.com Lunar Corp., Madison, WI), as previously described (Collison et al 2011). …”

“…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).…”