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

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 ß-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.

Dietary trans-fat combined with monosodium glutamate induces dyslipidemia and impairs spatial memory.

AIMS: Recent evidence suggests that intake of excessive dietary fat, particularly saturated fat and trans-hydrogenated oils (trans-fatty acids: TFA) can impair learning and memory. Central obesity, which can be induced by neonatal injections of monosodium Glutamate (MSG), also impairs learning and memory. To further clarify the effects of dietary fat and MSG, we treated C57BL/6J mice with either a TFA-enriched diet, dietary MSG, or a combination of both and examined serum lipid profile and spatial memory compared to mice fed standard chow. Spatial learning was assessed at 6, 16 and 32 weeks of age in a Morris Water Maze (MWM). The subjects were given four days of training to find a hidden platform and a fifth day of reversal learning, in which the platform was moved to a new location. RESULTS: The TFA+MSG combination caused a central adiposity that was accompanied by impairment in locating the hidden platform in the MWM. Females in the TFA+MSG group showed a greater impairment compared to the other diet groups, and also showed elevated levels of fasting serum LDL-C and T-CHOL:HDL-C ratio, together with the lowest levels of HDL-C. Similarly, males in the TFA+MSG diet group were less successful than control mice at locating the hidden platform and had the highest level of abdominal adiposity and elevated levels of fasting serum LDL-C. CONCLUSION: Dietary trans-fat combined with MSG increased central adiposity, promoted dyslipidemia and impaired spatial learning.