Something to make you go hmm?. High fat feeding in rodents generally leads to obesity and insulin resistance whereas in humans this is only seen if dietary carbohydrate is also high, the result of the anabolic effect of poor regulation of glucose and insulin. Kennedy, et al.[14] studied C57Bl/6 mice on a high fat, ketogenic diet (KD) and showed that they displayed all the characteristics of humans on a low-carbohydrate diet: weight loss without caloric restriction, increased energy expenditure, improved glucose tolerance, and lowered serum insulin and leptin levels. The KD in Kennedy, et al.. was 95% energy derived from fat and 5% from protein. Such a diet is rather extreme compared to a diet that might be consumed by a human even in an experimental setting: first, 5% energy from protein is very low and second, whereas there is no dietary requirement for carbohydrate, in humans, the effects attributed to the unique metabolic state associated with carbohydrate restriction have not generally required such an extreme fat/protein ratio. On the other hand, it seemed possible that, because of the small brain size and therefore limited requirements for glucose, very low carbohydrate would be necessary to reproduce in a rodent model the effect of CRDs seen in humans. We have confirmed, in work to be published elsewhere, that moderate lowering of carbohydrate had little effect on mice. We therefore tried to repeat Kennedy’s experiment at more traditional levels of protein while maintaining zero carbohydrate. To our surprise, we observed the phenotype usually associated with the high fat-fed-mouse model. Animals became obese and insulin-resistant and gained substantially more weight per calorie than mice fed normal chow. We describe here the results of these experiments. The outcomes suggest that the results found by Kennedy, et al.[14] were a consequence of the low levels of dietary protein, possibly to the point of protein deprivation. In the current study, we tested a zero-carbohydrate diet that had a higher protein content (20%). Mice on the zero-carbohydrate diet, despite similar caloric intake, consistently gained more weight than animals consuming standard chow, attaining a dramatic difference by week 16 (46.1±1.38g vs. 30.4±1.00g for the chow group). In sum, the response of mice to a carbohydrate-free diet was greater weight gain and metabolic disruptions in distinction to the response in humans where low carbohydrate diets cause greater weight loss than isocaloric controls. The results suggest that rodent models of obesity may be most valuable in the understanding of how metabolic mechanisms can work in ways different from the effect in humans.
Posted on: Fri, 11 Apr 2014 14:53:54 +0000
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