The title of the paper is : "Diet-induced central obesity and insulin resistance in rabbits".
This study looked at whether a high fat/ high sucrose diet administered to rabbits could result in obesity and insulin resistance. Male japanese white rabbits were dispersed into control and experimental groups. Control rabbits were fed a normal chow diet where as experimental group rabbits were fed the high fat/ high sucrose diet for 36 weeks. Plasma triglycerides, total cholesterol, insulin and glucose levels were measured. Intravenous glucose tolerance tests were also conducted to analyze glucose metabolism. Adipose tissue build up was also compared between the experimental and control rabbits. (Zhao et al. 2008)
The results found no significant difference in triglyceride, total cholesterol, glucose or insulin levels between the two groups over the course of the trial. However, the high fat/high sucrose fed rabbits showed impeded glucose clearance in connection with higher levels of insulin secretion compared to the control rabbits. Control rabbits also had less adipose tissue accumulation than rabbits in the experimental group. These results suggest that the high fat/ high sucrose diet leads to the induction of insulin resistance and weight gain in rabbits. The study then suggests that rabbits can thus be used as a model for research on human insulin resistance and obesity. (Zhao et al. 2008)
Rabbits do appear to be a better model than rodents for studying insulin resistance in humans as their lipoprotein profile is more similar. The high fat/ high sucrose diet fed to the rats also resulted in disorders which mimic those found in humans. The figures presented in the article, such as those labelled figure 1 clearly show the increase glucose and insulin levels in the experimental rabbits compared to the control rabbits during the glucose clearance tests which indicates induced insulin resistance.
Although the amount of food consumption was no different among the two groups as clearly shown in figure 2, there was a significant increase in body weight of the high fat/ high sucrose fed rabbits. (Zhao et al. 2008)
As shown in both figures above taken from the study, the claims that a high fat/ high sucrose diet can result in insulin resistance and obesity seem to be supported. This study was tested on male rabbits, it should be repeated with females to see if the same results will occur.
To further explore this topic, more long term complications associated with insulin resistance and obesity in rabbits should be measured, for example the progression of heart disease such as arteriosclerosis. It could also be tested if whether these results can be reversed with a return to a healthier diet or treated with exercise. In order to test these treatments, you could take four groups of insulin resistant obese rabbits, subject one to no treatment as a control, treat one with a healthier chow only diet, treat the third group with increased exercise and treat the fourth group with improved diet and an increase in exercise. All groups could be measured for triglyceride level, total cholesterol, glucose and insulin levels as done in this study. Body weight measures and glucose tolerance tests could also be conducted to determine if there are any significant changes to the groups before and after treatments as well as compare the results between groups. It has been suggested that insulin resistance resulting in type 2 diabetes can often be treated or reversed with a switch to a healthier diet and increased exercise. Thus the expected result of these trials would be that all of the treatment groups would have a decrease in insulin resistance and improved overall health compared to the control group. The most significant effects would be expected in the rabbit group treated with both a healthy diet and exercise.
References:
Zhao, S., Chu, Y., Zhang, C., Lin, Y., Xu, K., Yang, P., et al. (2008). Diet-induced central obesity and insulin resistance in rabbits. Journal of Animal Physiology & Animal Nutrition, 92(1), 105-111. doi:10.1111/j.1439-0396.2007.00723.x.
