The main findings of the present study show an improvement of bone tissue in obese rats. The obesity induced by the HF/HS diet was characterized by an increase in total, visceral and central fat masses without change of lean mass. As expected, the ageing process occurred during the period of investigation has produced deleterious effects on bone tissue in both Control and HF/HS diet groups. However, compared to the Control diet, the HF/HS diet has induced a higher total bone mineral density, a lower cortical porosity and a bone remodelling favouring bone formation as shown by the positive uncoupling index and the increase in bone osteoid surface on tibia. The vertebrae bone micro architecture improved as well (increase in trabecular thickness). Furthermore, it is relevant to note that bone tissue response to obesity was different according to the bone site analyzed.
We chose to control the food intake so that all groups consumed equal amounts of calories each day, which ensured that any diet effect was due to the macronutrient composition and not due to differences of energy consumed by each group. This method guaranteed that accumulation of fat was mainly due to supplementation of saturated fatty acid and/or sucrose. In a previous study, Dourmashkin et al. have concluded that both HF and HS diets were able to increase body weight and fat mass . In the present study, we could state that increase in body weight and fat accumulation were due to both sucrose and saturated fatty acids.
The lipid profile analysis showed that HF/HS diet had induced significantly lower triglycerides, HDL cholesterol and free fatty acid levels compared to the standard diet. These results could point out a lesser lipid mobilization in obese rats. Whereas most studies have shown that high fat diet may induce an increase of these lipids levels [23, 24], other studies reported that lipids levels were unchanged or even decreased [25, 26].
Result from oral glucose tolerance test showed that HF/HS group had a higher area under the curve for glucose but not for insulin. For the same insulin secretion, the glucose “peak” response was significantly higher and the return time to the basal level was longer in HF/HS group compared to control. These results suggest that the HF/HS diet group was not able to adequately respond to the elevated glucose levels as their insulin concentrations were similar to those of the control group that had significantly lower glucose levels. Although the HF/HS diet rats may have developed an impaired glucose tolerance, there was no evidence that HF/HS rats had developed an insulin resistance. Unfortunately, the present results are not in accordance with those observed currently in human. Contrary to the human response, the animal response seems to be more complex to analyze and interpret.
Insulin resistance and type2 diabetes without obesity are associated with low bone mineral density and increased risk of fracture in both humans and animals [27, 28]. In the present study, the improvement of bone quality could be also explained by the absence of insulin resistance in obese rats.
In previous studies using female rats, the HF/HS diet has been shown to induce adverse effects on bone health especially on cortical bone morphology and bone mineral content of vertebrae [7, 8]. A recent study  showed that female and male rats responded differently to a diet-induced obesity. A possible explanation for this difference could be the gender-specific changes in leptin or ghrelin under the HF feeding . Indeed, Harris et al. demonstrated that male mice fed with high fat diet had developed a leptin resistance in response to an injection of exogenous leptin whereas female mice remained leptin sensitive. They concluded that the development of leptin resistance in mice fed with HF diet is dependent upon the gender. Furthermore, one must consider that using female animals implicate additional hormonal effects of estrogen on bone metabolism, morphology and biomechanics .
Bone tissue is a modeling structure subjected to many intrinsic and extrinsic factors. On one hand, the benefit of a diet-induced obesity on bone could be explained by the mechanical loading caused by the excess of body mass. On the other hand, adipose tissue is known to be an active endocrine organ secreting many biological active molecules such as leptin and adiponectin. In our study the adiponectin level was not affected by the obesogenic diet. However, the leptin level was almost twice in obese group compared to the control group. Leptin effects on bone are complex depending of its central or peripherial pathways  and on its serum concentration . The central effect of leptin favors resorption through the sympathetic nervous system . A high bone mass phenotype has been observed in leptin-deficient ob/ob mice which could not be explained by their adiposity since mice lacking adipocytes displays the same phenotype . In our study, it is possible that obese rats would have developed a leptin endogenous resistance which has been shown in obese mice fed with high fat diet . Leptin resistance increases with fat mass storage and age [37, 38]. This phenomenon could then explain the difference of results observed between our study and those who worked on leaner and younger rats [7, 8, 11]. Leptin has also a direct anabolic effect within the bone micro-environment by stimulating the differentiation of bone marrow mesenchymal stem cells into osteoblastic cell lineage . These elements could explain a possible implication of leptin in the higher bone mass observed in obese rats in our study.
After adjustments for total and fat mass, the differences in the bone parameters observed between obese and control rats remained unchanged in vertebrae but became not significant in the tibia. This suggests a site-dependent response possibly due to the increase of mechanical loading provided by the excess of fat mass. While fat mass could partly explain the improvement of bone quality of the tibia (a loaded bone site), vertebrae (a non loaded bone site) was not affected by this factor. These results are in concordance with previous studies, which found that obesity and functional load, affected regional bone mineral density in a different manner [40, 41]. These results also suggest that mechanical loading is not the only parameter contributing to the improvement of bone health in obese rats. Other parameters are also implicated among which, leptin seems to play an important role.