There has been considerable inconsistency regarding the potential relationship between dyslipidemia and bone metabolism. The inflammatory stimulation through the receptor activator of the nuclear factor kappa-B ligand (RANKL)/ receptor activator of the nuclear factor kappa-B (RANK)/ osteoprotegerin (OPG) pathway could be the infrastructural mechanism for hypercholesterolemia-induced bone loss.In this study, we investigated the effect of dyslipidemia on RANKL and OPG alongside with pro-inflammatory cytokines. Thirty male C57Bl/6 mice (4 weeks old) were randomized to two purified diet groups (15 animals in each group), high fat, low carbohydrate diet (HFLCD) and its matched low fat, high carbohydrate diet (LFHCD). After 12 weeks of feeding in standard situations, the plasma concentration of lipid profile, interleukin (IL) 1Beta, IL-6, tumor necrosis factor-alpha (TNF-α) and RANKL, OPG, and RANKL: OPG ratio were measured.In the present study, although the body weight significantly increased during 12 weeks in HFLCD and LFHCD groups, there were no significant differences in food intake, food efficiency ratio and weight gain between the two groups. The LFHCD group had significantly higher median RANKL and RANKL/OPG ratio. There was no significant difference in plasma IL-1β, IL-6 and TNF-α concentration between LFHCD and HFLCD groups.These unexpected findings from LFHCD, that seem to be as a result of its higher carbohydrate proportion in comparison to HFLCD, implicate dietary carbohydrate rather than dietary fat as a more significant nutritional factor contributing to change in RANKL level and RANKL: OPG ratio.