Background and objectives: Menopause is accompanied by higher prevalence of atherogenic lipid profiles, central obesity, and insulin resistance. Hepatic steatosis is frequent in postmenopausal women. Fetuin-A level is strongly related to liver fat content. Its role in menopausal metabolic derangements is largely unknown. We aimed to investigate the relation between fetuin-A and the development of menopausal metabolic complications related to obesity and if caloric restriction/estrogen supplementation could alleviate these abnormalities. Methods: Adult female Wistar rats were either bilaterally ovariectomized (OVX) (30 rats) or sham operated (sham group, n=10 rats). OVX rats were randomly subdivided into ovariectomized group (OVX), ovariectomized group treated with 17-β estradiol (OVX+E2), and ovariectomized- caloric restricted group (OVX+CR) (n=10/group). Thirteen weeks following surgery, serum levels of glucose, insulin, lipids, fetuin-A and adiponectin were estimated. Weight of visceral fat and triacylglycerol (TAG) content of liver were assessed. Results: Serum fetuin-A level was increased following ovariectomy (113%, P<0.001). This was associated with increased visceral adiposity, abnormal lipid profile, insulin resistance, hypoadiponectinaemia and excessive accumulation of hepatic triacylglycerol (TAG). However, estrogen (E2) supplementation/caloric restriction (CR) significantly suppressed elevated Fetuin-A (by 41.9%, P<0.001 and 31.2%, P<0.001, respectively). In addition, CR was equally effective as E2 replacement in reversing metabolic abnormalities. Conclusion: Fetuin-A could be one of the factors contributing to the development of metabolic complications related to menopausal obesity. Caloric restriction alone can ameliorate those complications without the hazardous effects of estrogen replacement; possibly, through inhibition of serum fetuin-A level.