Menopausal women are at greater risk of developing metabolic syndrome with reduced endothelial nitric oxide synthase (eNOS) activity. Hormone replacement therapy increases eNOS activity and normalizes some characteristics of metabolic syndrome. We hypothesized that nitric oxide (NO) supplementation should have a therapeutic effect in this syndrome. We examined the effect of dietary nitrite on mice model with postmenopausal metabolic syndrome induced by ovariectomy (OVX) with high fat diet (HF). C57BL/6 female mice were divided into five groups, sham+normal fat diet (NF), sham+ HF, OVX+HF without or with sodium nitrite (50mg and 150mg/L) in drinking water. Daily food intake and weekly body weight were monitored for 18 weeks. OVX and HF significantly reduced plasma levels of nitrate/nitrite (NOx), and developed obesity with visceral hypertrophic adipocytes, and increased transcriptional levels of monocyte chemoattractant protein-1 (MCP-1), tumor necrotizing factor-α (TNF-α) and interleukin-6 (IL-6) in visceral fat tissues. The proinflammatory state in the adipocytes provoked severe hepatosteatosis and insulin resistance in OVX+HF group compared with sham+NF group. However, dietary nitrite significantly suppressed adipocyte hypertrophy and transcriptions of proinflammatory cytokines in visceral fat in a dose dependent manner. The improvement of visceral inflammatory state consequently reversed the hepatosteatosis and insulin resistance observed in OVX+HF mice. These results suggest that endogenous NO defect might underlie postmenopausal metabolic syndrome, and dietary nitrite provides an alternative source of NO, and subsequently compensating for metabolic impairments of this syndrome.