The increased risk for cardiometabolic disease with the onset of menopause is widely studied and likely precipitated by the decline in endogenous estradiol (E2)， yet the precise mechanisms are unknown. The gut microbiome is involved in estrogen metabolism and has been linked to metabolic disease， suggesting its potential involvement in the postmenopausal phenotype. Furthermore， menopause-associated risk factors， as well as gut ecology， are altered with exercise. Therefore， we studied microbial changes in an ovariectomized (OVX vs. Sham) rat model of high (HCR) and low (LCR) intrinsic aerobic capacity (n = 8-10/group) in relation to changes in body weight/composition， glucose tolerance， and liv... More
The increased risk for cardiometabolic disease with the onset of menopause is widely studied and likely precipitated by the decline in endogenous estradiol (E2)， yet the precise mechanisms are unknown. The gut microbiome is involved in estrogen metabolism and has been linked to metabolic disease， suggesting its potential involvement in the postmenopausal phenotype. Furthermore， menopause-associated risk factors， as well as gut ecology， are altered with exercise. Therefore， we studied microbial changes in an ovariectomized (OVX vs. Sham) rat model of high (HCR) and low (LCR) intrinsic aerobic capacity (n = 8-10/group) in relation to changes in body weight/composition， glucose tolerance， and liver triglycerides (TG). Nine weeks after OVX， HCR rats were moderately protected against regional adipose tissue gain and liver TG accumulation (P < 0.05 for both). Microbial diversity and number of the Bacteroidetes phylum were significantly increased in LCR with OVX， but unchanged in HCR OVX relative to Sham. Plasma short-chain fatty acids (SCFA)， produced by bacteria in the gut and recognized as metabolic signaling molecules， were significantly greater in HCR Sham relative to LCR Sham rats (P = 0.05) and were decreased with OVX in both groups. These results suggest that increased aerobic capacity may be protective against menopause-associated cardiometabolic risk and that gut ecology， and production of signaling molecules such as SCFA， may contribute to the mediation.
