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BackgroundCardiovascular disease is the leading cause of mortality in postmenopausal women. Follicle‐stimulating hormone (FSH) shows negative associations with obesity and diabetes mellitus in postmenopausal women. We aimed to study the associations between FSH and 10‐year risk of atherosclerotic cardiovascular disease (ASCVD) in postmenopausal women.Methods and Results SPECT‐China (the Survey on Prevalence in East China for Metabolic Diseases and Risk Factors) is a 22‐site, population‐based study conducted during 2014–2015. This study included 2658 postmenopausal women. A newly developed effective tool for 10‐year ASCVD risk prediction among Chinese was adopted. Regression analyses were performed to assess the relationship among FSH, 10‐year ASCVD risk, and multiple cardiometabolic risk factors. With the increase in FSH quartiles, the mean 10‐year ASCVD risk in postmenopausal women decreased from 4.9% to 3.3%, and most metabolic parameters were significantly ameliorated (all P for trend <0.05). In regression analyses, a 1‐SD increment in ln‐FSH was negatively associated with continuous (B −0.12, 95% confidence interval, −0.16, −0.09, P<0.05) and categorical (odds ratio 0.65, 95% confidence interval, 0.49, 0.85, P<0.05) 10‐year ASCVD risk. These significant associations existed in subgroups with or without medication use, obesity, diabetes mellitus, hypertension, and dyslipidemia. Body mass index and waist circumference (both B −0.35, 95% confidence interval, −0.40, −0.30, P<0.05) had the largest associations of all metabolic measures, and blood pressure had the smallest association.ConclusionsSerum FSH levels were negatively associated with 10‐year ASCVD risk in postmenopausal women. Among cardiometabolic factors, obesity indices had the largest associations with FSH. These results indicated that a low FSH might be a risk factor or a biomarker for cardiovascular disease risk in postmenopausal women.

In addition to acting as building blocks for biosynthesis, amino acids might serve as signaling regulators in various physiological and pathological processes. However, it remains unknown whether amino acid levels affect the activities of hematopoietic stem cells (HSCs). By using a genetically encoded fluorescent sensor of the intracellular levels of branched-chain amino acids (BCAAs), we could monitor the dynamics of BCAA metabolism in HSCs. A mitochondrial-targeted 2C-type Ser/Thr protein phosphatase (PPM1K) promotes the catabolism of BCAAs to maintain MEIS1 and p21 levels by decreasing the ubiquitination-mediated degradation controlled by the E3 ubiquitin ligase CDC20. PPM1K deficiency led to a notable decrease in MEIS1/p21 signaling to reduce the glycolysis and quiescence of HSCs, followed by a severe impairment in repopulation activities. Moreover, the deletion of Ppm1k dramatically extended survival in a murine leukemia model. These findings will enhance the current understanding of nutrient signaling in metabolism and function of stem cells.

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