Table 1.

Potential factors and associated mechanisms underlying racial/ethnic differences in serum antimüllerian hormone (AMH) levels.

Factors	Nature of association with AMH	Potential mechanism/s
Genetic factors
JARID2 gene	Marginal association with serum AMH level in genome-wide association studies [37, 39]	JARID2 negatively regulates cell growth and proliferation and is expressed in both human and mouse ovaries [38]
FMR1 genotype	AMH ≤ 0.8 ng/mL was significantly associated with the number of CGG repeats [40]	Theoretical altered FMR1 gene expression
BRCA1 mutation	BRCA1 mutation carriers display significantly lower serum AMH levels [48]	Loss of BRCA1 increases DNA double-strand breaks in human and mouse oocytes and is associated with reduced oocyte survival in mice [48]
Environmental factors
Obesity	Inverse correlation between BMI and serum AMH [57–59, 61]	Lipotoxic effects on granulosa cells [60] Leptin decreases AMH gene expression in cumulus and granulosa cells [64] Adiponectin modulates ovarian steroidogenesis [63]
Smoking	Smoking is inversely correlated with AMH [37, 71, 72]	Polycyclic aromatic hydrocarbons cause oocyte destruction in mice [77, 78] Nicotine and/or its metabolites accumulate in granulosa cells and induce their apoptosis [79, 82] Cigarette smoke metabolites are associated with follicular oxidative stress [75]
Vitamin D deficiency	Decreased serum vitamin D levels are associated with lower serum AMH levels [65, 66]	Vitamin D-receptor complex binds the vitamin D response element on the AMH gene promoter resulting in upregulation of AMH gene expression [68]

JARID2: jumonji AT rich interactive domain 2; FMR1: fragile X mental retardation; BRCA1: breast cancer 1; AMH: antim$\ddot{\text{u}}$llerian hormone.