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Table 2 Sexual dimorphism in four main cardiovascular disease-related metabolites

From: Sex, gut microbiome, and cardiovascular disease risk

Metabolite Men Women Cardiovascular disease risk
Branched-chain amino acids Serum branched-chain amino acids
Branched-chain 2-oxoacid dehydrogenase
Serum branched-chain amino acids
Branched-chain 2-oxo acid dehydrogenase
Increased risk of insulin resistance and type II diabetes in men compared to women
- Possible mechanisms include female sex hormone regulation of branched-chain 2-oxoacid dehydrogenase and enrichment of the gut microbial Bacteroides-Prevotella group in men [30, 72].
Short-chain fatty acids Short-chain fatty acids
Dietary fiber intake
PPAR-γ
Short-chain fatty acids
Dietary fiber intake
PPAR-γ
Increased susceptibility to dyslipidemia in men compared to women
- Possible mechanisms include 17β-estradiol-mediated increase in PPAR-γ receptor expression and decreased dietary fiber intake in men [20, 82].
Trimethylamine N-oxide TLR expression
FMO3 expression
Secondary bile acids
TLR expression
FMO3 expression
Secondary bile acids
Greater thrombotic risk in women compared to men
- Possible mechanism: increased TLR and trimethylamine N-oxide activation of platelets. [54, 55].
Accelerated trimethylamine N-oxide production in women compared to men
- Possible mechanisms: gonadal hormone regulation of hepatic FMO3 expression and increased secondary bile acid activation of Farnesoid X receptor [43, 87].
Lipopolysaccharide TLR4 expression
TLR2 signaling
TLR4 expression
TLR2 signaling
Estrogens, progesterone, and testosterone regulate LPS-mediated signaling through TLR4 [62,63,64].
  1. FMO3 flavin monooxygenase-3, PPAR-γ peroxisome proliferator activating receptor gamma, TLR toll-like receptor