|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
↑ Short-chain fatty acids|
↑ Dietary fiber intake
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].
↓ 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].
↓ TLR4 expression|
↓ TLR2 signaling
↑ TLR4 expression|
↑ TLR2 signaling
|Estrogens, progesterone, and testosterone regulate LPS-mediated signaling through TLR4 [62,63,64].|