Endocrine Abstracts

Anti-Müllerian hormone (AMH, Müllerian inhibiting substance) is a protein hormone expressed by the Sertoli cells of the testes and the granulosa cells of the ovaries. AMH is best known for its paracrine functions in reproductive organ development and function. The hormonal roles of AMH are largely unexplored, but functions are emerging in growth and brain development. To date, there is no putative function for AMH in the blood of adults. AMH belongs to the TGF-β superfamily, and shares signalling components with the BMP sub-family, which contributes to the regulation of blood pressure and cardiovascular morphology. We therefore postulated that AMH may be a hormonal regulator of the vasculature.

The potential function of AMH was examined in a cross-sectional study, which correlated the levels of AMH in 153 healthy mature men to their cardiovascular status. This included measurement of the exterior diameter of the abdominal aorta by ultrasound (4–7 MHz).

The men’s level of serum AMH negatively correlated with the external diameter of their aortas at both the mid-infrarenal and distal-infrarenal sites. The suprarenal aorta, in contrast, has limited capacity for remodelling and its diameter did not associate with the men’s level of serum AMH (r=−0.10). In regression models, the association of AMH to aortic diameter (r=−0.37, P<0.001) was equal but opposite to the men’s body surface area (BSA), which is the strongest known determinant of aortic diameter. The association between AMH and aorta was independent of the men’s lipid profile, history of smoking and intimal thickness of their carotid artery, indicating that AMH may affect aortic diameter independent of atherosclerosis.

In conclusion, the results are consistent with AMH being a hormone in adults, with one of its functions relating to an aspect(s) of cardiovascular physiology, which directly or indirectly regulates the remodeling of the aorta.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.