%0 Journal Article
%T Maternal AMPK pathway activation with uterine artery blood flow and fetal growth maintenance during hypoxia.
%A Moore LG
%A Lorca RA
%A Gumina DL
%A Wesolowski SR
%A Reisz JA
%A Cioffi-Ragan D
%A Houck JA
%A Banerji S
%A Euser AG
%A D'Alessandro A
%A Hobbins JC
%A Julian CG
%J Am J Physiol Heart Circ Physiol
%V 0
%N 0
%D 2024 Jul 19
%M 39028630
%F 5.125
%R 10.1152/ajpheart.00193.2024
%X High altitude (HA) hypoxia lowers uterine artery (UtA) blood flow during pregnancy and birth weight. Adenosine monophosphate kinase (AMPK) activation has selective, uteroplacental vasodilator effects which lessen hypoxia-associated birth weight reductions. In this study, we determined the relationship between AMPK-pathway gene expression and metabolites in the maternal circulation during HA pregnancy as well as with the maintenance of UtA blood flow and birth weight at HA. HA (2793 m) vs low altitude (LA; 1640 m) residents had smaller UtA diameters at weeks 20 and 34, lower UtA blood flow at week 20, and lower birth weight babies. At week 34, HA vs LA women had decreased expression of up- and down-stream AMPK-pathway genes. Expression of the a-1 AMPK catalytic subunit, PRKAA1, correlated positively with UtA diameter and blood flow at week 20 (HA) and 34 (LA). Downstream AMPK-pathway gene expression positively correlated with week 20 fetal biometry at both altitudes and with UtA diameter and birth weight at LA. Reduced gene expression of AMPK activators and downstream targets in HA versus LA women, together with positive correlations between PRKAA1 gene expression, UtA diameter, and blood flow suggest that greater sensitivity to AMPK activation at mid-gestation at HA may help offset later depressant effects of hypoxia on fetal growth.