BACKGROUND: Effective fetal growth requires adequate maternal nutrition coupled to active transport of nutrients across the placenta, which, in turn requires @entity855 . Epidemiological and experimental evidence has shown that impaired maternal nutrition in utero results in an adverse postnatal phenotype for the offspring. Placental mitochondrial function might link maternal food intake to fetal growth since impaired placental @entity855 production, in response to poor maternal nutrition, could be a pathway linking maternal food intake to reduced fetal growth. METHOD: We assessed the effects of maternal diet on placental water content, @entity855 levels and mitochondrial DNA (mtDNA) content in @entity19 at embryonic (E) day 18 (E18). Females maintained on either low- (LPD) or normal- (NPD) protein diets were mated with NPD males. RESULTS: To investigate the possibility of an underlying mitochondrial stress response, we studied cultured @entity1 trophoblast cells (BeWos). High throughput imaging showed that @entity3689 starvation induces changes in mitochondrial morphology that suggest stress-induced mitochondrial hyperfusion. This is a defensive response, believed to increase mitochondrial efficiency, that could underlie the increase in @entity855 observed in placenta. CONCLUSIONS: These findings reinforce the pathophysiological links between maternal diet and conceptus mitochondria, potentially contributing to metabolic programming. The quiet embryo hypothesis proposes that pre-implantation embryo survival is best served by a relatively low level of metabolism. This may extend to post-implantation trophoblast responses to nutrition.

Is Placental Mitochondrial Function a Regulator that Matches Fetal and Placental Growth to Maternal Nutrient Intake in the XXXX ?

@entity19 :: ('10090', 'Species') :: ['mice'] @entity1 :: ('9606', 'Species') :: ['human'] @entity3689 :: ('D000596', 'Chemical') :: ['amino acid'] @entity855 :: ('MESH:D000255', 'Chemical') :: ['ATP']
@entity19 :: (10090,Species) :: ['Mouse']
