Mayeur 2013 PhD Thesis

From Bioblast
Publications in the MiPMap
Mayeur S (2013) Retard de croissance intra-utรฉrin et vulnรฉrabilitรฉ au syndrome mรฉtabolique: recherche de marqueurs placentaires dans un modรจle de dรฉnutrition maternelle prรฉnatale et chez l'Homme. PhD Thesis 1-225.

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Mayeur S (2013) PhD Thesis

Abstract: Being small size at birth from malnutrition is associated with an increased risk to develop type 2 diabetes and cardiovascular and metabolic diseases in adulthood. The placental capacity to supply adequate amount of nutrients and oxygen to the fetus represents one of the main determiner of the fetal growth. Despite its critical roles during prenatal development, few studies have investigated the effects of maternal diet on the placental physiology and functions. Our aim was to explore the placental adaptive proteomic processes implicated in response to a maternal suboptimal nutrition.

Rat term placentas from 70% food-restricted (FR30) mothers were used for a proteomic screen. Placental mitochondrial functions were evaluated using molecular and functional approaches and ATP production was measured. RESULTS โ€“ FR30 drastically reduced both placental and fetal weights. FR30 placentas displayed 14 identified proteins differentially expressed, including several mitochondrial proteins suggesting specific alterations of these organelles. FR30 induced a marked increase of placental mtDNA content and changes in mitochondrial functions including modulation of the expression of numerous genes implicated in both mitochondrial biogenesis and bioenergetic pathways. Mitochondria under FR30 conditions showed higher oxygen consumption but fail to maintain their critical ATP production.

We provide first evidence that maternal suboptimal nutrition induces mitochondrial abnormalities in the placenta of growth-restricted fetuses. Although maternal calorie restriction induces mitochondrial adaptive processes such as an increase of both mitochondrial biogenesis and bioenergetic efficiency; placental ATP production was drastically reduced. This disturbance may be implicated in reduction of the placental capacity to actively transport nutrients that may strengthen the effect of maternal undernutrition on the development of the fetus. Our data suggest that placental mitochondrial defects may be implicated, at least in part, in pathologies of feto-placental growth.

Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Diabetes 

Organism: Rat  Tissue;cell: Genital  Preparation: Isolated mitochondria 

Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, CIV, NS, ROX  HRR: Oxygraph-2k 

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