Mayeur 2013 PhD Thesis: Difference between revisions

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Mayeur S (2013) Retard de croissance intra-utérin et vulnérabilité au syndrome métabolique: recherche de marqueurs placentaires dans un modèle de dénutrition maternelle prénatale 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 – 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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 {{Publication
-|title=Mayeur S (2013) Retard de croissance intrauterin et vulnerabilite au syndrome metabolique: recherche de marqueurs placentaires dans un modele de denutrition maternelle prenatale et chez l'homme. PhD Thesis 1-225.
+|title=Mayeur S (2013) Retard de croissance intra-utérin et vulnérabilité au syndrome métabolique: recherche de marqueurs placentaires dans un modèle de dénutrition maternelle prénatale et chez l'Homme. PhD Thesis 1-225.
+|info=[https://tel.archives-ouvertes.fr/tel-00829097/document PDF]
 |authors=Mayeur S
 |year=2013
 |journal=PhD Thesis
-|abstract=De nombreuses données indiquent qu’un petit poids à la naissance, résultant en partie d’une sousnutrition
+|abstract=Being small size at birth from malnutrition is associated with an increased
-materno-foetale, est associé à une augmentation de la morbidité et de la mortalité durant la période
+risk to develop type 2 diabetes and cardiovascular and metabolic diseases in adulthood.
-néonatale, et conduit également à un risque accru de développer à l'âge adulte un syndrome métabolique
+The placental capacity to supply adequate amount of nutrients and oxygen to the fetus
-(diabète de type 2, obésité, hypertension artérielle et dyslipidémie). Les mécanismes de cette
+represents one of the main determiner of the fetal growth. Despite its critical roles during
-programmation prénatale sont encore mal connus et impliqueraient plusieurs molécules et systèmes
+prenatal development, few studies have investigated the effects of maternal diet on the
-physiologiques distincts. De nombreuses études suggèrent que le placenta serait impliqué dans la
+placental physiology and functions. Our aim was to explore the placental adaptive proteomic
-programmation de ces pathologies métaboliques. En effet, celui-ci constitue un organe de communication
+processes implicated in response to a maternal suboptimal nutrition.
-entre la mère et son foetus et participe à la régulation de l'homéostasie foetale. En raison de la proportion
-croissante de femmes présentant des troubles de la nutrition durant la grossesse et en lien avec leurs
+Rat term placentas from 70% food-restricted
-répercussions potentielles chez la descendance, il est nécessaire de mieux comprendre les interactions entre
+(FR30) mothers were used for a proteomic screen. Placental mitochondrial functions were
-l’alimentation maternelle et l’unité foeto-placentaire et d’identifier les mécanismes impliqués dans les
+evaluated using molecular and functional approaches and ATP production was measured.
-altérations de la croissance foetale. En conséquent, le placenta constitue un organe de choix pour étudier les
+RESULTS – FR30 drastically reduced both placental and fetal weights. FR30 placentas
-interactions entre l’alimentation maternelle et le foetus au cours de la grossesse. Durant cette thèse, nous
+displayed 14 identified proteins differentially expressed, including several mitochondrial
-avons tenté d’identifier de nouvelles voies moléculaires placentaires impliquées dans le contrôle de la
+proteins suggesting specific alterations of these organelles. FR30 induced a marked increase
-croissance foetale chez le rat, puis étudié l'expression de ces facteurs dans des placentas humains provenant
+of placental mtDNA content and changes in mitochondrial functions including modulation of
-de grossesses impliquant des anomalies de la croissance foetale.
+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.
 }}
 {{Labeling
-|area=Respiration
+|area=Respiration, Exercise physiology;nutrition;life style
+|diseases=Diabetes
+|organism=Rat
+|tissues=Genital
+|preparations=Isolated mitochondria
+|couplingstates=LEAK, OXPHOS, ET
+|pathways=N, S, CIV, NS, ROX
 |instruments=Oxygraph-2k
 }}