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Background: The postnatal failures of expression of the hepatic glucose-6-phosphatase system suggest there are developmental deficiencies in the mechanism to ‘switch-on’ this key enzyme of gluconeogenesis at the time of birth in both preterm and term infants. The evidence for hormonal regulation of this critical enzyme system in animal studies, in adult humans, and studies of cell lines make the possible failure of hormonal control around the time of birth an important hypothesis to test, but before this can be done, further studies of perinatal metabolism and its hormonal control need to be undertaken. Objective: To describe the hormonal and metabolic profiles of ‘unstressed’ term infants delivered by elective caesarean section. Methods: One hundred and fifty three women who had an elective caesarean section for a singleton pregnancy at term in Ninewells Hospital and Medical School, Dundee were recruited between July 2004 and April 2006. Maternal venous blood was taken for glucose and lactate estimations. Umbilical venous cord blood was obtained for the measurement of glucose, lactate, 3-hydroxybutyrate, free fatty acids, amino acids (alanine, arginine, citruline, cystine, GABA, glutamic acid, glutamine, glycine, histidine, isoleucine, leucine, lysine, methionine ornithine, phenyalanine, serine,taurine, threonine, tyrosine and valine), insulin, glucagon, human growth hormone, cortisol, catechols (EPI, NE, DA, DOPA, DHPG, DOPAC) and their sulfated conjugates (EPI sulfate, NE sulfate, DA sulfate, DOPA sulfate, DHPG sulfate, DOPAC sulfate), and blood gas and acid-base profiles. Results The mean maternal glucose and lactate levels were 4.28 mmol/l and 1.8 mmol/l respectively. Three infants were hypoglycaemic with umbilical blood glucose levels of less than 2.6 mmol/l. The mean infant glucose and lactate levels were as expected for full term infants at 3.3 mmol/l and 2.2 mmol/l respectively. High mean levels of insulin and catechols were noted at birth. There was a significant positive association between umbilical venous cord glucose levels and maternal venous glucose levels (p=<0.001) but no association of umbilical venous cord glucose levels with amino acids, insulin, glucagon, human growth hormone, cortisol and catechols. Conclusions: This extensive data set of levels of metabolites and hormones in infants at birth acts as a reference source and will be valuable for evaluating any effects of antenatal or intrapartum factors on the hormonal and metabolic profiles of infants at birth as well as to investigate the mechanisms to ‘switch-on’ the key enzyme glucose-6-phosphatase. Objective: To describe the hormonal and metabolic profiles of ‘unstressed’ term infants delivered by elective caesarean section. Methods: One hundred and fifty three women who had an elective caesarean section for a singleton pregnancy at term in Ninewells Hospital and Medical School, Dundee were recruited between July 2004 and April 2006. Maternal venous blood was taken for glucose and lactate estimations. Umbilical venous cord blood was obtained for the measurement of glucose, lactate, 3-hydroxybutyrate, free fatty acids, amino acids (alanine, arginine, citruline, cystine, GABA, glutamic acid, glutamine, glycine, histidine, isoleucine, leucine, lysine, methionine ornithine, phenyalanine, serine, taurine, threonine, tyrosine and valine), insulin, glucagon, human growth hormone, cortisol, catechols (EPI, NE, DA, DOPA, DHPG, DOPAC) and their sulfated conjugates (EPI sulfate, NE sulfate, DA sulfate, DOPA sulfate, DHPG sulfate, DOPAC sulfate), and blood gas and acid-base profiles. Results: The mean maternal glucose and lactate levels were 4.28 mmol/l and 1.8 mmol/l respectively. Three infants were hypoglycaemic with umbilical blood glucose levels of less than 2.6 mmol/l. The mean infant glucose and lactate levels were as expected for full term infants at 3.3 mmol/l and 2.2 mmol/l respectively. High mean levels of insulin and catechols were noted at birth. There was a significant positive association between umbilical venous cord glucose levels and maternal venous glucose levels (p=<0.001) but no association of umbilical venous cord glucose levels with amino acids, insulin, glucagon, human growth hormone, cortisol and catechols.

Le diabète de type 1 (DT1) se caractérise par la destruction auto-immune des cellules ß des îlots de Langerhans du pancréas productrices d’insuline, entraînant un état d’hyperglycémie chronique. Malgré une prise en charge très fine de la maladie, s’appuyant sur l’insulinothérapie fonctionnelle, les personnes vivant avec le DT1 sont fréquemment sujettes à des épisodes hypoglycémiques et hyperglycémiques en raison de difficultés à adapter le traitement insulinique, notamment lors de l’activité physique. L’activité physique procure de nombreux bénéfices pour la santé que l’on ait ou non un diabète. Cependant, dans le cadre du DT1, les excursions glycémiques lors de l’activité physique peuvent conduire à des barrières à l’activité physique dans cette population ou peuvent limiter les performances sportives d’athlètes vivant avec le DT1. L’objectif de cette thèse était triple : 1) Étudier les barrières à l’activité physique chez les enfants et adultes vivant avec le DT1 et à leurs liens avec les excursions glycémiques réellement vécues dans la vie quotidienne et d’autant plus autour de l’activité physique, 2) Chez des enfants vivant avec le DT1, comparer deux types d’exercice (exercice aérobie continu vs. intermittent intense), représentatifs de leur activité physique spontanée, et explorer leurs effets sur les variations glycémiques à l’exercice et à la récupération précoce et tardive et, 3) Mesurer la glycémie en continu, à l’exercice et à la récupération, chez des sportifs en endurance qui n’ont pas de diabète, afin de comprendre les mécanismes impliqués dans la régulation de la glycémie lors d’épreuves d’ultra-endurance et de transposer ces résultats chez des sportifs vivant avec le DT1. Les résultats montrent que : 1) Chez les enfants, plus le temps passé <54 mg.dL-1 les nuits suivant les séances d'activités physiques augmente, plus la peur de l'hypoglycémie est importante. Chez les adultes, étonnamment, ceux qui déclarent le moins l’hypoglycémie comme une barrière à l’activité physique sont ceux qui ont le plus grand pourcentage de séances d’activités physiques entraînant une baisse de glycémie; 2) Le risque hypoglycémique n’est pas supérieur lors d’un exercice continu modéré représentatif de l’activité physique spontanée des enfants et, cet exercice semble efficace pour diminuer l’hyperglycémie retrouvée les jours inactifs sur la même période de temps; 3) Un risque hyperglycémique existe lors des phases intenses de la course et pendant 48 heures de récupération lors d’un ultra-trail réalisé chez des athlètes qui n’ont pas de diabète. Ce risque hyperglycémique à la récupération pourrait être en lien avec les dommages musculaires. / Type 1 diabetes (T1D) is characterized by the autoimmune destruction of the insulin-producing ß-cells of the islets of Langerhans in the pancreas, leading to a state of chronic hyperglycemia. Despite very sophisticated management of the disease, based on functional insulin therapy, people living with T1D are frequently subject to hypoglycemic and hyperglycemic episodes because of difficulties in adapting insulin treatment, particularly during physical activity. Physical activity has many health benefits, whether or not you have diabetes. However, in the context of T1D, glycemic excursions during physical activity may lead to barriers to physical activity in this population or may limit the sporting performance of athletes living with T1D. The aim of this thesis was threefold: 1) Investigate the barriers to physical activity in children and adults living with T1D and their links with the glycemic excursions actually experienced in daily life and all the more so around physical activity, 2) In children living with T1D, compare two exercise modalities (continuous aerobic exercise vs. intense intermittent), representative of their spontaneous physical activity, and explore their effects on glycemic variations during exercise and early and late recovery and, 3) Measure glycemia continuously, during exercise and recovery, in endurance athletes without diabetes in order to understand the mechanisms involved in regulating glycaemia during ultra-endurance events and transpose these results to athletes living with T1D. The results show that: 1) In children, the greater the time spent <54 mg.dL-1 on the nights following physical activity sessions, the greater the fear of hypoglycemia. Surprisingly, among adults, those who least reported hypoglycemia as a barrier to physical activity were those who had the highest percentage of physical activity sessions resulting in a drop in blood glucose levels; 2) The risk of hypoglycemia is no greater during continuous moderate exercise representative of the spontaneous physical activity of children, and this exercise appears to be effective in reducing the hyperglycemia found on inactive days over the same period of time; 3) A hyperglycemic risk exists during the intense phases of the race and during 48 hours of recovery during an ultra-trail run carried out in athletes who do not have diabetes. This hyperglycemic risk during recovery could be related to muscle damage.