Clinical endocrinology · 2006
Lower ability to oxidize lipids in adult patients with growth hormone (GH) deficiency: reversal under GH treatment.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Brandou F, Aloulou I, Razimbaud A, Fédou C, Mercier J, Brun J F
Аннотация
BACKGROUND: The aim of the study was to characterize lipid oxidation at exercise in adults with growth hormone deficiency (GHD) and to evaluate the effect of 6 and 12 months of GH replacement therapy on substrate carbohydrate (CHO) and lipid utilization at exercise.
PATIENTS AND MEASUREMENTS: Twenty-five patients with GHD and 40 matched controls participated in the study. Ten of the 25 GH-deficient patients were treated with recombinant GH for 12 months. Anthropometric measurements and exercise calorimetry were performed before and after treatment. Maximal fat oxidation and the crossover point [that is the percentage of the theoretical maximal power (Wmax th) where CHO become the predominant fuel used for oxidation] were determined.
RESULTS AND CONCLUSION: The GH-deficient patients exhibited a highly significant shift in the balance of substrate oxidation during exercise, towards a decrease in fat oxidation, and a shift towards lower intensities of the crossover (52 +/- 5.5%vs. 72.6 +/- 6.6% of Wmax th, P < 0.03) and maximal fat oxidation (131.04 +/- 14 vs. 234.4 +/- 30.1 mg/min, P < 0.03) in the GHD and control groups, respectively. However, GH treatment at 6 and 12 months partially reversed this defect, resulting in an increase (+83%, P < 0.001) in the maximal ability to oxidize fat during exercise. These findings are consistent with the hypothesis that a lack of GH reduces the ability to oxidize lipids during exercise and that GH treatment restores this muscular metabolic property.
PATIENTS AND MEASUREMENTS: Twenty-five patients with GHD and 40 matched controls participated in the study. Ten of the 25 GH-deficient patients were treated with recombinant GH for 12 months. Anthropometric measurements and exercise calorimetry were performed before and after treatment. Maximal fat oxidation and the crossover point [that is the percentage of the theoretical maximal power (Wmax th) where CHO become the predominant fuel used for oxidation] were determined.
RESULTS AND CONCLUSION: The GH-deficient patients exhibited a highly significant shift in the balance of substrate oxidation during exercise, towards a decrease in fat oxidation, and a shift towards lower intensities of the crossover (52 +/- 5.5%vs. 72.6 +/- 6.6% of Wmax th, P < 0.03) and maximal fat oxidation (131.04 +/- 14 vs. 234.4 +/- 30.1 mg/min, P < 0.03) in the GHD and control groups, respectively. However, GH treatment at 6 and 12 months partially reversed this defect, resulting in an increase (+83%, P < 0.001) in the maximal ability to oxidize fat during exercise. These findings are consistent with the hypothesis that a lack of GH reduces the ability to oxidize lipids during exercise and that GH treatment restores this muscular metabolic property.
Предметные рубрики MeSH
AdenomaAdultAnalysis of VarianceBody CompositionCarbohydrate MetabolismCase-Control StudiesCross-Sectional StudiesEnergy MetabolismExerciseExercise TestFemaleFollow-Up StudiesGrowth HormoneHuman Growth HormoneHumansHypopituitarismLipid MetabolismMaleMuscle, SkeletalOxygen ConsumptionPituitary NeoplasmsTime Factors