The Journal of clinical endocrinology and metabolism · 2015
Resting Energy Expenditure Is Decreased in Pseudohypoparathyroidism Type 1A.
СтатьяПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
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Roizen Jeffrey D, Danzig Jennifer, Groleau Veronique, McCormack Shana, Casella Alex, Harrington Jennifer, Sochett Etienne, Tershakovec Andrew, Zemel Babette S, Stallings Virginia A, Levine Michael A
Аннотация
CONTEXT: Pseudohypoparathyroidism type 1A (PHP1A) is caused by loss-of-function mutations on the maternally inherited GNAS allele and is associated with early-onset obesity, neurocognitive defects, and resistance to multiple hormones. The role of energy intake vs central regulation of energy expenditure in the pathophysiology of obesity remains unclear.
OBJECTIVE: The aim of this study was to evaluate resting energy expenditure (REE) in participants with PHP1A.
DESIGN: We assessed REE, biochemical, endocrine, and auxological status of 12 participants with PHP1A who had normal or elevated body mass index; controls were a cohort of 156 obese participants.
SETTING: This study took place at Children's Hospital in Philadelphia and Sick Children's Hospital in Toronto.
MAIN OUTCOME MEASURES: REE as a percent of predicted REE was the outcome measure.
RESULTS: PHP1A participants had normal endocrine status while receiving appropriate hormone replacement therapy, but had significantly decreased REE as a percent of predicted REE (using the modified Schofield equation).
CONCLUSION: Our results are consistent with REE being the principal cause of obesity in PHP1A rather than it being caused by excessive energy intake or endocrine dysfunction.
OBJECTIVE: The aim of this study was to evaluate resting energy expenditure (REE) in participants with PHP1A.
DESIGN: We assessed REE, biochemical, endocrine, and auxological status of 12 participants with PHP1A who had normal or elevated body mass index; controls were a cohort of 156 obese participants.
SETTING: This study took place at Children's Hospital in Philadelphia and Sick Children's Hospital in Toronto.
MAIN OUTCOME MEASURES: REE as a percent of predicted REE was the outcome measure.
RESULTS: PHP1A participants had normal endocrine status while receiving appropriate hormone replacement therapy, but had significantly decreased REE as a percent of predicted REE (using the modified Schofield equation).
CONCLUSION: Our results are consistent with REE being the principal cause of obesity in PHP1A rather than it being caused by excessive energy intake or endocrine dysfunction.