期刊
ENDOCRINOLOGY
卷 157, 期 2, 页码 666-678出版社
ENDOCRINE SOC
DOI: 10.1210/en.2015-1753
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资金
- National Institutes of Health (NIH) [R01 DK089038]
- Columbia Diabetes Research Center Mouse Phenotyping and Histopathology Cores NIH [P30 DK063608]
- National Center for Advancing Translational Sciences, through NIH Grant [UL1 TR000040]
- Howard Hughes Medical Institute-funded Med into Grad Program
- NIH [T32 GM008464]
- Russ Berrie Foundation
Although most adults can lose weight by dieting, a well-characterized compensatory decrease in energy expenditure promotes weight regain more than 90% of the time. Using mice with impaired hypothalamic leptin signaling as a model of early-onset hyperphagia and obesity, we explored whether this unfavorable response to weight loss could be circumvented by early intervention. Early-onset obesity was associated with impairments in the structure and function of brown adipose tissue mitochondria, which were ameliorated by weight loss at any age. Although decreased sympathetic tone in weight-reduced adults resulted in net reductions in brown adipose tissue thermogenesis and energy expenditure that promoted rapid weight regain, this was not the case when dietary interventions were initiated at weaning. Enhanced energy expenditure persisted even after mice were allowed to resume overeating, leading to lasting reductions in adiposity. These findings reveal a time window when dietary interventions can produce metabolic improvements that are stably maintained.
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