Attenuation of obesity by early-life food restriction in genetically hyperphagic male OLETF rats: Peripheral mechanisms

Mariana Schroeder, Timothy H. Moran, Aron Weller

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16 Scopus citations


The alarming increase in childhood, adolescent and adult obesity has exposed the need for understanding early factors affecting obesity and for treatments that may help prevent or moderate its development. In the present study, we used the OLETF rat model of early-onset hyperphagia induced obesity, which become obese as a result of the absence of CCK1 receptors, to examine the influence of partial food restriction on peripheral adiposity-related parameters during and after chronic and early short-term food restriction. Pair feeding (to the amount of food eaten by control, LETO rats) took place from weaning until postnatal day (PND) 45 (early) or from weaning until PND90 (chronic). We examined fat pad weight (brown, retroperitoneal, inguinal and epididymal); inguinal adipocyte size and number; and plasma leptin, oxytocin and creatinine levels. We also examined body weight, feeding efficiency and spontaneous intake after release from food-restriction. The results showed that chronic food restriction produced significant reductions in adiposity parameters, hormones and body weight, while early food restriction successfully reduced long-term body weight, intake and adiposity, without affecting plasma measurements. Early (and chronic) dieting produced promising long-term effects that may imply the reorganization of both peripheral and central mechanisms that determine energy balance and further support the theory suggesting that early interventions may effectively moderate obesity, even in the presence of a genetic tendency.

Original languageEnglish
Pages (from-to)455-462
Number of pages8
JournalHormones and Behavior
Issue number4-5
StatePublished - Apr 2010

Bibliographical note

Funding Information:
This work was supported partly by a grant from the US-Israel Binational Research Foundation (AW and THM), and partly by NIH/NIDDK — RO1 DK57609 (PI: THM, sub-contract: AW).


  • Animal models
  • Early-onset obesity
  • Food restriction
  • Obesity


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