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Physiol Behav. 2016 Apr 1;157:246-57. doi: 10.1016/j.physbeh.2016.02.003. Epub 2016 Feb 2.

Diet-induced obesity resistance of adult female mice selectively bred for increased wheel-running behavior is reversed by single perinatal exposure to a high-energy diet.

Author information

1
Groningen Institute for Evolutionary Life Sciences (GELIFES), Unit Behavioral Neuroscience, University of Groningen, The Netherlands; Center for Isotope Research (CIO), Energy and Sustainability Research Institute Groningen (ESRIG), University of Groningen, The Netherlands. Electronic address: st.guidotti@gmail.com.
2
Groningen Institute for Evolutionary Life Sciences (GELIFES), Unit Behavioral Neuroscience, University of Groningen, The Netherlands. Electronic address: neele.meyer1@gmail.com.
3
Department of Pathology and Medical Biology, University of Groningen, The Netherlands. Electronic address: ewaprzybyt@gmail.com.
4
Groningen Institute for Evolutionary Life Sciences (GELIFES), Unit Behavioral Neuroscience, University of Groningen, The Netherlands. Electronic address: a.j.w.scheurink@rug.nl.
5
Department of Pathology and Medical Biology, University of Groningen, The Netherlands. Electronic address: m.c.harmsen@umcg.nl.
6
Department of Biology, University of California, Riverside, CA, USA. Electronic address: theodore.garland@ucr.edu.
7
Groningen Institute for Evolutionary Life Sciences (GELIFES), Unit Behavioral Neuroscience, University of Groningen, The Netherlands; Center for Isotope Research (CIO), Energy and Sustainability Research Institute Groningen (ESRIG), University of Groningen, The Netherlands. Electronic address: gertjan.van.dijk@rug.nl.

Abstract

Female mice from independently bred lines previously selected over 50 generations for increased voluntary wheel-running behavior (S1, S2) resist high energy (HE) diet-induced obesity (DIO) at adulthood, even without actual access to running wheels, as opposed to randomly bred controls (CON). We investigated whether adult S mice without wheels remain DIO-resistant when exposed - via the mother - to the HE diet during their perinatal stage (from 2 weeks prior to conception until weaning on post-natal day 21). While S1 and S2 females subjected to HE diet either perinatally or from weaning onwards (post-weaning) resisted increased adiposity at adulthood (as opposed to CON females), they lost this resistance when challenged with HE diet during these periods combined over one single cycle of breeding. When allowed one-week access to wheels (at week 6-8 and at 10 months), however, tendency for increased wheel-running behavior of S mice was unaltered. Thus, the trait for increased wheel-running behavior remained intact following combined perinatal and post-weaning HE exposure, but apparently this did not block HE-induced weight gain. At weaning, perinatal HE diet increased adiposity in all lines, but this was only associated with hyperleptinemia in S lines irrespective of gender. Because leptin has multiple developmental effects at adolescence, we argue that a trait for increased physical activity may advance maturation in times of plenty. This would be adaptive in nature where episodes of increased nutrient availability should be exploited maximally. Associated disturbances in glucose homeostasis and related co-morbidities at adulthood are probably pleiotropic side effects.

KEYWORDS:

Developmental switch; Glucose homeostasis; Leptin; Obesity; Physical activity; Reproductive age; Voluntary exercise

PMID:
26850290
DOI:
10.1016/j.physbeh.2016.02.003
[Indexed for MEDLINE]

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