Abstract
We investigated whether long-lived weight-reduced αMUPA mice differ from their wild types in postnatal body composition and leptin level, and whether these differences are affected by maternal-borne factors. Newborn αMUPA and wild type mice had similar body weight and composition up to the third postnatal week, after which αMUPA mice maintained lower body weight due to lower fat-free mass. Both strains showed a surge in leptin levels at the second postnatal week, initiating earlier in αMUPA mice, rising higher and lasting longer than in the wild types, mainly in females. Leptin level in dams’ serum and breast milk, and in their pup’s stomach content were also higher in αMUPA than in the WT during the surge peak. Leptin surge preceded the strain divergence in body weight, and was associated with an age-dependent decrease in the leptin:fat mass ratio—suggesting that postnatal sex and strain differences in leptin ontogeny are strongly influenced by processes independent of fat mass, such as production and secretion, and possibly outside fat tissues. Dam removal elevated corticosterone level in female pups from both strains similarly, yet mitigated the leptin surge only in αMUPA–eliminating the strain differences in leptin levels. Overall, our results indicate that αMUPA’s postnatal leptin surge is more pronounced than in the wild type, more sensitive to maternal deprivation, less related to pup’s total adiposity, and is associated with a lower post-weaning fat-free mass. These strain-related postnatal differences may be related to αMUPA’s higher milk-borne leptin levels. Thus, our results support the use of αMUPA mice in future studies aimed to explore the relationship between maternal (i.e. milk-borne) factors, postnatal leptin levels, and post-weaning body composition and energy homeostasis.
Highlights
Postnatal perturbations in pups physiology often lead to long-term adverse effects–a phenomenon known as “the developmental origins of health and disease” [1]
We explored the postnatal ontogeny of body composition, and its association with leptin ontogeny
Body weight of αMUPA mice became noticeably lower than their wild type (WT) by P20 in both sexes, and significantly so by Pups were weaned at day 24 (P24) (Fig 1A)
Summary
Postnatal perturbations in pups physiology often lead to long-term adverse effects–a phenomenon known as “the developmental origins of health and disease” [1]. Leptin’s serum level is correlated with body fat and its main role is in signaling a negative energy balance [8] This role of leptin is absent in pre-weaning rodents [2,3,9,10]. Postnatal leptin level in rodents shows a transient increase peaking at the 2nd postnatal week, termed leptin surge [11,12,13] This surge is related, to a varying degree, to leptin’s mRNA expression levels in white and brown fat and in gastric epithelial cells, as well as to total fat mass [7,13,14,15,16,17]. The causality between leptin surge level and post-weaning body weight is hard to prove [30,31], as these phenotypes seem to be associated with mode of leptin delivery, pups’ sex and diet, and most importantly, with maternal diet during gestation and lactation
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