Leptin alters metabolic rates before acquisition  of its anorectic effect in developing neonatal mice

Mistry, Anahita M.; Swick, Andrew G.; Romsos, Dale R.

doi:10.1152/ajpregu.1999.277.3.r742

Cited by 135 publications

(160 citation statements)

References 20 publications

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“…The high levels of ir-leptin that we found in mares' colostrum and transitional milk are consistent with the suggestion of Mistry et al [19] that the peptide's thermoregulatory role in the neonate differs from the anorectic role in adults, acquired most likely at the time of weaning.…”

Section: Milk Constituents and Hormone Determinationssupporting

confidence: 92%

“…Emerging evidence has indicated that leptin in milk may be involved in the regulation of growth, and in particular in the development and maturation of the neonatal gut, the immune system and the neuroendocrine system [12,24]. Leptin in milk may also exert a more general regulatory activity until organ systems begin to function autonomously [19].…”

Section: Introductionmentioning

confidence: 99%

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Major constituents, leptin, and non-protein nitrogen compounds in mares' colostrum and milk

Salimei¹,

Varisco²,

Rosi³

2002

Reprod. Nutr. Dev.

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-Five Haflinger mares were hand-milked at 0 h (pre-suckle) and 6 h (postsuckle), 12, 24, 48, 72 and 96 h after parturition. Total solids, protein, fat, lactose, calculated gross energy content, leptin and non-protein nitrogen components (urea, a-amino nitrogen, creatinine and allantoin) were determined. The levels of the major constituents differed significantly in pre-suckle colostrum from subsequent samples. Leptin levels were the highest in whole (9 ng . mL -1 of immunoreactive human equivalent HE ± 0.48 ng . mL -1 , SEM) and skimmed (7.8 ng HE . mL -1 ± 0.52 ng . mL -1 , SEM) pre-suckle colostrum, declined sharply at 6 hours postpartum, and more slowly subsequently. Mean urea concentration was constant at around 5.0 mM, while a-amino N increased over the observation period and creatinine and allantoin decreased. These findings provide a further indication that mares' milk can be regarded as a functional food. mares' milk / colostrum / major constituents / leptin / non-protein nitrogenRésumé -Principaux constituants, leptine et métabolites d'azote non protéique dans le colostrum et le lait de jument. Cinq juments Haflinger ont été traitées à la main aux temps 0 (avant tétée) et 6 (après tétée), 12, 24, 48, 72 et 96 heures après le poulinage. Les paramètres évalués sur ces échantillons ont été les principaux constituants de la sécrétion mammaire (matière sèche, protéines, lipides, lactose), le contenu énergétique brut et la leptine ; en plus, on a considéré les teneurs en urée, a-aminoacides, créatinine et allantoïne. Une différence significative a été observée entre les valeurs enregistrées dans le colostrum prélevé avant la tétée et dans les autres échantillons. De même, des variations dynamiques concernant la leptine immunoréactive ont été relevées au cours de l'essai : les valeurs étaient les plus fortes dans le lait entier (9 ng . mL -1 équivalent de leptine humaine HE ± 0,48 ng . mL -1 , SEM) et dans le colostrum écrémé (7,8 ng HE . mL -1 ± 0,52 ng . mL -1 , SEM) prélevés avant la tétée. La concentration en urée était en moyenne de 5,0 mM et la concentration en azote des a-aminoacides dénote des bilans différents par rapport à celui mis en évidence pour la créatinine et pour l'allantoïne. Ces résultats contribuent à faire considérer le lait de jument comme un aliment fonctionnel.lait de jument / colostrum / constituants du lait / leptine / non-protein nitrogen Reprod. Nutr. Dev. 42 (2002) 65-72 65

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Section: Milk Constituents and Hormone Determinationssupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Major constituents, leptin, and non-protein nitrogen compounds in mares' colostrum and milk

Salimei¹,

Varisco²,

Rosi³

2002

Reprod. Nutr. Dev.

View full text Add to dashboard Cite

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“…In newborn rodents, a peak of leptin appears during the second week of life, which is not related to the regulation of food intake (Ahima et al 1998, Mistry et al 1999, Proulx et al 2002. This peak has been related to a maternal origin through lactation (Stocker et al 2004, Bautista et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Early leptin blockade predisposes fat-fed rats to overweight and modifies hypothalamic microRNAs

Benoît¹,

Ould-Hamouda²,

Crépin³

et al. 2013

Journal of Endocrinology

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Perinatal leptin impairment has long-term consequences on energy homeostasis leading to body weight gain. The underlying mechanisms are still not clearly established. We aimed to analyze the long-term effects of early leptin blockade. In this study, newborn rats received daily injection of a pegylated rat leptin antagonist (pRLA) or saline from day 2 (d2) to d13 and then body weight gain, insulin/leptin sensitivity, and expression profile of microRNAs (miRNAs) at the hypothalamic level were determined at d28, d90, or d153 (following 1 month of high-fat diet (HFD) challenge). We show that pRLA treatment predisposes rats to overweight and promotes leptin/insulin resistance in both hypothalamus and liver at adulthood. pRLA treatment also modifies the hypothalamic miRNA expression profile at d28 leading to the upregulation of 34 miRNAs and the downregulation of four miRNAs. For quantitative RT-PCR confirmation, we show the upregulation of rno-miR-10a at d28 and rno-miR-200a, rno-miR-409-5p, and rno-miR-125a-3p following HFD challenge. Finally, pRLA treatment modifies the expression of genes involved in energy homeostasis control such as UCPs and AdipoRs. In pRLA rat muscle, Ucp2/3 and Adipor1/r2 are upregulated at d90. In liver, pRLA treatment upregulates Adipor1/r2 following HFD challenge. These genes are known to be involved in insulin resistance and type 2 diabetes. In conclusion, we demonstrate that the impairment of leptin action in early life promotes insulin/leptin resistance and modifies the hypothalamic miRNA expression pattern in adulthood, and finally, this study highlights the potential link between hypothalamic miRNA expression pattern and insulin/leptin responsiveness.

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“…17,18 At this stage, leptin regulates metabolic rate and hypothalamic neuropeptides expression, but not food intake. [19][20][21] These observations could be, at least partially, explained by the kinetic in the development of neuronal hypothalamic network, which begins in rodents only after birth (day 6) to be achieved at the end of the second postnatal week. 22 During that temporal window, neuronal projections are developing to interconnect the different hypothalamic nuclei responsible for food intake regulation, and leptin appears to play a crucial role in this phenomenon.…”

Section: Introductionmentioning

confidence: 99%

Early postnatal leptin blockage leads to a long-term leptin resistance and susceptibility to diet-induced obesity in rats

et al. 2008

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Objective: Using a recombinant rat leptin antagonist, we investigated the effects of early postnatal leptin disruption on long-term leptin sensitivity and metabolic phenotype. Design: Three groups of 10 newborn female Wistar rats were injected subcutaneously with either saline (control) or leptin antagonist (at 2.5 or 7.5 mg g À1 day À1 ) from postnatal day 2 to day 13. Results: At weaning (day 28), antagonist-treated rats presented similar body weight (BW) compared to control animals. At 3 months of age, there was no significant change in BW, food intake and leptin or insulin levels between groups. Only a disturbed relationship between circulating insulin and glucose levels was observed in antagonist-treated animals. At 4 months of age, treated animals developed a leptin resistance appreciated by the lack of response to a 7-days leptin treatment (1 mg kg À1 day À1 ) in term of decrease in food intake and BW. At 8 months of age, following 3 months of high-energy diet, rlepm7.5 animals presented higher BW gain associated with increased body fatness and striking hyperleptinaemia as compared to control animals. Conclusion: The blockage of leptin action during the critical period of early life in rodents has long-term consequences by altering the capacity to respond to leptin during adulthood, thus predisposing the animals to obesity. These findings clearly demonstrate the physiological importance of the postnatal leptin surge for the optimal onset of the metabolic regulation, at least in rodents, and its implication in the prevention of unfavourable developmental programming.

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Leptin alters metabolic rates before acquisition of its anorectic effect in developing neonatal mice

Cited by 135 publications

References 20 publications

Major constituents, leptin, and non-protein nitrogen compounds in mares' colostrum and milk

Major constituents, leptin, and non-protein nitrogen compounds in mares' colostrum and milk

Early leptin blockade predisposes fat-fed rats to overweight and modifies hypothalamic microRNAs

Early postnatal leptin blockage leads to a long-term leptin resistance and susceptibility to diet-induced obesity in rats

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