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The effect of neonatal leptin treatment on postnatal weight gain in male rats is dependent on maternal nutritional status during pregnancy

The effect of neonatal leptin treatment on postnatal weight gain in male rats is dependent on maternal nutritional status during pregnancy
The effect of neonatal leptin treatment on postnatal weight gain in male rats is dependent on maternal nutritional status during pregnancy
An adverse prenatal environment may induce long-term metabolic consequences, in particular obesity, hyperleptinemia, insulin resistance, and type 2 diabetes. Although the mechanisms are unclear, this "programming" has generally been considered an irreversible change in developmental trajectory. Adult offspring of rats subjected to undernutrition (UN) during pregnancy develop obesity, hyperinsulinemia, and hyperleptinemia, especially in the presence of a high-fat diet. Using this model of maternal UN, we have recently shown that neonatal leptin treatment in females reverses the postnatal sequelae induced by developmental programming. To examine possible gender-related effects of neonatal leptin treatment, the present study investigated the effect of neonatal leptin treatment on the metabolic phenotype of adult male offspring. Leptin treatment (recombinant rat leptin, 2.5 microg/g.d, sc) from postnatal d 3-13 resulted in a transient slowing of neonatal weight gain, particularly in programmed offspring. Neonatal leptin treatment of male offspring from normally nourished mothers caused an increase in diet-induced weight gain and related metabolic sequelae, including hyperinsulinemia and increased total body adiposity compared with saline-treated controls. This occurred without an increase in caloric intake. These effects were specific to offspring of normal pregnancies and were not observed in offspring of mothers after UN during pregnancy. In the latter, neonatal leptin treatment conferred protection against the development of the programmed phenotype, particularly in those fed the chow diet postnatally. These data further reinforce the importance of leptin in determining long-term energy homeostasis, and suggest that leptin's effects are modulated by gender and both prenatal and postnatal nutritional status.
programming, gender, weight, pharmacology, animals, insulin, homeostasis, adipose tissue, malnutrition, insulin-resistance, glucose, adult, bone density, analysis, phenotype, leptin, metabolism, mothers, insulin resistance, consequences, diet, physiopathology, female, maternal, maternal nutrition physiology, obesity, c-peptide, blood, diabetes, weight gain, newborn, blood glucose, pregnancy, eating, resistance, development, wistar, rats, nutritional status, rat, drug effects, male, physiology, undernutrition, environment
0013-7227
1906-1913
Vickers, M.H.
0fa7133b-53c7-4b48-9863-1b55e53baa5e
Gluckman, P.D.
492295c0-ef71-4871-ad5a-771c98e1059a
Coveny, A.H.
4d63188d-c04c-405a-bd06-2b28955df08e
Hofman, P.L.
c8936c79-0cc8-4de9-8b73-db6e6933ceb3
Cutfield, W.S.
6b21b06f-1f06-4601-b5e9-91b2c6336770
Gertler, A.
8b608753-63e0-4e35-bca1-4ca2e230e4b8
Breier, B.H.
21c929cc-573f-4cec-8a78-0e68b3fd48f0
Harris, M.
b0e2d8cb-44f8-47a5-8e1b-6ca9c04fe776
Vickers, M.H.
0fa7133b-53c7-4b48-9863-1b55e53baa5e
Gluckman, P.D.
492295c0-ef71-4871-ad5a-771c98e1059a
Coveny, A.H.
4d63188d-c04c-405a-bd06-2b28955df08e
Hofman, P.L.
c8936c79-0cc8-4de9-8b73-db6e6933ceb3
Cutfield, W.S.
6b21b06f-1f06-4601-b5e9-91b2c6336770
Gertler, A.
8b608753-63e0-4e35-bca1-4ca2e230e4b8
Breier, B.H.
21c929cc-573f-4cec-8a78-0e68b3fd48f0
Harris, M.
b0e2d8cb-44f8-47a5-8e1b-6ca9c04fe776

Vickers, M.H., Gluckman, P.D., Coveny, A.H., Hofman, P.L., Cutfield, W.S., Gertler, A., Breier, B.H. and Harris, M. (2008) The effect of neonatal leptin treatment on postnatal weight gain in male rats is dependent on maternal nutritional status during pregnancy. Endocrinology, 149 (4), 1906-1913. (doi:10.1210/en.2007-0981).

Record type: Article

Abstract

An adverse prenatal environment may induce long-term metabolic consequences, in particular obesity, hyperleptinemia, insulin resistance, and type 2 diabetes. Although the mechanisms are unclear, this "programming" has generally been considered an irreversible change in developmental trajectory. Adult offspring of rats subjected to undernutrition (UN) during pregnancy develop obesity, hyperinsulinemia, and hyperleptinemia, especially in the presence of a high-fat diet. Using this model of maternal UN, we have recently shown that neonatal leptin treatment in females reverses the postnatal sequelae induced by developmental programming. To examine possible gender-related effects of neonatal leptin treatment, the present study investigated the effect of neonatal leptin treatment on the metabolic phenotype of adult male offspring. Leptin treatment (recombinant rat leptin, 2.5 microg/g.d, sc) from postnatal d 3-13 resulted in a transient slowing of neonatal weight gain, particularly in programmed offspring. Neonatal leptin treatment of male offspring from normally nourished mothers caused an increase in diet-induced weight gain and related metabolic sequelae, including hyperinsulinemia and increased total body adiposity compared with saline-treated controls. This occurred without an increase in caloric intake. These effects were specific to offspring of normal pregnancies and were not observed in offspring of mothers after UN during pregnancy. In the latter, neonatal leptin treatment conferred protection against the development of the programmed phenotype, particularly in those fed the chow diet postnatally. These data further reinforce the importance of leptin in determining long-term energy homeostasis, and suggest that leptin's effects are modulated by gender and both prenatal and postnatal nutritional status.

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More information

Published date: 2008
Keywords: programming, gender, weight, pharmacology, animals, insulin, homeostasis, adipose tissue, malnutrition, insulin-resistance, glucose, adult, bone density, analysis, phenotype, leptin, metabolism, mothers, insulin resistance, consequences, diet, physiopathology, female, maternal, maternal nutrition physiology, obesity, c-peptide, blood, diabetes, weight gain, newborn, blood glucose, pregnancy, eating, resistance, development, wistar, rats, nutritional status, rat, drug effects, male, physiology, undernutrition, environment

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Local EPrints ID: 61585
URI: http://eprints.soton.ac.uk/id/eprint/61585
ISSN: 0013-7227
PURE UUID: 395c5296-8ca5-4e14-b673-1929cf1ab82a

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Date deposited: 09 Sep 2008
Last modified: 15 Mar 2024 11:27

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Contributors

Author: M.H. Vickers
Author: P.D. Gluckman
Author: A.H. Coveny
Author: P.L. Hofman
Author: W.S. Cutfield
Author: A. Gertler
Author: B.H. Breier
Author: M. Harris

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