Relevant bibliographies by topics / Postnatal overfeeding

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Postnatal overfeeding'

Author: Grafiati
Published: 20 April 2024
Last updated: 31 July 2025

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Journal articles on the topic "Postnatal overfeeding"

1

Sousa, Diana, Mariana Rocha, Andreia Amaro, et al. "Exposure to Obesogenic Environments during Perinatal Development Modulates Offspring Energy Balance Pathways in Adipose Tissue and Liver of Rodent Models." Nutrients 15, no. 5 (2023): 1281. http://dx.doi.org/10.3390/nu15051281.

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Obesogenic environments such as Westernized diets, overnutrition, and exposure to glycation during gestation and lactation can alter peripheral neuroendocrine factors in offspring, predisposing for metabolic diseases in adulthood. Thus, we hypothesized that exposure to obesogenic environments during the perinatal period reprograms offspring energy balance mechanisms. Four rat obesogenic models were studied: maternal diet-induced obesity (DIO); early-life obesity induced by postnatal overfeeding; maternal glycation; and postnatal overfeeding combined with maternal glycation. Metabolic parameter
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2

Castellano, Juan M., Agnete H. Bentsen, Miguel A. Sánchez-Garrido, et al. "Early Metabolic Programming of Puberty Onset: Impact of Changes in Postnatal Feeding and Rearing Conditions on the Timing of Puberty and Development of the Hypothalamic Kisspeptin System." Endocrinology 152, no. 9 (2011): 3396–408. http://dx.doi.org/10.1210/en.2010-1415.

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Kiss1 neurons have recently emerged as a putative conduit for the metabolic gating of reproduction, with leptin being a regulator of hypothalamic Kiss1 expression. Early perturbations of the nutritional status are known to predispose to different metabolic disorders later in life and to alter the timing of puberty; however, the potential underlying mechanisms remain poorly defined. Here we report how changes in the pattern of postnatal feeding affect the onset of puberty and evaluate key hormonal and neuropeptide [Kiss1/kisspeptin (Kp)] alterations linked to these early nutritional manipulatio
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3

You, Su, Franziska Götz, W. Rohde, and G. Dörner. "Early Postnatal Overfeeding and Diabetes Susceptibility." Experimental and Clinical Endocrinology & Diabetes 96, no. 06 (2009): 301–6. http://dx.doi.org/10.1055/s-0029-1211023.

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4

Mićić, Bojana, Ana Djordjevic, Nataša Veličković, et al. "AMPK Activation as a Protective Mechanism to Restrain Oxidative Stress in the Insulin-Resistant State in Skeletal Muscle of Rat Model of PCOS Subjected to Postnatal Overfeeding." Biomedicines 11, no. 6 (2023): 1586. http://dx.doi.org/10.3390/biomedicines11061586.

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Polycystic ovary syndrome (PCOS) is a common endocrinopathy in women of reproductive age, often associated with obesity and insulin resistance. Childhood obesity is an important predisposing factor for the development of PCOS later in life. Being particularly interested in the interplay between prepubertal obesity and hyperandrogenemia, we investigated the effects of early postnatal overfeeding, accomplished by reducing litter size during the period of suckling, on energy sensing and insulin signaling pathways in the gastrocnemius muscle of a rat model of PCOS-induced by 5α-dihydrotestosterone
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5

Kappeler, Laurent, Carlos De Magalhaes Filho, Patricia Leneuve, et al. "Early Postnatal Nutrition Determines Somatotropic Function in Mice." Endocrinology 150, no. 1 (2008): 314–23. http://dx.doi.org/10.1210/en.2008-0981.

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Increasing evidence suggests a developmental origin for a number of human diseases, notably after intrauterine or postnatal nutrient deprivation. Nutritional changes readily translate into alterations of somatic growth. However, whereas intrauterine growth retardation often shows postnatal catch-up growth, recovery from food restriction immediately after birth is limited. Therefore, we investigated whether early postnatal nutrition (undernutrition and overfeeding) modifies plasticity of growth through developmental control of the somatotropic hormone axis. We used cross-fostering in mice to in
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6

Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, et al. "Influence of postnatal overfeeding on postnatal heart development in juvenile mice." Archives of Cardiovascular Diseases Supplements 15, no. 2 (2023): 192. http://dx.doi.org/10.1016/j.acvdsp.2023.03.029.

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7

Du, Susu, Xiaolei Zhu, Nan Zhou, Wen Zheng, Wei Zhou, and Xiaonan Li. "Curcumin alleviates hepatic steatosis by improving mitochondrial function in postnatal overfed rats and fatty L02 cells through the SIRT3 pathway." Food & Function 13, no. 4 (2022): 2155–71. http://dx.doi.org/10.1039/d1fo03752h.

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Postnatal overfeeding damaged mitochondrial biogenesis and antioxidant response, and increased hepatic lipids and the severity of high-fat-induced NAFLD, while curcumin alleviated hepatic steatosis, at least partially, by enhancing mitochondrial function through SIRT3.
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8

Mićić, Bojana, Ana Teofilović, Ana Djordjevic, Nataša Veličković, Djuro Macut, and Danijela Vojnović Milutinović. "AMPK Activation Is Important for the Preservation of Insulin Sensitivity in Visceral, but Not in Subcutaneous Adipose Tissue of Postnatally Overfed Rat Model of Polycystic Ovary Syndrome." International Journal of Molecular Sciences 23, no. 16 (2022): 8942. http://dx.doi.org/10.3390/ijms23168942.

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Polycystic ovary syndrome (PCOS) is a well-known reproductive syndrome usually associated with obesity, insulin resistance, and hyperinsulinemia. Although the first signs of PCOS begin early in adolescence, it is underexplored whether peripubertal obesity predisposes women to PCOS metabolic disturbances. To highlight that, we examined the impact of postnatal overfeeding-induced obesity, achieved by litter size reduction during the suckling period, on metabolic disturbances associated with visceral and subcutaneous adipose tissue (VAT and SAT) function in the 5α-dihydrotestosterone (5α-DHT)-ind
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9

Boubred, Farid, Laurent Daniel, Christophe Buffat, et al. "Early postnatal overfeeding induces early chronic renal dysfunction in adult male rats." American Journal of Physiology-Renal Physiology 297, no. 4 (2009): F943—F951. http://dx.doi.org/10.1152/ajprenal.90704.2008.

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Low birth weight is associated with an increased risk of hypertension and renal dysfunction at adulthood. Such an association has been shown to involve a reduction of nephron endowment and to be enhanced by accelerated postnatal growth in humans. However, while low-birth-weight infants often undergo catch-up growth, little is known about the long-term vascular and renal effects of accelerated postnatal growth. We surimposed early postnatal overfeeding (OF; reduction of litter size during the suckling period) to appropriate-birth-weight (NBW+OF) and intrauterine growth restriction (IUGR; IUGR+O
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10

Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, et al. "Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents." International Journal of Molecular Sciences 21, no. 24 (2020): 9427. http://dx.doi.org/10.3390/ijms21249427.

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Nutritional environment in the perinatal period has a great influence on health and diseases in adulthood. In rodents, litter size reduction reproduces the effects of postnatal overnutrition in infants and reveals that postnatal overfeeding (PNOF) not only permanently increases body weight but also affects the cardiovascular function in the short- and long-term. In addition to increased adiposity, the metabolic status of PNOF rodents is altered, with increased plasma insulin and leptin levels, associated with resistance to these hormones, changed profiles and levels of circulating lipids. PNOF
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Dissertations / Theses on the topic "Postnatal overfeeding"

1

Rigal, Eve. "Impact à long terme de la programmation nutritionnelle postnatale sur le risque cardio-métabolisme et sur la sensibilité aux lésions d'ischémie-reperfusion in vivo chez la souris." Electronic Thesis or Diss., Bourgogne Franche-Comté, 2023. http://www.theses.fr/2023UBFCI017.

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Les troubles nutritionnels survenant pendant les périodes fœtales et postnatales peuvent être responsables d'une prédisposition aux maladies cardio-métaboliques à l'âge adulte. Le modèle de Suralimentation PostNatale (SAPN), induit par la réduction de la taille des portées, récapitule de façon pertinente les mécanismes physiopathologiques d’une programmation d’un risque cardio-métabolique accru chez l’individu, qu’il soit de sexe masculin ou féminin. Cependant, dans le domaine préclinique, la majorité des travaux a été conduit chez des rongeurs mâles de 2 à 4 mois d’âge.Chez les souris mâles,
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