Relevant bibliographies by topics / Postnatal overfeeding

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Academic literature on the topic 'Postnatal overfeeding'

Author: Grafiati
Published: 20 April 2024

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Journal articles on the topic "Postnatal overfeeding"

1

Sousa, Diana, Mariana Rocha, Andreia Amaro, Marcos Divino Ferreira-Junior, Keilah Valéria Naves Cavalcante, Tamaeh Monteiro-Alfredo, Cátia Barra, 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 (March 4, 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 parameters, energy expenditure, and storage pathways in visceral adipose tissue (VAT) and the liver were analyzed. Maternal DIO increased VAT lipogenic [NPY receptor-1 (NPY1R), NPY receptor-2 (NPY2R), and ghrelin receptor], but also lipolytic/catabolic mechanisms [dopamine-1 receptor (D1R) and p-AMP-activated protein kinase (AMPK)] in male offspring, while reducing NPY1R in females. Postnatally overfed male animals only exhibited higher NPY2R levels in VAT, while females also presented NPY1R and NPY2R downregulation. Maternal glycation reduces VAT expandability by decreasing NPY2R in overfed animals. Regarding the liver, D1R was decreased in all obesogenic models, while overfeeding induced fat accumulation in both sexes and glycation the inflammatory infiltration. The VAT response to maternal DIO and overfeeding showed a sexual dysmorphism, and exposure to glycotoxins led to a thin-outside-fat-inside phenotype in overfeeding conditions and impaired energy balance, increasing the metabolic risk in adulthood.
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2

You, Su, Franziska Götz, W. Rohde, and G. Dörner. "Early Postnatal Overfeeding and Diabetes Susceptibility." Experimental and Clinical Endocrinology & Diabetes 96, no. 06 (July 16, 2009): 301–6. http://dx.doi.org/10.1055/s-0029-1211023.

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3

Castellano, Juan M., Agnete H. Bentsen, Miguel A. Sánchez-Garrido, Francisco Ruiz-Pino, Magdalena Romero, David Garcia-Galiano, Enrique Aguilar, 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 (June 28, 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 manipulations. Female rats were raised in litters of different sizes: small (four pups per dam: overfeeding), normal (12 pups per dam), and large litters (20 pups per litter: underfeeding). Postnatal overfeeding resulted in persistently increased body weight and earlier age of vaginal opening, as an external sign of puberty, together with higher levels of leptin and hypothalamic Kiss1 mRNA. Conversely, postnatal underfeeding caused a persistent reduction in body weight, lower ovarian and uterus weights, and delayed vaginal opening, changes that were paralleled by a decrease in leptin and Kiss1 mRNA levels. Kisspeptin-52 immunoreactivity (Kp-IR) in the hypothalamus displayed similar patterns, with lower numbers of Kp-IR neurons in the arcuate nucleus of postnatally underfed animals, and a trend for increased Kp-positive fibers in the periventricular area of early overfed rats. Yet, gonadotropin responses to Kp at puberty were similar in all groups, except for enhanced responsiveness to low doses of Kp-10 in postnatally underfed rats. In conclusion, our data document that the timing of puberty is sensitive to both overfeeding and subnutrition during early (postnatal) periods and suggest that alterations in hypothalamic expression of Kiss1/kisspeptin may underlie at least part of such programming phenomenon.
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4

Mićić, Bojana, Ana Djordjevic, Nataša Veličković, Sanja Kovačević, Teodora Martić, Djuro Macut, and Danijela Vojnović Milutinović. "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 (May 30, 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 (DHT). The combination of overfeeding and DHT treatment caused hyperinsulinemia and decreased systemic insulin sensitivity. Early postnatal overfeeding induced defects at critical nodes of the insulin signaling pathway in skeletal muscle, which was associated with reduced glucose uptake in the presence of hyperandrogenemia. In this setting, under a combination of overfeeding and DHT treatment, skeletal muscle switched to mitochondrial β-oxidation of fatty acids, resulting in oxidative stress and inflammation that stimulated AMP-activated protein kinase (AMPK) activity and its downstream targets involved in mitochondrial biogenesis and antioxidant protection. Overall, a combination of overfeeding and hyperandrogenemia resulted in a prooxidative and insulin-resistant state in skeletal muscle. This was accompanied by the activation of AMPK, which could represent a potential therapeutic target in insulin-resistant PCOS patients.
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5

Kappeler, Laurent, Carlos De Magalhaes Filho, Patricia Leneuve, Jie Xu, Nadège Brunel, Christos Chatziantoniou, Yves Le Bouc, and Martin Holzenberger. "Early Postnatal Nutrition Determines Somatotropic Function in Mice." Endocrinology 150, no. 1 (September 18, 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 induce changes in early nutrition, and examined endocrine growth regulation and the development of specific disease phenotypes in adults. We showed that underfeeding during the early postnatal period delayed growth, whereas overfeeding accelerated it. In both cases, final body size was permanently altered. We found coordinated alterations in pituitary GH, plasma IGF-I and acid labile subunit, and gene expression of hypothalamic GHRH during postnatal development. These changes were consistent with the observed phenotypes. Alterations in the somatotropic axis persisted throughout adulthood. Although limited to the early postnatal period, both underfeeding and overfeeding led to reduced glucose tolerance later in life. These metabolic abnormalities were in line with defective insulin secretion in restricted mice and insulin resistance in overfed mice. Moreover, both restricted and overfed mice had increased arterial blood pressure, suggestive of vascular impairment. Our findings indicate a significant link between early postnatal diet, somatotropic development, and specific late onset diseases in mice. We suggest that, together with other hormones like leptin, IGF-I may play a role in modulating hypothalamic stimulation of the developing somatotropic function. Early postnatal nutrition determines adult activity of the GH axis through an early modulation of hypothalamic GHRH stimulation, probably via hormones like leptin or IGF-I.
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Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, Francesca Rochais, Geoffrey Dogon, Luc Rochette, Marianne Zeller, and Catherine Vergely. "Influence of postnatal overfeeding on postnatal heart development in juvenile mice." Archives of Cardiovascular Diseases Supplements 15, no. 2 (May 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 (August 11, 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)-induced animal model of PCOS. We analyzed markers of insulin signaling, lipid metabolism, and energy sensing in the VAT and SAT. Our results showed that postnatally overfed DHT-treated Wistar rats had increased VAT mass with hypertrophic adipocytes, together with hyperinsulinemia and increased HOMA index. In the VAT of these animals, insulin signaling remained unchanged while lipogenic markers decreased, which was accompanied by increased AMPK activation. In the SAT of the same animals, markers of lipogenesis and lipolysis increased, while the activity of AMPK decreased. Taken together, obtained results showed that postnatal overfeeding predisposes development of PCOS systemic insulin resistance, most likely as a result of worsened metabolic function of SAT, while VAT preserved its tissue insulin sensitivity through increased activity of AMPK.
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9

Boubred, Farid, Laurent Daniel, Christophe Buffat, Jean-Marc Feuerstein, Michel Tsimaratos, Charles Oliver, Françoise Dignat-George, Martine Lelièvre-Pégorier, and Umberto Simeoni. "Early postnatal overfeeding induces early chronic renal dysfunction in adult male rats." American Journal of Physiology-Renal Physiology 297, no. 4 (October 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+OF) pups, obtained after a maternal gestational low-protein diet. Blood pressure (systolic blood pressure; SBP) and renal function (glomerular filtration rate; GFR) were measured in young and aging offspring. Glomerulosclerosis and nephron number were determined in aging offspring (22 mo). Nephron number was reduced in both IUGR and IUGR+OF male offspring (by 24 and 26%). GFR was reduced by 40% in 12-mo-old IUGR+OF male offspring, and both NBW+OF and IUGR+OF aging male offspring had sustained hypertension (+25 mmHg) and glomerulosclerosis, while SBP and renal function were unaffected in IUGR aging offspring. Female offspring were unaffected. In conclusion, in this experimental model, early postnatal OF in the neonatal period has major long-lasting effects. Such effects are gender dependent. Reduced nephron number alone, associated with IUGR, may not be sufficient to induce long-lasting physiological alterations, and early postnatal OF acts as a “second hit.” Early postnatal OF is a suitable model with which to study the long-term effects of postnatal growth in the pathogenesis of vascular disorders and renal disease.
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10

Josse, Marie, Eve Rigal, Nathalie Rosenblatt-Velin, Luc Rochette, Marianne Zeller, Charles Guenancia, and Catherine Vergely. "Programming of Cardiovascular Dysfunction by Postnatal Overfeeding in Rodents." International Journal of Molecular Sciences 21, no. 24 (December 11, 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 animals present elevated arterial blood pressure with altered vascular responsiveness to vasoactive substances. The hearts of overfed rodents exhibit hypertrophy and elevated collagen content. PNOF also induces a disturbance of cardiac mitochondrial respiration and produces an imbalance between oxidants and antioxidants. A modification of the expression of crucial genes and epigenetic alterations is reported in hearts of PNOF animals. In vivo, a decreased ventricular contractile function is observed during adulthood in PNOF hearts. All these alterations ultimately lead to an increased sensitivity to cardiac pathologic challenges such as ischemia-reperfusion injury. Nevertheless, caloric restriction and physical exercise were shown to improve PNOF-induced cardiac dysfunction and metabolic abnormalities, drawing a path to the potential therapeutic correction of early nutritional programming.
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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, la SAPN a induit un surpoids associé à des désordres du métabolisme glucidique de façon précoce et permanente (4 à 18 mois). La fonction contractile cardiaque était diminuée par la SAPN et la sensibilité des cœurs aux lésions d’ischémie-reperfusion (I/R) induites in vivo était accrue et associée à une augmentation de la masse du tissu adipeux péricardique ainsi que de son statut inflammatoire. Chez les femelles, la SAPN à induit des altérations cardio métaboliques similaires, cependant, la sensibilité des cœurs aux lésions d’I/R induites in vivo n’a pas été impactée.Ces résultats montrent qu’une SAPN prédispose l’organisme des souris mâles et femelles aux maladies cardio-métaboliques précocement (dès 4 mois) et durablement (jusqu’à 18 mois de vie), mais qu’elle n’affecte que les mâles pour la susceptibilité aux lésions ischémiques cardiaques.Ce modèle original de SAPN constitue un modèle préclinique pertinent de syndrome métabolique tel qu’il est généralement constaté chez l’humain, et sur lequel des études physiopathologiques et thérapeutiques plus représentatives de la pathologie clinique pourraient être menées
Nutritional disorders occurring during the foetal and postnatal periods may be responsible for a predisposition to cardio-metabolic diseases in adulthood. The PostNatal OverFeeding (PNOF) model, induced by litter size reduction, pertinently recapitulates the pathophysiological mechanisms of a programmed increase of cardiometabolic risk in Humans. However, most of preclinical data has been obtained in young male animals.In male mice, PNOF induced an increase in body weight associated with glucose metabolism impairment at young and older ages (4 to 18 months). Cardiac contractile function was reduced by PNOF and the sensitivity of hearts to in vivo ischemia-reperfusion (I/R) injury was increased and associated with an augmentation in pericardial adipose tissue mass and inflammatory status. In females, PNOF induced similar cardio-metabolic alterations, however, the sensitivity of hearts to I/R lesions induced in vivo was not impacted.These results show that PNOF predisposes the organism of male and female mice to cardio-metabolic diseases from the young (4 months) to the older ages (up to 18 months); however, PNOF only affects males for an increased sensitivity to ischemic cardiac lesions.This original model of PNOF could constitute a model of “natural” metabolic syndrome on which physiopathological and therapeutic studies could be carried out
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