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  1. Artikel ; Online: Neonatal overnutrition, but not neonatal undernutrition, disrupts CCK-induced hypophagia and neuron activation of the nucleus of the solitary tract and paraventricular nucleus of hypothalamus of male Wistar rats.

    Wunderlich, Ana Luiza Machado / Martins, Andressa Busetti / de Souza, Camila Franciele / Stopa, Larissa Rugila S / Monteiro, Érica Cristina A M / Aguiar, Danielly D / Guergolette, Rhauany P / Zaia, Cássia Thaïs B V / Uchôa, Ernane Torres

    Brain research bulletin

    2023  Band 195, Seite(n) 109–119

    Abstract: Metabolic programming may be induced by reduction or enhancement of litter size, which lead to neonatal over or undernutrition, respectively. Changes in neonatal nutrition can challenge some regulatory processes in adulthood, such as the hypophagic ... ...

    Abstract Metabolic programming may be induced by reduction or enhancement of litter size, which lead to neonatal over or undernutrition, respectively. Changes in neonatal nutrition can challenge some regulatory processes in adulthood, such as the hypophagic effect of cholecystokinin (CCK). In order to investigate the effects of nutritional programming on the anorexigenic function of CCK in adulthood, pups were raised in small (SL, 3 pups per dam), normal (NL, 10 pups per dam), or large litters (LL, 16 pups per dam), and on postnatal day 60, male rats were treated with vehicle or CCK (10 µg/Kg) for the evaluation of food intake and c-Fos expression in the area postrema (AP), nucleus of solitary tract (NTS), and paraventricular (PVN), arcuate (ARC), ventromedial (VMH), and dorsomedial (DMH) nuclei of the hypothalamus. Overnourished rats showed increased body weight gain that was inversely correlated with neuronal activation of PaPo, VMH, and DMH neurons, whereas undernourished rats had lower body weight gain, inversely correlated with increased neuronal activation of PaPo only. SL rats showed no anorexigenic response and lower neuron activation in the NTS and PVN induced by CCK. LL exhibited preserved hypophagia and neuron activation in the AP, NTS, and PVN in response to CCK. CCK showed no effect in c-Fos immunoreactivity in the ARC, VMH, and DMH in any litter. These results indicate that anorexigenic actions, associated with neuron activation in the NTS and PVN, induced by CCK were impaired by neonatal overnutrition. However, these responses were not disrupted by neonatal undernutrition. Thus, data suggest that an excess or poor supply of nutrients during lactation display divergent effects on programming CCK satiation signaling in male adult rats.
    Mesh-Begriff(e) Rats ; Male ; Animals ; Paraventricular Hypothalamic Nucleus/metabolism ; Cholecystokinin/pharmacology ; Cholecystokinin/metabolism ; Rats, Wistar ; Solitary Nucleus/metabolism ; Rats, Sprague-Dawley ; Hypothalamus/metabolism ; Neurons/metabolism ; Proto-Oncogene Proteins c-fos/metabolism ; Overnutrition/metabolism ; Malnutrition ; Body Weight ; Eating
    Chemische Substanzen Cholecystokinin (9011-97-6) ; Proto-Oncogene Proteins c-fos
    Sprache Englisch
    Erscheinungsdatum 2023-02-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 197620-5
    ISSN 1873-2747 ; 0361-9230
    ISSN (online) 1873-2747
    ISSN 0361-9230
    DOI 10.1016/j.brainresbull.2023.02.012
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Neonatal overnutritional programming impairs the hypophagia and neuron activation induced by acute lipopolysaccharide in adult male rats.

    Wunderlich, Ana Luiza / Stopa, Larissa / Martins, Andressa Busetti / de Souza, Camila Franciele / Monteiro, Érica / Aguiar, Danielly / Guergolette, Rhauany / Shishido, Polyana / Zaia, Cassia Thais / Uchoa, Ernane

    Nutritional neuroscience

    2023  Band 27, Heft 7, Seite(n) 734–744

    Abstract: Nutritional status during critical windows in early development can challenge metabolic functions and physiological responses to immune stress in adulthood, such as the systemic inflammation induced by lipopolysaccharide (LPS). The aim of this study was ... ...

    Abstract Nutritional status during critical windows in early development can challenge metabolic functions and physiological responses to immune stress in adulthood, such as the systemic inflammation induced by lipopolysaccharide (LPS). The aim of this study was to investigate the long-term effects of post-natal over- and undernutrition on the anorexigenic effect of LPS and its association with neuronal activation in the brainstem and hypothalamus of male rats. Animals were raised in litters of 3 (small - SL), 10 (normal - NL), or 16 (large - LL) pups per dam. On post-natal day 60, male rats were treated with LPS (500 µg/Kg) or vehicle for the evaluation of food intake and c-Fos expression in the area postrema (AP), nucleus of solitary tract (NTS), and paraventricular (PVN), arcuate (ARC), ventromedial (VMH), and dorsomedial (DMH) nuclei of the hypothalamus. SL, NL, and LL animals showed a decreased food consumption after LPS treatment. In under- and normonourished animals, peripheral LPS induced an increase in neuronal activation in the brainstem, PaV, PaMP, and ARC and a decrease in the number of c-Fos-ir neurons in the DMH. Overnourished rats showed a reduced hypophagic response, lower neuron activation in the NTS and PaMP, and no response in the DMH induced by LPS. These results indicate that early nutritional programming displays different responses to LPS, by means of neonatal overnutrition decreasing LPS-mediated anorexigenic effect and neuronal activation in the NTS and hypothalamic nuclei.
    Mesh-Begriff(e) Animals ; Male ; Lipopolysaccharides/administration & dosage ; Neurons/drug effects ; Proto-Oncogene Proteins c-fos/metabolism ; Rats, Wistar ; Hypothalamus/metabolism ; Hypothalamus/drug effects ; Animals, Newborn ; Eating ; Overnutrition ; Brain Stem/drug effects ; Rats ; Female ; Nutritional Status
    Chemische Substanzen Lipopolysaccharides ; Proto-Oncogene Proteins c-fos
    Sprache Englisch
    Erscheinungsdatum 2023-08-31
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 1447449-9
    ISSN 1476-8305 ; 1028-415X
    ISSN (online) 1476-8305
    ISSN 1028-415X
    DOI 10.1080/1028415X.2023.2250967
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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