Altered Fos immunoreactivity in the hypothalamus after glucose administration in pre- and post-weaning malnourished rats

Miñana-Solis, María del Carmen; Ángeles-Castellanos, Manuel; Buijs, Ruud M.; Escobar, Carolina

doi:10.1179/147683010x12611460764246

Cited by 3 publications

(9 citation statements)

References 49 publications

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“…In agreement with our previous studies and with others, 6,7,18,19 we found that low-protein malnutrition during gestation and lactation as well as from weaning to P55 induced a long-lasting slowdown growth on the offspring. This leads to maintain low body weight of MGL-R and MPW-R rats until P90 in spite of a balanced diet nutritional rehabilitation.…”

Section: Discussionsupporting

confidence: 95%

“…The 6% casein and the balanced diet have been previously employed by our group and others for similar studies. 7,15,16 Control and malnourished groups were obtained as described elsewhere. 6 Briefly, control (C) rats were born to dams nourished with a balanced diet during gestation and lactation and were maintained in the same nutritional condition until post-natal (P) day 90.…”

Section: Nutritional Conditionsmentioning

confidence: 99%

“…7 Briefly, after 16 hours of food deprivation (food was removed at 18:00 hours), conscious rats were weighed and then received an intraperitoneal bolus (IPB) of glucose as performed for a glucose tolerance test. Glucose solution was administered in a dose of 1 g/kg of body weight (1 g/ 10 ml glucose solution in NaCl 0.9%).…”

Section: Intraperitoneal Bolus Of Glucose and Perfusionmentioning

confidence: 99%

“…6 Our group and others have evidenced that peripheral metabolic disarrangement due to malnutrition correlate with neural alterations in hypothalamic nuclei involved in energy homeostasis. [7][8][9] These studies have reported that peripheral and hypothalamic signals providing metabolic balance information are altered in malnourished animals.…”

Section: Introductionmentioning

confidence: 95%

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Early and post-weaning malnutrition impairs alpha-MSH expression in the hypothalamus: a possible link to long-term overweight

Miñana-Solis

Escobar

2011

Nutritional Neuroscience

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The present study explored the effects of early and post-weaning malnutrition and nutritional rehabilitation on orexigenic (orexin (ORX) and neuropeptide Y (NPY)) and anorexigenic peptides (alpha-melanocyte stimulating hormone (alpha-MSH)) expressed in hypothalamic nuclei. Male Wistar rats were malnourished during gestation-lactation (MGL) or from weaning to post-natal day 55 (MPW; P55). Two groups of rats were rehabilitated with a balanced diet until P90 (MGL-R and MPW-R, respectively). After a glucose tolerance test (GTT) brains were processed for immunohistochemistry. Malnourished groups were hyperglycemic after GTT. ORX expression did not display any difference. Only MGL rats showed increased NPY immunoreactivity in ARC and PVN nuclei, and both malnourished groups showed low alpha-MSH expression in the PVN and DMH, as compared with their controls. After nutritional rehabilitation rats showed normal GTT, increased rate of body and adipose tissue weights and high proportion of food ingestion. Both rehabilitated groups maintained low alpha-MSH expression in the PVN, indicating a deleterious long-lasting effect.

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Section: Discussionsupporting

confidence: 95%

Section: Nutritional Conditionsmentioning

confidence: 99%

Section: Intraperitoneal Bolus Of Glucose and Perfusionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

See 2 more Smart Citations

Early and post-weaning malnutrition impairs alpha-MSH expression in the hypothalamus: a possible link to long-term overweight

Miñana-Solis

Escobar

2011

Nutritional Neuroscience

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“…However, there are few report similar nutritional deficiency protocol as ours. 40) Further studies are needed to clarify the brain region responsible for the enhancement of the 5-HT 1A agonist induced head weaving reseponse in our postweaning PM model.…”

Section: Discussionmentioning

confidence: 99%

Enhanced Behavioral Response to Serotonin-Related Agonists in Postweaning Protein Malnourished Mice

Sato

Nakagawasai

Hayashi

et al. 2012

Biological & Pharmaceutical Bulletin

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We investigated whether postweaning protein malnutrition (PM) affects serotonergic systems. Mice were fed a PM diet or normal protein (control) diet from weaning (21 d of age). Twenty days later, we tested for behavioral effects of the selective serotonin (5-HT) 1A Key words protein malnutrition; serotonin 1A ; serotonin syndrome; head weaving; post-weaning period; mouse Serotonin (5-HT) is involved in the control of numerous physiological functions (e.g. food intake, thermoregulation, sleep patterns and nociception) 1) as well as in some psychiatric disorders such as anxiety and depression.2) These multiple actions are mediated through activation of at least 15 different families of serotonergic receptors.3) The 5-HT 1A receptor is one of the best described receptor subtypes and may be present on presynaptic as well as postsynaptic neurons.4) 5-HT 1A agonists have been successfully used in the treatment of anxiety disorders in human.5) However, excessive stimulation of postsynaptic 5-HT 1A receptor can lead to the 5-HT syndrome, a toxic condition displaying multiple clinical features. 6) In rodents, the administration of high doses of 5-HT 1A agonist, e.g. 8-hydroxy-N,N-dipropyl-2-aminotetralin (8-OH-DPAT), also elicits a 5-HT syndrome with typical major behavioral components such as flat body posture, hind limb abduction, forepaw treading, and head weaving. 7)5-HT concentrations are strongly influenced by undernourishment.8) 5-HT is synthesized from the amino acid precursor tryptophan and therefore is dependent on the latter's bioavailability. Brain levels of both are believed to increase as a result of metabolic adaptation to protein deficiency, which induces a decrease in the molar ratio of bound tryptophan to albumin. 9)However, some studies have reported either a decrease or no changes in brain serotonin levels following protein malnutrition (PM).10-12) Several experimental studies have focused on the consequences of prenatal (i.e., gestation period) and early postnatal (i.e., lactation period) malnutrition. PM during these developmental stages causes various atypical behaviors in rats, such as reduced anxiety, 13) decreased social interaction, 14) increased depressive behavior, 15) prepulse inhibition deficit 16) and impairment of memory-related behavior. 17) Moreover, a reduction in 5-HT 1A receptor levels and 5-HT uptake sites was reported in the hippocampus of prenatal PM rats.12) Since the 5-HT 1A receptor is considered to be a key receptor via which 5-HT participates in hippocampal dependent learning and memory functions, 18) PM may impact on cognitive performances as well. Thus, it is considered that the developmental period extending from gestation to weaning is critical with regards to PM. However, it has become apparent that brain development continues through adolescence.19) The age range for which the brain is vulnerable to the effects of malnutrition is potentially much greater than previously suspected but the threshold for malnutrition necessary to produce the behavioral alterations is unk...

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Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration

Koçoğlu

Uygul

et al. 2022

Folia Morphol

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Background:Nesfatin-1 is a newly identified satiety peptide that has regulatory effects on food intake and glucose metabolism, and is located in the hypothalamic nuclei, including the supraoptic nucleus (SON). In this study, we have investigated the hypothesis that nesfatin-1 neurons are activated by refeeding and intraperitoneal (ip) glucose injection and that the glutamatergic system has regulatory influences on nesfatin-1 neurons in the SON. Materials and methods:The first set of experiments analyzed activation of nesfatin-1 neurons after refeeding as a physiological stimulus and the effectiveness of the glutamatergic system on this physiological stimulation. The subjects were randomly divided into three groups: fasting group, refeeding group and antagonist (CNQX+refeeding) group. The second set of experiments analyzed activation of nesfatin-1 neurons by glucose injection as a metabolic stimulus and the effectiveness of the glutamatergic system on this metabolic stimulation. The subjects were randomly divided into three groups: saline group, glucose group and antagonist (CNQX+glucose) group. Results:Refeeding significantly increased the number of activated nesfatin-1 neurons by approximately 66%, and intraperitoneal glucose injection activated these neurons by about 55%, compared to the fasting and saline controls. The injections of glutamate antagonist (CNQX) greatly decreased the number of activated nesfatin-1 neurons. Conclusions:This study suggested that nesfatin-1 neurons were activated by peripheral and/or metabolic signals and that this effect was mediated through the glutamatergic system.

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Altered Fos immunoreactivity in the hypothalamus after glucose administration in pre- and post-weaning malnourished rats

Cited by 3 publications

References 49 publications

Early and post-weaning malnutrition impairs alpha-MSH expression in the hypothalamus: a possible link to long-term overweight

Early and post-weaning malnutrition impairs alpha-MSH expression in the hypothalamus: a possible link to long-term overweight

Enhanced Behavioral Response to Serotonin-Related Agonists in Postweaning Protein Malnourished Mice

Glutamate receptor antagonist suppresses the activation of nesfatin-1 neurons following refeeding or glucose administration

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