Nutritional Regulation of IGF-I Expression during Brain Development in Mice

Çalıkoğlu, Ali S.; Karayal, Aysen F.; D’Ercole, A. Joseph

doi:10.1203/00006450-200102000-00011

Cited by 31 publications

(19 citation statements)

References 34 publications

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“…Representative hematoxylin and eosin histology (original magnification ×100) of distal ileal sections from the experimental mice at day 27 after weaning and refeeding. Blunted expression of IGF-1 in the ileum mucosa from malnourished apoE null mice at day 27 (B and D), after the refeeding protocol (day [21][22][23][24][25][26][27], in comparison with the rehabilitated malnourished wild-type controls (A and C), using immunoblotting and immunohistochemistry, respectively. Distal ileum sections were used at 200× magnification for panels C and D. Insulinlike growth factor α receptor expression from distal ileal sections (original magnification ×100).…”

Section: Discussionmentioning

confidence: 99%

“…Newborn litters were adjusted to 7 to 8 pups. Undernutrition was induced by separating half the pups in each litter from their lactating dams for defined periods each day (4 hours on day 1, 8 hours on day 2, and 12 hours thereafter), according to protocol adapted from Calikoglu et al [21]. Both apoE-ko and wild-type mice underwent the same protocol for induction of undernutrition.…”

Section: Undernutrition Modelmentioning

confidence: 99%

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Apolipoprotein E knockout mice have accentuated malnutrition with mucosal disruption and blunted insulin-like growth factor I responses to refeeding

et al. 2006

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Apolipoprotein E (apoE) is synthesized mainly in the liver and in the brain and is critical for cholesterol metabolism and recovery from brain injury. However, although apoE mRNA increases at birth, during suckling, and after fasting in rat liver, little is known about its role in early postnatal development. Using an established postnatal malnutrition model and apoE knock-out (ko) mice, we examined the role of apoE in intestinal adaptation responses to early postnatal malnutrition. Wild-type and apoE-ko mice were separated from their lactating dams for defined periods each day (4 hours on day 1, 8 hours on day 2, and 12 hours thereafter). We found significant growth deficits, as measured by weight gain or tail length, in the apoE-ko mice submitted to a malnutrition challenge, as compared with malnourished wild type, especially during the second week of postnatal development (P < .05). In addition, apoE-ko animals failed to show growth catch-up after refeeding, compared with wild-type malnourished controls. Furthermore, we found shorter crypts and reduced villus height and area in the apoE-ko malnourished mice, compared with controls, after refeeding. Insulinlike growth factor 1 expression was also blunted in the ileum in apoE-ko mice after refeeding, compared with wild-type controls, which exhibited full insulinlike growth factor 1 expression along the intestinal crypts, villi, and in the muscular layer. Taken together, these findings suggest the importance of apoE in coping with a malnutrition challenge and during the intestinal adaptation after refeeding. NIH Public Access

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Section: Discussionmentioning

confidence: 99%

Section: Undernutrition Modelmentioning

confidence: 99%

Apolipoprotein E knockout mice have accentuated malnutrition with mucosal disruption and blunted insulin-like growth factor I responses to refeeding

et al. 2006

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“…50−53 In the case of nutrient depletion, the relative preservation of brain growth to organ growth appears to be due to several mechanisms including a direct signaling of tyrosine kinases that is uncoupled from the mTOR pathway in the brain, 54 or differential regulation of the IGF1 pathway in the brain. 53 Thus, it appears that 5-HT would not be essential in such mechanisms preserving brain growth in the face of nutrient loss.…”

Section: Acs Chemical Neurosciencementioning

confidence: 99%

Postnatal Growth Defects in Mice with Constitutive Depletion of Central Serotonin

Narboux-Nême

Angenard

Mosienko

et al. 2012

ACS Chem. Neurosci.

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Although the trophic actions of serotonin (5-HT) are well established, only few developmental defects have been reported in mouse strains with constitutive hyposerotonergia. We analyzed postnatal growth and cortical development in three different mutant mouse strains with constitutive reductions in central 5-HT levels. We compared two previously published mouse strains with severe (−95%) depletions of 5-HT, the tryptophan hydroxylase (Tph) 2 −/− mouse line and VMAT2 sert-cre mice, with a new strain, in which VMAT2 deletion is driven by Pet1 (VMAT2 pet1-cre ) in 5-HT raphe neurons leading to partial (−75%) reduction in brain 5-HT levels. We find that normal embryonic growth and postnatal growth retardation are common features of all these mouse strains. Postnatal growth retardation varied from mild to severe according to the extent of the brain 5-HT reduction and gender. Normal growth was reinstated in VMAT2 sert-cre mice by reconstituting central 5-HT stores. Growth abnormalities could not be linked to altered food intake or temperature control. Morphological study of the cerebral cortex over postnatal development showed a delayed maturation of the upper cortical layers in the VMAT2 sert-cre and Tph2 −/− mice, but not in the VMAT2 pet1-cre mice. No changes in layer-specific gene expression or morphological alterations of barrel cortex development were found. Overall, these observations sustain the notion that central 5-HT signaling is required for the preweaning growth spurt of mouse pups. Brain development appeared to be immune to severe central 5-HT depletion for its overall growth during prenatal life, whereas reduced brain growth and delayed cortical maturation development occurred during postnatal life. Reduced developmental 5-HT signaling during postnatal development might modulate the function and fine structure of neural circuits in ways that affect adult behavior.

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“…Furthermore, recent evidence indicates that long-lasting decrements in hippocampal plasticity occur in mice subjected to early environmental stress, such as maternal separation [6,7]. It has also been shown that undernutrition reduces peripheral circulating concentrations of insulin-like growth factor (IGF-1) [8]. …”

Section: Introductionmentioning

confidence: 99%

Prolonged maternal separation induces undernutrition and systemic inflammation with disrupted hippocampal development in mice

et al. 2016

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Objective Prolonged maternal separation (PMS) in the first two weeks of life has been associated with poor growth with lasting effects in the brain structure and function. This study aimed to investigate whether PMS-induced undernutrition could cause systemic inflammation and changes in nutrition-related hormonal levels, affecting hippocampal structure and neurotransmission in C57BL/6J suckling mice. Methods This study assessed mouse growth parameters coupled with IGF-1 serum levels. In addition, leptin, adiponectin and corticosterone serum levels were measured following PMS. Hippocampal stereology and the amino acid levels were also assessed. Furthermore, we measured myelin basic protein and synapthophysin (SYN) expression in the overall brain tissue and hippocampal SYN immunolabeling. For behavioral tests, we analyzed the ontogeny of selected neonatal reflexes. PMS was induced by separating half the pups in each litter from their lactating dams for defined periods each day (4h on day 1, 8h on day 2, and 12h thereafter). A total of 67 suckling pups were used in this study. Results PMS induced significant slowdown in weight gain and growth impairment. Significant reductions in serum leptin and IGF-1 levels were found following PMS. Total CA3 area and volume were reduced, specifically affecting the pyramidal layer in PMS mice. CA1 pyramidal layer area was also reduced. Overall hippocampal SYN immunolabeling was lower, especially in CA3 field and dentate gyrus. Furthermore, PMS reduces hippocampal aspartate, glutamate, and GABA levels, as compared with unseparated controls. Conclusion Altogether, these findings suggest that PMS causes significant growth deficits and alterations in hippocampal morphology and neurotransmission.

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Nutritional Regulation of IGF-I Expression during Brain Development in Mice

Cited by 31 publications

References 34 publications

Apolipoprotein E knockout mice have accentuated malnutrition with mucosal disruption and blunted insulin-like growth factor I responses to refeeding

Apolipoprotein E knockout mice have accentuated malnutrition with mucosal disruption and blunted insulin-like growth factor I responses to refeeding

Postnatal Growth Defects in Mice with Constitutive Depletion of Central Serotonin

Prolonged maternal separation induces undernutrition and systemic inflammation with disrupted hippocampal development in mice

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