Effects of early postnatal growth restriction and subsequent catch-up growth on body composition, insulin sensitivity, and behavior in neonatal rats

Jou, Ming Yu; Lönnerdal, Bo; Griffin, Ian J.

doi:10.1038/pr.2013.27

Cited by 15 publications

(19 citation statements)

References 19 publications

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“…; Jou et al . ) have shown more rapid recovery of body weight when pups were refed on a higher plane of nutrition than in our study. This rapid refeeding, however, was associated with greater adipose tissue accretion; skeletal muscle was not evaluated.…”

Section: Discussioncontrasting

confidence: 49%

Ribosome abundance regulates the recovery of skeletal muscle protein mass upon recuperation from postnatal undernutrition in mice

Fiorotto

Davis

Sosa

et al. 2014

The Journal of Physiology

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Key pointsr Inadequate nutrient intake during early life can programme a low adult muscle mass. We have used a mouse model to identify the developmental window when the skeletal musculature is vulnerable to programming and to identify factors that limit the muscle's ability to respond when normal nutrition is restored.r We established that the developmental age when nutritional rehabilitation occurs following an episode of poor nutrition, rather than the duration or severity of the nutrient restriction, is the critical factor that determines if muscle mass can be recuperated.r The ability to recover depends on whether the muscles' translational capacity, i.e. ribosomal abundance, can increase sufficiently to raise protein synthesis rates sufficiently to accelerate protein deposition.r We show that the ability to increase ribosomal abundance was associated with increased expression of the nucleolar transcription factor UBF (upstream binding factor), which regulates RNA polymerase 1 activity and rRNA transcription, the limiting factor for ribosomal production.Abstract Nutritionally-induced growth faltering in the perinatal period has been associated with reduced adult skeletal muscle mass; however, the mechanisms responsible for this are unclear. To identify the factors that determine the recuperative capacity of muscle mass, we studied offspring of FVB mouse dams fed a protein-restricted diet during gestation (GLP) or pups suckled from postnatal day 1 (PN1) to PN11 (E-UN), or PN11 to PN22 (L-UN) on protein-restricted or control dams. All pups were refed under control conditions following the episode of undernutrition. Before refeeding, and 2, 7 and 21 days later, muscle protein synthesis was measured in vivo. There were no long-term deficits in protein mass in GLP and E-UN offspring, but in L-UN offspring muscle protein mass remained significantly smaller even after 18 months (P < 0.001). E-UN differed from L-UN offspring by their capacity to upregulate postprandial muscle protein synthesis when refed (P < 0.001), a difference that was attributable to a transient increase in ribosomal abundance, i.e. translational capacity, in E-UN offspring (P < 0.05); translational efficiency was similar across dietary treatments. The postprandial phosphorylation of Akt and extracellular signal-regulated protein kinases were similar among treatments. However, activation of the ribosomal S6 kinase 1 via mTOR (P < 0.02), and total upstream binding factor abundance were significantly greater in E-UN than L-UN offspring (P < 0.02). The results indicate that the capacity of muscles to recover following perinatal undernutrition depends on developmental age as this establishes whether ribosome abundance can be enhanced sufficiently to promote the protein synthesis rates required to accelerate protein deposition for catch-up growth.

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Section: Discussioncontrasting

confidence: 49%

Ribosome abundance regulates the recovery of skeletal muscle protein mass upon recuperation from postnatal undernutrition in mice

Fiorotto

Davis

Sosa

et al. 2014

The Journal of Physiology

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“…The floor of the dark chamber was composed of a metal grid through which a small electrical charge (2.0 mA) could be passed. Testing was carried out over 2d: a training (habituation) day and a testing (learning) day as previously described [18, 19]. Data are expressed as time (s) taken to enter the dark chamber on d2 of the test, designated as retention latency.…”

Section: Methodsmentioning

confidence: 99%

Effects of iron supplementation on growth, gut microbiota, metabolomics and cognitive development of rat pups

Alexeev

Slupsky

et al. 2017

PLoS ONE

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BackgroundIron deficiency is common during infancy and therefore iron supplementation is recommended. Recent reports suggest that iron supplementation in already iron replete infants may adversely affect growth, cognitive development, and morbidity.MethodsNormal and growth restricted rat pups were given iron daily (30 or 150 μg/d) from birth to postnatal day (PD) 20, and followed to PD56. At PD20, hematology, tissue iron, and the hepatic metabolome were measured. The plasma metabolome and colonic microbial ecology were assessed at PD20 and PD56. T-maze (PD35) and passive avoidance (PD40) tests were used to evaluate cognitive development.ResultsIron supplementation increased iron status in a dose-dependent manner in both groups, but no significant effect of iron on growth was observed. Passive avoidance was significantly lower only in normal rats given high iron compared with controls. In plasma and liver of normal and growth-restricted rats, excess iron increased 3-hydroxybutyrate and decreased several amino acids, urea and myo-inositol. While a profound difference in gut microbiota of normal and growth-restricted rats was observed, with iron supplementation differences in the abundance of strict anaerobes were observed.ConclusionExcess iron adversely affects cognitive development, which may be a consequence of altered metabolism and/or shifts in gut microbiota.

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“…The passive avoidance test was performed according to the protocol described by Jou et al (21) with slight changes. It was a 3-d test, including habituation, training, and testing.…”

Section: Passive Avoidance Testmentioning

confidence: 99%

Milk osteopontin promotes brain development by up‐regulating osteopontin in the brain in early life

Jiang

Prell²,

Lönnerdal

2018

FASEB j.

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Osteopontin (OPN) is a pleiotropic protein and is abundantly present in milk. Its functions include immune modulation and cellular proliferation and differentiation. OPN is highly expressed in the brain. We investigated the effects of milk-derived OPN on brain development of mouse pups. Wild-type (WT) dams producing OPN milk and OPN knockout (KO) dams producing OPN milk nursed WT pups (OPN), yielding 2 pup treatment groups, OPN OPN and OPN OPN, for comparison. Preliminary studies supported use of this model by showing high concentrations of OPN in milk of WT dams and no OPN in milk of OPN KO dams, and production of similar amounts of milk by WT and KO dams. The ability of ingested milk OPN to enter the brain was revealed by appearance of orally gavaged [I]-labeled and antibody-probed milk OPN in brains of pups. Brain OPN mRNA levels were similar in both nursed groups, but the brain OPN protein level was significantly lower in the OPN OPN group at postnatal days 6 and 8. Behavior tests showed impaired memory and learning ability in OPN OPN pups. In addition, our study revealed increased expression of myelination-related proteins and elevated proliferation and differentiation of NG-2 glia into oligodendrocytes in the brain of OPN OPN pups, accompanied by increased activation of ERK-1/2 and PI3K/Akt signaling. We concluded that milk OPN can play an important role in brain development and behavior in infancy by promoting myelination.-Jiang, R., Prell, C., Lönnerdal, B. Milk osteopontin promotes brain development by up-regulating osteopontin in the brain in early life.

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Effects of early postnatal growth restriction and subsequent catch-up growth on body composition, insulin sensitivity, and behavior in neonatal rats

Abstract: Early postnatal growth retardation is associated with poorer medium-term growth and poorer developmental outcome. Increased catch-up growth is associated with improved developmental outcome but with increased body adiposity, without any significant effect on glucose homeostasis.

Cited by 15 publications

References 19 publications

Ribosome abundance regulates the recovery of skeletal muscle protein mass upon recuperation from postnatal undernutrition in mice

Ribosome abundance regulates the recovery of skeletal muscle protein mass upon recuperation from postnatal undernutrition in mice

Effects of iron supplementation on growth, gut microbiota, metabolomics and cognitive development of rat pups

Milk osteopontin promotes brain development by up‐regulating osteopontin in the brain in early life

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