Sex differences in statural growth impairment in Crohnʼs disease: Role of IGF-1

Gupta, Neera; Lustig, Robert H.; Kohn, Michael A.; McCracken, Marjorie F.; Vittinghoff, Eric

doi:10.1002/ibd.21617

Cited by 52 publications

(52 citation statements)

References 42 publications

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“…However, during states of pure malnutrition (such as in anorexia nervosa), IGF-1 levels are low, demonstrating GH resistance [25], [26]. Although IGF-1 is commonly seen as a marker of nutritional status, IGFBP-3 is more stable in states of under nutrition and is more commonly seen as an indicator of adequate GH signaling [27]. That hsCRP was associated with higher GH levels and lower levels of IGF-1 and IGFBP-3 (suggesting lower hepatic response to GH) suggests against poor nutrition as the only reason for these associations, particularly given the lower levels of IGFBP-3 [27].…”

Section: Discussionmentioning

confidence: 99%

Systemic inflammation, growth factors, and linear growth in the setting of infection and malnutrition

et al. 2017

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ObjectivesDeficits in weight gain and linear growth are seen frequently among children in areas where malnutrition and recurrent infections are common. Although both inflammation and malnutrition can result in growth hormone (GH) resistance, the interrelationships of infection, inflammation, and growth deficits in developing areas remain unclear. The aim of this study was to evaluate relationships between low levels of systemic inflammation, growth factors, and anthropometry in a case–control cohort of underweight and normal weight children in northern Brazil.MethodsWe evaluated data from 147 children ages 6 to 24 mo evaluated in the MAL-ED (Interactions of Malnutrition and Enteric Disease) case–control study following recruitment from a nutrition clinic for impoverished families in Fortaleza, Brazil. We used nonparametric tests and linear regression to evaluate relationships between current symptoms of infections (assessed by questionnaire), systemic inflammation (assessed by high-sensitivity C-reactive protein [hsCRP]), the GH insulin-like growth factor-1 (IGF-1) axis, and measures of anthropometry. All models were adjusted for age and sex.ResultsChildren with recent symptoms of diarrhea, cough, and fever (compared with those without symptoms) had higher hsCRP levels; those with recent diarrhea and fever also had lower IGF-1 and higher GH levels. Stool myeloperoxidase was positively associated with serum hsCRP. hsCRP was in turn positively associated with GH and negatively associated with IGF-1 and IGF-binding protein-3 (IGFBP-3), suggesting a state of GH resistance. After adjustment for hsCRP, IGF-1 and IGFBP-3 were positively and GH was negatively associated with Z scores for height and weight.ConclusionsInfection and inflammation were linked to evidence of GH resistance, whereas levels of GH, IGF-1, and IGFBP-3 were associated with growth indices independent of hsCRP. These data implicate complex interrelationships between infection, nutritional status, GH axis, and linear growth in children from a developing area.

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Section: Discussionmentioning

confidence: 99%

Systemic inflammation, growth factors, and linear growth in the setting of infection and malnutrition

et al. 2017

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“…At the initial withdrawl, males and females showed a similar degree of seizure behavior, however, on subsequent withdrawal bouts, males had robust increases in seizure severity while females did not. Interestingly, this was not associated with estrogen levels or with sex differences in blood alcohol levels Veatch et al, 2007), although sex differences in blood IGF-1 levels have been reported (Chaler et al, 2009; Gupta et al, 2011). …”

Section: Introductionmentioning

confidence: 87%

Estrogen-IGF-1 interactions in neuroprotection: Ischemic stroke as a case study

Sohrabji

2015

Frontiers in Neuroendocrinology

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The steroid hormone 17b-estradiol and the peptide hormone insulin-like growth factor (IGF)-1 independently exert neuroprotective actions in neurologic diseases such as stroke. Only a few studies have directly addressed the interaction between the two hormone systems, however, there is a large literature that indicates potentially greater interactions between the 17b-estradiol and IGF-1 systems. The present review focuses on key issues related to this interaction including IGF-1 and sex differences and common activation of second messenger systems. Using ischemic stroke as a case study, this review also focuses on independent and cooperative actions of estrogen and IGF-1 on neuroprotection, blood brain barrier integrity, angiogenesis, inflammation and post-stroke epilepsy. Finally, the review also focuses on the astrocyte, a key mediator of post stroke repair, as a local source of 17b-estradiol and IGF-1. This review thus highlights areas where significant new research is needed to clarify the interactions between these two neuroprotectants.

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“…This suggested influences beyond the delivery of calories alone. Growth deficits not explained by nutrition alone have been proposed to result predominantly from inflammation [19, 20, 21, 22, 23, 24] or from suppression of growth factors in the setting of inflammation [25, 26]. …”

Section: Discussionmentioning

confidence: 99%

Mice with infectious colitis exhibit linear growth failure and subsequent catch-up growth related to systemic inflammation and IGF-1

et al. 2017

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In developing communities, intestinal infection is associated with poor weight gain and linear-growth failure. Prior translational animal models have focused on weight gain investigations into key contributors to linear growth failure have been lacking. We hypothesized that murine intestinal infection with Citrobacter-rodentium would induce linear-growth failure associated with systemic inflammation and suppressed serum levels of insulin-like growth factor-1 (IGF-1). We evaluated 4 groups of mice infected or sham-infected on day-of-life 28: uninfected-controls, wild-type C.-rodentium-infected, partially-attenuated C. rodentium-infected (with deletion of 3 serine protease genes involved in colonization), and pair-fed (given the amount of daily food consumed by the wild-type C.-rodentium group). Relative to the uninfected group, mice infected with wild-type C. rodentium exhibited temporal associations of lower food intake, weight loss, linear-growth failure, higher IL-6 and TNF-α and lower IGF-1. However, relative to the pair-fed group, the C.-rodentium-infected group only differed significantly by linear growth and systemic inflammatory cytokines. Between post-infection days 15–20, the infected group exhibited resolution of systemic inflammation. Between days 16–20, both wild-type C.-rodentium and pair-fed groups exhibited rapid linear-growth velocities exceeding the uninfected and mutant C.-rodentium groups; during this time levels of IGF-1 increased to match the uninfected group. We submit this as a model providing important opportunities to study mechanisms of catch-up growth related to intestinal inflammation. We conclude that in addition to known effects of weight loss, infection with C. rodentium induces linear-growth failure potentially related to systemic inflammation and low levels of IGF-1, with catch-up of linear growth following resolution of inflammation.

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Sex differences in statural growth impairment in Crohnʼs disease: Role of IGF-1

Abstract: Background-Growth impairment in Crohn's disease (CD) is more common in males than females for unknown reasons. Since insulin-like growth factor 1 (IGF-1) is required for statural growth, we hypothesized that IGF-1 levels are lower in males with CD.

Cited by 52 publications

References 42 publications

Systemic inflammation, growth factors, and linear growth in the setting of infection and malnutrition

Systemic inflammation, growth factors, and linear growth in the setting of infection and malnutrition

Estrogen-IGF-1 interactions in neuroprotection: Ischemic stroke as a case study

Mice with infectious colitis exhibit linear growth failure and subsequent catch-up growth related to systemic inflammation and IGF-1

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