An inadequate glycaemic response to glucagon is linked to insulin resistance in preterm infants?

Jackson, Lesley; Burchell, Ann; McGeechan, Anne; Hume, Robert

doi:10.1136/fn.88.1.f62

Cited by 23 publications

(12 citation statements)

References 35 publications

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“…These data are in accordance with previous studies showing abnormalities in glucose homeostasis in preterm infants in both neonatal and early infant period [36,37]. Later in life, children and adults born preterm display reduced insulin sensitivity and increased insulin secretion [8,18].…”

Section: Discussionsupporting

confidence: 82%

Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

et al. 2015

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Aims: To investigate whether short children born very preterm (<32 weeks of gestation) exhibit features of growth hormone (GH) resistance compared to term peers. Methods: We studied 26 prepubertal children (aged 7.0 ± 2.0 years) with short stature (height adjusted for parents' heights <10th percentile), who were born appropriate for gestational age and either very preterm (n = 11) or at term (n = 15). Children underwent insulin-like growth factor-1 (IGF-1) generation test via a daily recombinant human GH (rhGH) dose (0.05 mg/kg/day) over 4 consecutive days. Hormone and binding proteins were measured at baseline and day 5. Results: At baseline, preterm children had lower IGF-binding protein 1 (IGFBP-1; -22%; p = 0.049) and IGFBP-3 (-24%; p = 0.013) concentrations than term children. Preterm children also had insulin concentrations that tended to be 39% higher (p = 0.059) than term peers. After stimulation, IGF-1 and IGFBP-3 concentrations increased similarly in term and preterm groups, while GH-binding protein (GHBP) concentrations decreased in both groups. Preterm children had higher GHBP (+50%; p = 0.049), insulin (+86%; p = 0.005), and leptin (+107%; p = 0.020) but lower IGFBP-1 (-47%; p = 0.006) concentrations than term children following rhGH stimulation. Conclusions: Preterm children who are short for genetic height potential show no evidence of GH resistance that would explain their short stature. However, there was indirect evidence of insulin resistance in the preterm children, as previously described in this group.

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Section: Discussionsupporting

confidence: 82%

Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

et al. 2015

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“…Furthermore, the QUICKI has been validated against homeostatic model assessment 52 and has been used in neonates before. 53 Measurement of the QUICKI was carried out at term age and samples taken at the time of routine (pre-feed) blood tests.…”

Section: Quantitative Insulin Sensitivity Check Indexmentioning

confidence: 99%

Nutritional Evaluation and Optimisation in Neonates (NEON) trial of amino acid regimen and intravenous lipid composition in preterm parenteral nutrition: a randomised double-blind controlled trial

et al. 2016

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Health. This issue may be freely reproduced for the purposes of private research and study and extracts (or indeed, the full report) may be included in professional journals provided that suitable acknowledgement is made and the reproduction is not associated with any form of advertising.The WestminsterResearch online digital archive at the University of Westminster aims to make the research output of the University available to a wider audience. Copyright and Moral Rights remain with the authors and/or copyright owners.Whilst further distribution of specific materials from within this archive is forbidden, you may freely distribute the URL of WestminsterResearch: ((http://westminsterresearch.wmin.ac.uk/).In case of abuse or copyright appearing without permission e-mail repository@westminster.ac.uk This journal is a member of and subscribes to the principles of the Committee on Publication Ethics (COPE) (www.publicationethics.org/). EFFICACY AND MECHANISM EVALUATION Efficacy and Mechanism EvaluationEditorial contact: nihredit@southampton.ac.ukThe full EME archive is freely available to view online at www.journalslibrary.nihr.ac.uk/eme. Print-on-demand copies can be purchased from the report pages of the NIHR Journals Library website: www.journalslibrary.nihr.ac.uk Criteria for inclusion in the Efficacy and Mechanism Evaluation journalReports are published in Efficacy and Mechanism Evaluation (EME) if (1) they have resulted from work for the EME programme, and (2) they are of a sufficiently high scientific quality as assessed by the reviewers and editors. EME programmeThe Efficacy and Mechanism Evaluation (EME) programme was set up in 2008 as part of the National Institute for Health Research (NIHR) and the Medical Research Council (MRC) coordinated strategy for clinical trials. The EME programme is broadly aimed at supporting 'science driven' studies with an expectation of substantial health gain and aims to support excellent clinical science with an ultimate view to improving health or patient care.Its remit includes evaluations of new treatments, including therapeutics (small molecule and biologic), psychological interventions, public health, diagnostics and medical devices. Treatments or interventions intended to prevent disease are also included.The EME programme supports laboratory based or similar studies that are embedded within the main study if relevant to the remit of the EME programme. Studies that use validated surrogate markers as indicators of health outcome are also considered.For more information about the EME programme please visit the website: http://www.nets.nihr.ac.uk/programmes/eme This reportThe research reported in this issue of the journal was funded by the EME programme as project number 08/99/04. The contractual start date was in February 2010. The final report began editorial review in January 2015 and was accepted for publication in October 2015. The authors have been wholly responsible for all data collection, analysis and interpretation, and for writing up their work. The EME edit...

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“…Several studies have reported that many neonates produce an inadequate glucose raising response to decreases in glucose infusion [58] and to a bolus of glucagon [73]. Additionally, it has been shown that many preterm infants have concentrations of hepatic glucose-6-phosphatase, the rate limiting enzyme in gluconeogenesis, below the limit of normal term infants [74].…”

Section: Discussionmentioning

confidence: 99%

Modeling the glucose regulatory system in extreme preterm infants

Compte¹,

Chase²,

Russell³

et al. 2011

Computer Methods and Programs in Biomedicine

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BACKGROUNDPremature infants represent a significant proportion of the neonatal intensive care population. Blood glucose homeostasis in this group is often disturbed by immaturity of endogenous regulatory systems and the stress of their condition. Hypo-and hyperglycemia are frequently reported in very low birth weight infants, and more mature infants often experience low levels of glycemia. A model capturing the unique fundamental dynamics of the neonatal glucose regulatory system could be used to develop better blood glucose control methods.

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An inadequate glycaemic response to glucagon is linked to insulin resistance in preterm infants?

Abstract: Some preterm infants show an inadequate glycaemic response to glucagon and have features suggestive of insulin resistance. The potential long term implications of such insulin resistance may have appreciable public health consequences.

Cited by 23 publications

References 35 publications

Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

Response to IGF-1 Generation Test in Short Prepubertal Children Born Very Preterm or at Term

Nutritional Evaluation and Optimisation in Neonates (NEON) trial of amino acid regimen and intravenous lipid composition in preterm parenteral nutrition: a randomised double-blind controlled trial

Modeling the glucose regulatory system in extreme preterm infants

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