Growth Hormone Secretion in Protein Energy Malnutrition

Günöz, Hülya; Neyzi, Olcay; E, Sencer; Molvalílar, S; Argün, Ali Saltuk

doi:10.1111/j.1651-2227.1981.tb05734.x

Cited by 5 publications

(1 citation statement)

References 21 publications

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“…No entanto, o aumento na resposta observado nos grupos PC-N e PC-R, que pode ser comparável entre os dois grupos, foi melhor do que o observado no grupo DPE, apesar de a resposta não ter sido tão elevada quanto a dos controles normais e ainda ser considerada como secreção subnormal de GH. Esses achados podem indicar que os pacientes com DPE não foram capazes de obter uma resposta adequada do GH ao estímulo com hipoglicemia insulínica, conforme também observou Günöz et al 16 . Nos portadores de PC, a doença pode estar relacionada a uma resposta hipofisária subnormal, o que é evidenciado pelo nível significativamente menor de GH basal em nossos pacientes com PC se comparados aos pacientes com DPE, especialmente se considerarmos a possibilidade de uma deficiência nutricional não identificada no grupo PC-R. Além disso, os valores de GH após estímulo foram significativamente menores no grupo PC-R se comparados aos do grupo REF (p c = 0,04), e até mesmo as crianças com PC-N não foram capazes de aumentar significativamente os níveis de GH (≥ 10 ng/mL) e apresentaram pico de GH mais baixo do que o dos controles normais.…”

Section: Discussionunclassified

Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy

Hegazi¹,

Soliman²,

Hasaneen³

et al. 2012

J Pediatr (Rio J)

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Objective: To assess growth hormone (GH)/insulin like growth factor-1 (IGF-1) axis as a possible non-nutritional factor for growth retardation in children with cerebral palsy (CP). Methods:A case-control study was conducted at a tertiary university hospital. Thirty children with CP (seven children with normal growth [CP-N] and 23 with retarded growth [CP-R]), 30 children with protein energy malnutrition (PEM), and 30 healthy children (REF group) underwent an assessment of growth parameters, serum IGF-1, basal GH, and peak GH after stimulation with insulin.Results: PEM patients had higher basal GH levels than CP-N, CP-R and REF groups (p = 0.026, p < 0.001, and p < 0.001 respectively). After insulin stimulation, CP-N, CP-R, and PEM patients had lower GH levels compared to the REF group (p = 0.04, p = 0.007, and p = 0.036 respectively). IGF-1 levels were lower in CP-R group compared to CP-N and REF groups (p = 0.037 and p < 0.001 respectively), and in PEM group compared to CP-N and REF groups (p < 0.001 and p < 0.001 respectively). Conclusions:CP-R patients failed to demonstrate the same high basal GH response as PEM patients, and responded inadequately to the insulin stimulation test, but they had IGF-1 levels comparable to those of PEM patients. On the other hand, CP-N patients behaved as controls regarding their basal GH and IGF-1 levels, but failed to respond adequately to the insulin stimulation test. The PEM group presented high basal GH and low IGF-1 levels. These findings suggest that nonnutritional factors contribute to growth retardation in CP children. J Pediatr (Rio J). 2012;88(3):267-74:GH, IGF-1, cerebral palsy, children. ResumoObjetivo: Avaliar o eixo hormônio de crescimento (GH)/fator de crescimento semelhante à insulina 1 (IGF-1) como possível fator não nutricional para o retardo de crescimento em crianças com paralisia cerebral (PC). Conclusões:Os pacientes com PC-R não demonstraram a mesma resposta basal elevada do GH apresentada pelos pacientes com DPE, e responderam de forma inadequada ao estímulo com insulina, mas apresentaram níveis de IGF-1 comparáveis aos dos pacientes com DPE. Por outro lado, os pacientes com PC-N tiveram comportamento semelhante ao dos controles com relação aos níveis basais de GH e IGF-1, mas não responderam adequadamente ao estímulo com insulina. O grupo DPE apresentou GH basal elevado e IGF-1 baixo. Esses achados sugerem que fatores não nutricionais contribuem para o retardo de crescimento em crianças com PC. Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy Não foram declarados conflitos de interesse associados à publicação deste artigo.Como citar este artigo: Hegazi MA, Soliman OE, Hasaneen BM, El-Arman M, El-Galel NA, El-Deek BS. Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy. J Pediatr (Rio J). 2012;88(3):267-74.Artigo submetido em 27.11.11, aceito em 14.03.12.http://dx

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Section: Discussionunclassified

Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy

Hegazi¹,

Soliman²,

Hasaneen³

et al. 2012

J Pediatr (Rio J)

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Diverging metabolic programmes and behaviours during states of starvation, protein malnutrition, and cachexia

Olson

Marks

Grossberg

2020

J cachexia sarcopenia muscle

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Background Our evolutionary history is defined, in part, by our ability to survive times of nutrient scarcity. The outcomes of the metabolic and behavioural adaptations during starvation are highly efficient macronutrient allocation, minimization of energy expenditure, and maximized odds of finding food. However, in different contexts, caloric deprivation is met with vastly different physiologic and behavioural responses, which challenge the primacy of energy homeostasis. Methods We conducted a literature review of scientific studies in humans, laboratory animals, and non-laboratory animals that evaluated the physiologic, metabolic, and behavioural responses to fasting, starvation, protein-deficient or essential amino acid-deficient diets, and cachexia. Studies that investigated the changes in ingestive behaviour, locomotor activity, resting metabolic rate, and tissue catabolism were selected as the focus of discussion. Results Whereas starvation responses prioritize energy balance, both protein malnutrition and cachexia present existential threats that induce unique adaptive programmes, which can exacerbate the caloric insufficiency of undernutrition. We compare and contrast the behavioural and metabolic responses and elucidate the mechanistic pathways that drive state-dependent alterations in energy seeking and partitioning. Conclusions The evolution of energetically inefficient metabolic and behavioural responses to protein malnutrition and cachexia reveal a hierarchy of metabolic priorities governed by discrete regulatory networks.

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Insulin-like growth factor (IGF) and IGF binding proteins in growth hormone dysregulation and abnormal glucose tolerance in small cell lung cancer patients

Reeve

Morgan

Clark

et al. 1995

European Journal of Cancer

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Growth Hormone Secretion in Protein Energy Malnutrition

Cited by 5 publications

References 21 publications

Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy

Growth hormone/insulin-like growth factor-1 axis: a possible non-nutritional factor for growth retardation in children with cerebral palsy

Diverging metabolic programmes and behaviours during states of starvation, protein malnutrition, and cachexia

Insulin-like growth factor (IGF) and IGF binding proteins in growth hormone dysregulation and abnormal glucose tolerance in small cell lung cancer patients

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