ArticleEndocrine connections2013
Lifetime congenital isolated GH deficiency does not protect from the development of diabetes.
Article in Endocrine connections, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- The state of Sergipe contribution to GH research: from Souza Leite to Itabaianinha syndrome.Archives of endocrinology and metabolism · 2022Review
- Do patients with Prader-Willi syndrome have favorable glucose metabolism?Orphanet journal of rare diseases · 2022Review
- Article
- Disruption of the GHRH receptor and its impact on children and adults: The Itabaianinha syndrome.Reviews in endocrine & metabolic disorders · 2021Review
- Growth Hormone Deficiency: Health and Longevity.Endocrine reviews · 2019Review
- Developments in our understanding of the effects of growth hormone on white adipose tissue from mice: implications to the clinic.Expert review of endocrinology & metabolism · 2016Article
- GH Receptor Deficiency in Ecuadorian Adults Is Associated With Obesity and Enhanced Insulin Sensitivity.The Journal of clinical endocrinology and metabolism · 2015Article
- Obesity, diabetes and cancer: insight into the relationship from a cohort with growth hormone receptor deficiency.Diabetologia · 2015Review
- Differential impact of selective GH deficiency and endogenous GH excess on insulin-mediated actions in muscle and liver of male mice.American journal of physiology. Endocrinology and metabolism · 2014Article
- Article
- Long- but not short-term adult-onset, isolated GH deficiency in male mice leads to deterioration of β-cell function, which cannot be accounted for by changes in β-cell mass.Endocrinology · 2014Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesAdult subjects with untreated, lifetime, isolated GH deficiency (IGHD) due to a homozygous GHRH receptor gene mutation (MUT/MUT) residing in Itabaianinha, Brazil, present with lower BMI, higher prevalence of impaired glucose tolerance (IGT), increased insulin sensitivity (IS), and reduced β-cell function (βCF) when compared with non-BMI-matched homozygous normal controls. However, the prevalence of diabetes mellitus (DM) in this cohort is unknown. Comparing their IS and βCF with BMI-matched individuals heterozygous for the same mutation (MUT/N) may be useful to elucidate the role of the GH-IGF1 axis in IS and βCF. The purposes of this work were to verify the prevalence of IGT and DM in adult MUT/MUT subjects from this kindred and to compare IS and βCF in MUT/MUT and MUT/N.
designCross-sectional study.
methodsWe studied most (51) of the living IGHD adults of this kindred who are GH naive. The oral glucose tolerance test (OGTT) could be performed in 34 subjects, fasting glucose was measured in 15, while two had a previous diagnosis of DM. The OGTT results of 24 MUT/MUT subjects were compared with those of 25 BMI-matched MUT/N subjects. IS was assessed by homeostatic model assessment of insulin resistance (HOMA-IR), quantitative IS check index, and oral glucose IS index for 2 and 3 h. βCF was assayed by HOMA-β, insulinogenic index, and the area under the curve of insulin:glucose ratio.
resultsThe prevalence of DM and IGT in IGHD was 15.68 and 38.23% respectively. IS was increased and βCF was reduced in MUT/MUT in comparison with MUT/N.
conclusionsLifetime, untreated IGHD increases IS, impairs βCF, and does not provide protection from diabetes.
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