ArticlePloS one2014
Whole-body insulin sensitivity rather than body-mass-index determines fasting and post-glucose-load growth hormone concentrations.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- High Incidence of Diabetes Mellitus After Distal Pancreatectomy and Its Predictors: A Long-term Follow-up Study.The Journal of clinical endocrinology and metabolism · 2024Article
- Increased GH/IGF-I Axis Activity Relates to Lower Hepatic Lipids and Phosphor Metabolism.The Journal of clinical endocrinology and metabolism · 2023Article
- Single Point Insulin Sensitivity Estimator in Pediatric Non-Alcoholic Fatty Liver Disease.Frontiers in endocrinology · 2022Article
- [The role of glucose and insulin in the metabolic regulation of growth hormone secretion].Problemy endokrinologii · 2021Review
- Is GH nadir during OGTT a reliable test for diagnosis of acromegaly in patients with abnormal glucose metabolism?Endocrine · 2019Article
- Updates in Diagnosis and Treatment of Acromegaly.European endocrinology · 2018Review
- Review
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9 authors at 2 institutions in 2 countries.
Funding
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Abstract
backgroundObese, non-acromegalic persons show lower growth hormone (GH) concentrations at fasting and reduced GH nadir during an oral glucose tolerance test (OGTT). However, this finding has never been studied with regard to whole-body insulin-sensitivity as a possible regulator.
methodsIn this retrospective analysis, non-acromegalic (NonACRO, n = 161) and acromegalic (ACRO, n = 35), non-diabetic subjects were subdivided into insulin-sensitive (IS) and -resistant (IR) groups according to the Clamp-like Index (CLIX)-threshold of 5 mg · kg(-1) · min(-1) from the OGTT.
resultsNon-acromegalic IS (CLIX: 8.8 ± 0.4 mg · kg(-1) · min(-1)) persons with similar age and sex distribution, but lower (p < 0.001) body-mass-index (BMI = 25 ± 0 kg/m2, 84% females, 56 ± 1 years) had 59% and 70%, respectively, higher (p < 0.03) fasting GH and OGTT GH area under the curve concentrations than IR (CLIX: 3.5 ± 0.1 mg · kg(-1) · min(-1), p < 0.001) subjects (BMI = 29 ± 1 kg/m2, 73% females, 58 ± 1 years). When comparing on average overweight non-acromegalic IS and IR with similar anthropometry (IS: BMI: 27 ± 0 kg/m2, 82% females, 58 ± 2 years; IR: BMI: 27 ± 0 kg/m2, 71% females, 60 ± 1 years), but different CLIX (IS: 8.7 ± 0.9 vs. IR: 3.8 ± 0.1 mg · kg(-1) · min(-1), p < 0.001), the results remained almost the same. In addition, when adjusted for OGTT-mediated glucose rise, GH fall was less pronounced in IR. In contrast, in acromegalic subjects, no difference was found between IS and IR patients with regard to fasting and post-glucose-load GH concentrations.
conclusionsCirculating GH concentrations at fasting and during the OGTT are lower in non-acromegalic insulin-resistant subjects. This study seems the first to demonstrate that insulin sensitivity rather than body-mass modulates fasting and post-glucose-load GH concentrations in non-diabetic non-acromegalic subjects.
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