Background/aims: Monogenic forms of growth hormone insensitivity (GHI) and its treatment with recombinant insulin-like growth factor-1 (rIGF-1) are both associated with glucose dysregulation. We used the information provided by continuous glucose monitoring systems (CGMS) for the clinical management of two children with monogenic GHI prior to the commencement of therapy as well as during the years when they received rIGF-1 treatment and continued to do so after the cessation of therapy.
Methods: We evaluated the extent of hyper- and hypoglycaemia with CGMS.
Results: In one patient, before treatment CGMS identified self-limiting nocturnal hypoglycaemia. Initiation of rIGF-1 treatment resulted in severe and persistent hypoglycaemia with an absence of spontaneous recovery. Corrective dietary measures were instituted. In a second patient, who had a poor growth response to rIGF-1 therapy, CGMS identified significant fluctuations in daytime glucose levels whilst on treatment with evidence of postprandial hyperglycaemia and both rebound and nocturnal hypoglycaemia. Given the lack of improved growth and the documented glucose dysregulation, treatment was stopped and repeat measurements with CGMS 1 month afterwards showed complete resolution.
Conclusions: We have demonstrated that CGMS is an effective tool to assess glucose dysregulation in patients with GHI and alters clinical management.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1159/000369096 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Metabolic effects of heterocyclic amines on insulin‑induced AKT phosphorylation and gluconeogenic gene expression are modified by N-acetyltransferase 2 genetic polymorphism.
Pharmacogenet Genomics
January 2025
Department of Pharmacology & Toxicology and Brown Cancer Center, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Objective: Heterocyclic amines (HCAs) are mutagens and carcinogens primarily generated when cooking meat at high temperatures or until well-done, and their major metabolic pathway includes hepatic N-hydroxylation via CYP1A2 followed by O-acetylation via N-acetyltransferase 2 (NAT2). NAT2 expresses a well-defined genetic polymorphism in humans resulting in rapid and slow acetylators. Recent epidemiological studies reported significant associations between dietary HCA exposure and insulin resistance and type II diabetes.
View Article and Find Full Text PDFType 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.
Burns Trauma
January 2025
Department of Critical Care Medicine, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, No. 321 Zhongshan Road, Gulou District, Nanjing, Jiangsu 210008, China.
Background: Non-thyroidal illness syndrome is commonly observed in critically ill patients, characterized by the inactivation of systemic thyroid hormones (TH), which aggravates metabolic dysfunction. Recent evidence indicates that enhanced TH inactivation is mediated by the reactivation of type 3 deiodinase (Dio3) at the tissue level, culminating in a perturbed local metabolic equilibrium. This study assessed whether targeted inhibition of Dio3 can maintain tissue metabolic homeostasis under septic conditions and explored the mechanism behind Dio3 reactivation.
View Article and Find Full Text PDFGlycolysis in asthma: Its role and potential as a diagnostic or therapeutic target.
Int Immunopharmacol
January 2025
Department of Respiratory and Critical Care Medicine, The Second Hospital of Jilin University, Changchun, Jilin, China. Electronic address:
Asthma is a heterogeneous disease characterized by chronic airway inflammation and hyperresponsiveness. A number of immune cells are involved in asthma pathogenesis, such as eosinophils, mast cells, T lymphocytes and neutrophils, as well as airway epithelial cells. Glycolysis plays a crucial role in glucose metabolism, and serves as a bridge between metabolic and inflammatory dysfunction.
View Article and Find Full Text PDFPrimitive to visceral endoderm maturation is essential for mouse epiblast survival beyond implantation.
iScience
January 2025
Mammalian Embryo and Stem Cell Group, University of Cambridge, Department of Physiology, Development and Neuroscience, Downing Street, Cambridge CB2 3DY, UK.
The implantation of the mouse blastocyst initiates a complex sequence of tissue remodeling and cell differentiation events required for morphogenesis, during which the extraembryonic primitive endoderm transitions into the visceral endoderm. Through single-cell RNA sequencing of embryos at embryonic day 5.0, shortly after implantation, we reveal that this transition is driven by dynamic signaling activities, notably the upregulation of BMP signaling and a transient increase in Sox7 expression.
View Article and Find Full Text PDFSemaglutide and laparoscopic sleeve gastrectomy in an adolescent with congenital adrenal hyperplasia due to 21-hydroxylase: a case report.
J Med Case Rep
January 2025
Department of Surgery, Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles and Keck School of Medicine of USC, Los Angeles, CA, USA.
Background: Classic congenital adrenal hyperplasia, primarily due to 21-hydroxylase deficiency, leads to impaired cortisol and aldosterone production and excess adrenal androgens. Lifelong glucocorticoid therapy is required, often necessitating supraphysiological doses in youth to manage androgen excess and growth acceleration. These patients experience higher obesity rates, hypertension, and glucose metabolism issues, complicating long-term health management.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!