Eating disorder in Down’s Syndrome and GLUT-1 Detection
Introduction The results of many previous studies report a high prevalence of overweight and obesity in children and adults with Down syndrome (hereinafter DS). According to different authors, the incidence of obesity in them varies between 23 and 70%. The age of onset of overweight formation was 2–3 years. Objectives Glucose transporter (abbreviated GLUT) is a large group of membrane proteins responsible for the transport of glucose across the cell membrane. Since glucose is a vital source of energy, these proteins are present in all types of living organisms. GLUT, or SLC2A, is a separate family of glucose transport proteins found in most mammalian cells. Thus, the human genome encodes twelve proteins of the GLUT family. They are transport uniporter proteins. Methods We studied PCR of scrapings of the mucous membrane of the inner side of the cheek to search for GLUT1 genes in 31 patients with DS, ьen and women aging from 8 to 39 years. The control group consisted of 67 healthy donors by the same ages and genders. Results It was found that the expression of GLUT1 genes was significantly reduced. A decrease in the expression of these genes correlated with an increase in body weight and symptoms of bulimia in patients with Down syndrome. Conclusions Eating disorders, namely bulimia, in DS is a serious condition that aggravates the course of the underlying disease. Hereditary factors affect the expression of glucose transporter genes. Taking these circumstances into account would help in developing personalized pharmacotherapy. Disclosure of Interest None Declared
Authors
- N. Kolmykova
- Dmitriy Labunskiy (ORCID: https://orcid.org/0000-0001-6629-6682)
- S. Kiryukhina
- V. Podsevatkin
- Г. Кукіна
Institutions
- National Research Mordovia State University (RU)
Publication Details
- Journal
- European Psychiatry
- Published
- 2025-04-01
- DOI
- https://doi.org/10.1192/j.eurpsy.2025.1399
- Primary Topic
- Eating Disorders and Behaviors
- Type
- article
- Field-Weighted Citation Impact
- 0.00