SavedAdd your journal

Journals / Batı Karadeniz Tıp Dergisi / 2026 / Cilt: 9 Sayı: 2

The Association between GHRL and LEP Gene Polymorphisms and ADHD: Evidence from a Pediatric Cohort

GHRL ve LEP Gen Polimorfizmleri ile DEHB Arasındaki İlişki: Pediatrik Kohorttan Kanıtlar

Ali Atabek Kilic(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0009-0003-1612-7591
Nilfer Şahin(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0000-0001-7120-1561
Aysegul Demirtas Bilgic(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0000-0002-6490-0169
Çilem Özdemir(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0000-0002-3821-3621
Murat Cenik(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0009-0002-6517-4522
Tuba Edgünlü(MUGLA SITKI KOCMAN UNIVERSITY, FACULTY OF MEDICINE)0000-0002-9300-9324
Pages
214–221
Publication Date
2025-08-31
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Further research is required to elucidate the mechanisms underlying this association.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Aim: Dopaminergic neurons and dopamine transporters show variations in Attention Deficit Hyperactivity Disorder (ADHD).
📊
Key Findings & Data:Furthermore, Ghrelin and leptin, hormones recognized for their neurotrophic effects, are significant in central nervous system regulation, influencing neuronal survival and development.
💡
Conclusion & Impact:Further research is required to elucidate the mechanisms underlying this association.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:DEHB · Gelişim · GHRL

Abstract

Aim: Dopaminergic neurons and dopamine transporters show variations in Attention Deficit Hyperactivity Disorder (ADHD). Furthermore, Ghrelin and leptin, hormones recognized for their neurotrophic effects, are significant in central nervous system regulation, influencing neuronal survival and development. Material and Methods: This study aimed to examine the potential relationship between Attention Deficit Hyperactivity Disorder (ADHD) and polymorphisms in the GHRL (rs34911341) and LEP (rs7799039) genes. The research sample consisted of 29 children diagnosed with ADHD and 24 age-matched healthy controls. Genotypic analysis was conducted using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: A significant difference in genotype distribution for the GHRL gene rs34911341 polymorphism was observed between the ADHD group and healthy controls (p = 0.036), whereas allele frequencies did not show a statistically significant difference (p = 0.207). In contrast, analysis of the LEP gene rs7799039 polymorphism revealed no significant differences in either genotype (p = 0.579) or allele frequencies (p = 0.558) between the two groups. Conclusion: These findings suggest a potential role for the GHRL rs34911341 polymorphism in the development or presentation of ADHD. Further research is required to elucidate the mechanisms underlying this association.

Özet

Amaç: Dopaminerjik nöronlar ve dopamin taşıyıcıları Dikkat Eksikliği Hiperaktivite Bozukluğu'nda (DEHB) farklılıklar gösterir. Ayrıca, nörotrofik etkileriyle tanınan hormonlar olan Ghrelin ve leptin, nöronal sağ kalımı ve gelişimi etkileyerek merkezi sinir sistemi düzenlemesinde önemlidir. Gereç ve Yöntemler: Bu çalışmanın amacı, DEHB ile GHRL (rs34911341) ve LEP (rs7799039) polimorfizmleri arasındaki ilişkiyi araştırmaktır. Çalışmaya DEHB tanısı almış 29 çocuk ve 24 sağlıklı çocuk dahil edildi. Genotipleme, PCR-RFLP (polimeraz zincir reaksiyonu-restriksiyon parça uzunluğu polimorfizmi) yöntemi aracılığıyla gerçekleştirildi. Bulgular: GHRL geni rs34911341 polimorfizminin genotip sıklığı, DEHB ve sağlıklı kontrol grupları arasında önemli ölçüde farklılık gösterdi (p=0,036), ancak alel sıklıkları önemli ölçüde farklılık göstermedi (p=0,207). LEP rs7799039 polimorfizmi için, iki grup arasında ne genotip ne de alel frekansları farklı değildi (genotip frekansı için p=0,579; alel frekansı için p=0,558). Sonuç: Bu bulgular, GHRL rs34911341 polimorfizminin DEHB'nin gelişiminde veya sunumunda potansiyel bir rolü olduğunu göstermektedir. Bu ilişkinin altında yatan mekanizmaları açıklamak için daha fazla araştırma gerekmektedir.

🔖

Cite This Article

Kilic, A. A., Şahin, N., Bilgic, A. D., Özdemir, Ç., Cenik, M., Edgünlü, T. (2025). The Association between GHRL and LEP Gene Polymorphisms and ADHD: Evidence from a Pediatric Cohort. Batı Karadeniz Tıp Dergisi, Cilt: 9 Sayı: 2, 214–221. https://doi.org/10.29058/mjwbs.1641420

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (22)

  1. Faraone, S. V., Asherson, P., Banaschewski, T., Biederman, J., Buitelaar, J. K., Ramos-Quiroga, J. A., Rohde, L. A., Sonuga- Barke, E. J. S., Tannock, R., & Franke, B. (2015). Attention- deficit/hyperactivity disorder. Nature Reviews Disease Primers, 1, Article 15020.
  2. Alvarez-Crespo, M., Skibicka, K. P., Farkas, I., Molnár, C. S., Egecioglu, E., Hrabovszky, E.,. & Dickson, S. L. (2012). The amygdala as a neurobiological target for ghrelin in rats: neuroanatomical, electrophysiological and behavioral evidence.
  3. Becer, E., & Ergoren, M. C. (2021). Dual effect of the GHRL gene variant in the molecular pathogenesis of obesity. Balkan Journal of Medical Genetics: BJMG, 24(1), 27.
  4. Gregoor, J. G., van der Weide, J., Mulder, H., Cohen, D., van Megen, H. J., Egberts, A. C., & Heerdink, E. R. (2009). Polymorphisms of the LEP-and LEPR gene and obesity in patients using antipsychotic medication. Journal of clinical psychopharmacology, 29(1), 21-25.
  5. araone S V., Biederman J, Mick E. The age-dependent decline of attention deficit hyperactivity disorder: a meta-analysis of follow- up studies. Psychological medicine. 2006;36(2):159-165. doi:10.1017/S003329170500471X
  6. Retz, W., Ginsberg, Y., Turner, D., Barra, S., Retz-Junginger, P., Larsson, H., & Asherson, P. (2021). Attention-Deficit/Hyperactivity Disorder (ADHD), antisociality and delinquent behavior over the lifespan. Neuroscience & Biobehavioral Reviews, 120, 236-248.
  7. Wu SY, Gau SSF. Correlates for academic performance and school functioning among youths with and without persistent attention-deficit/hyperactivity disorder. Research in Developmental Disabilities. 2013; 34(1):505-515. doi:10.1016/J. RIDD.2012.09.004
  8. Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ. Dopamine transporter density in patients with attention deficit hyperactivity disorder. Lancet. 1999;354(9196): 2132-2133. doi:10.1016/S0140-6736(99)04030-1
  9. Lange, M., Norton, W., Coolen, M., Chaminade, M., Merker, S., Proft, F., Schmitt, A., Vernier, P., Lesch, K.-P., & Bally-Cuif, L. (2012). The ADHD-susceptibility gene lphn3.1 modulates dopaminergic neuron formation and locomotor activity during zebrafish development. Molecular Psychiatry, 17(10), 946–954.
  10. Cherkasova, M. V., Faridi, N., Casey, K. F., O’Driscoll, G. A., Hechtman, L., Joober, R., Baker, G. B., Palmer, J., Dagher, A., Leyton, M., & Benkelfat, C. (2014). Amphetamine-induced dopamine release and neurocognitive function in treatment-naive adults with ADHD. Neuropsychopharmacology, 39(6), 1498– 1507.
  11. Swanson, J. M., Kinsbourne, M., Nigg, J., Lanphear, B., Stefanatos, G. A., Volkow, N., Taylor, E., Casey, B. J., Castellanos, F. X., & Wadhwa, P. D. (2007). Etiologic subtypes of attention- deficit/hyperactivity disorder: Brain imaging, molecular genetic and environmental factors and the dopamine hypothesis. Neuropsychology Review, 17(1), 39–59.
  12. Shi, X., Guan, K., Peng, X., Xu, B., Zhou, X., Wang, S., Xu, S., Zheng, M., Huang, J., Wan, X., Guan, W., Su, K.-P., Ye, M., Gao, X., Yin, Z., & Li, X. (2021). Ghrelin modulates dopaminergic neuron formation and attention deficit hyperactivity disorder-like behaviors: From animals to human models. Brain, Behavior, and Immunity, 94, 327–337.
  13. de Candia P, Matarese G. Leptin and ghrelin: Sewing metabolism onto neurodegeneration. Neuropharmacology. 2018;136:307- 316. doi:10.1016/J.NEUROPHARM.2017.12.025
  14. Schwartz MW, Baskin DG. Leptin and the brain: then and now. The Journal of Clinical Investigation. 2013;123(6):2344-2345. doi:10.1172/JCI69346
  15. Ahima RS, Bjorbæk C, Osei S, Flier JS. Regulation of Neuronal and Glial Proteins by Leptin: Implications for Brain Development. Endocrinology. 1999;140(6):2755-2762. doi:10.1210/ ENDO.140.6.6774
  16. Kohl M, Foulon C, Guelfi JD. [Hyperactivity and anorexia nervosa: behavioural and biological perspective]. L’encephale. 2004;30(5):492-499. doi:10.1016/S0013-7006(04)95463-2
  17. Zarouna S, Wozniak G, Papachristou AI. Mood disorders: A potential link between ghrelin and leptin on human body? World Journal of Experimental Medicine. 2015;5(2):103. doi:10.5493/ WJEM.V5.I2.103
  18. Lu XY, Kim CS, Fraser A, Zhang W. Leptin: A potential novel antidepressant. Proceedings of the National Academy of Sciences of the United States of America. 2006;103(5):1593-1598. doi:10.1073/PNAS.0508901103/SUPPL_FILE/08901FIG8. JPG
  19. Turkmenoglu, M.F., Pektas Demir S, Demirtas Bilgic, A., Ozdemir C, Gokdogan Edgunlu T. GHRL Gene Polymorphisms in Early Onset Psoriasis: Molecular and In silico Analyses. Clinical Dermatology Open Access Journal. 2023;8(4):1-8. doi:10.23880/cdoaj-16000316
  20. Steinle NI, Pollin TI, O’Connell JR, Mitchell BD, Shuldiner AR. Variants in the Ghrelin Gene Are Associated with Metabolic Syndrome in the Old Order Amish. The Journal of Clinical Endocrinology & Metabolism. 2005;90(12):6672-6677. doi:10.1210/JC.2005-0549
  21. Geisler, C. E., & Hayes, M. R. (2023). Metabolic hormone action in the VTA: Reward-directed behavior and mechanistic insights. Physiology & behavior, 268, 114236.
  22. Alvarez-Crespo, M., Skibicka, K. P., Farkas, I., Molnár, C. S., Egecioglu, E., Hrabovszky, E.,. & Dickson, S. L. (2012). The amygdala as a neurobiological target for ghrelin in rats: neuroanatomical, electrophysiological and behavioral evidence.