ABSTRACT

Background and Aims: Chronic kidney disease (CKD) is a major global health problem with increasing incidence and mortality rates. Its early stages are often asymptomatic, delaying diagnosis and treatment. This study aimed to evaluate the relationship between branched-chain amino acids (BCAAs), serotonin, and -catenin in CKD patients in Thi-Qar province, Iraq.
Methods: A case-control study was conducted involving 88 patients with CKD and 40 healthy controls. Blood samples were collected, and serum levels of BCAAs, serotonin and -catenin and were measured using enzyme-linked immunosorbent assay (ELISA) kits (Sunlong Biotech, China). Data were analyzed using SPSS version 11.5. The Mann-Whitney U test compared group means, and Spearman’s rank correlation assessed associations between variables. Statistical significance was defined as P<0.05.
Results: BCAA concentrations were significantly lower in CKD patients compared with controls (35.53 ± 3.37 μg/ml vs 61.06 ± 5.39 μg/ml; P<0.001). - catenin levels were also significantly reduced in CKD patients: (39.55 ± 9.62 pg/ml vs. 48.81 ± 13.74 pg/ml) ( P <0.001), while serotonin levels were significantly elevated in patients with CKD: (21.69 ± 6.95 ng/ml vs. 18.88 ± 3.3 ng/ml) (P < 0.001). There is a negative correlation between serum branched-chain amino acids and β-catenin and serotonin with correlation coefficients (r = -0.0761) and (r = -0.0949) respectively.
Conclusion: The findings suggest that low levels of branched-chain amino acids (BCAAs) in patients with CKD may be associated with impaired -catenin synthesis and elevated serotonin levels. These could be vital monitoring indicators in disease management. Early nutritional interventions, including amino acid supplementation, may benefit patients and warrant further investigation.

KEYWORDS

B- Catenin, Serotonin ,Branched chain amino acids and patients.

REFERENCES

1) Zhe N; Jiang Y; & Wu J. (2023). Amino acid metabolism in health and disease. Signal Transduction and Targeted Therapy, 8(345): 1–32. https://doi.org/10.1038/s41392-023-01569-3.ces
2) Pedro H; & Nilufar M.(2022). Kidney metabolism and acid–base control: back to the basics. European J. Physiology, 474: 919-934.
3) Martine G; Wulfmeyer V; Müller R; & Rinschen M. (2024). Amino acid metabolism in kidney health and disease. Nature Reviews Nephrology, 20: 771–788.
4) Neinast M; Jang C; Hui S; Murashige D; Chu Q; Morscher R; Li X; Zhan L; White E; Anthony T; Rabinowitz J; & Arany Z. (2019). Quantitative Analysis of the Whole-Body Metabolic Fate of Branched-Chain Amino Acids. Cell Metabolism, 29: 417–429.
5) Pinelopi K. (2025). Fueling kidney recovery: boosting BCAA metabolism to overcome nephrotoxic AKI. Am J Physiol Renal Physiol, 328: 596–598, doi:10.1152/ajprenal.00024.2025.
6) Philipp R; & Zimmermann A. (2024). Branched chain amino acids: physico chemical properties, industrial synthesis and role in signaling, metabolism and energy production. Amino Acids, 56(51): 1–27. https://doi.org/10.1007/s00726-024-03417-2.
7) Layman K; & Walker D. (2006). Potential importance of leucine in treatment of obesity and the metabolic syndrome. J.Nutr., 136(1): 319–323.
8) Lynch, C; & Adams S. (2014). Branched-chain amino acids in metabolic signaling and insulin resistance. Nature Reviews Endocrinology, 10(12):723–736. https://doi.org/10.1038/nrendo.2014.171.
9) Okekunle A; Zhang M; Wang Z; Liu X; Liu Y; & Wei W. (2019). Dietary branched-chain amino acids intake exhibited a different relationship with type 2 diabetes and obesity risk: a meta-analysis. Acta Diabetologica, 56: 187–195. https://doi.org/10.1007/s00592-018-1243-7.
10) Gagandeep M; Mora S; Madu G; & Adegoke O. (2021). Branched-chain amino acids: catabolism in skeletal muscle and implications for muscle and whole-body metabolism. Frontiers in Physiology, 12: 1-26.
11) Mahbub M; Arima K; Ikeda K; Fukunaga S; Yonemoto A; & Nakashima E. (2021). Association of plasma branched-chain and aromatic amino acids with reduction in kidney function evaluated in apparently healthy adults. J. Clin. Med., 10(22): 5234. https://doi.org/10.3390/jcm10225234
12) Shafi S; Khan H; & Bajpai P. (2024). Protein metabolism and its profiling for the diagnosis of metabolic disorders. Clinical applications of biomolecules in disease diagnosis. Springer, Singapore: 1-448. https://doi.org/10.1007/978-981-97-4723-8_3.
13) Knol . M; Wulfmeyer V; Müller R; & Rinschen M. (2024). Amino acid metabolism in kidney health and disease. Nature Reviews Nephrology, 20: 771–788. https://doi.org/10.1038/s41581-024-00872-8.
14) Aikaterini D; Vasilis T; & Eleni B; Dimova. (2022). The critical role of the branched chain amino acids (BCAAs) catabolism-regulating enzymes, branched-chain aminotransferase (BCAT) and branched-chain α-keto acid dehydrogenase (BCKD), in human pathophysiology. Int. J. Mol. Sci., 23(7): 4022.
15) Haizhou J; Feifan G; & Fei X. (2025). Role of branched-chain amino acid catabolism in the regulation of adipocyte metabolism. Endocrinology, 166(7):1-13.
16) Holeček M.(2018). Branched-chain amino acids in health and disease: metabolism, alterations in blood plasma, and as supplements. Nutrition & Metabolism, 15(33): 1–12. https://doi.org/10.1186/s12986-018-0271-1.
17) Cole J. (2015). Metabolism of BCAAs. Branched chain amino acids in clinical nutrition. Humana Press, New York, NY.: 1-30. https://doi.org/10.1007/978-1-4939-1923-9_2.
18) Hou Y; Hu S; Li X; He W; & Wu G. (2020). Amino acid metabolism in the liver: nutritional and physiological significance. Advances in experimental medicine and biology, Springer, Cham., 1st ed: 1-220.
19) https://doi.org/10.1016/ j.kint.2020.07.013.
20) María M; López-Maside L; Donapetry-García C; Fernández-Fernández C; & Sixto-Leal C. (2017). Enzymes involved in branched-chain amino acid metabolism in humans. Amino Acids, 49(6): 1005–1028.
21) Zhen Z; Müller D; Valdivia P; & Storch J. (2018). Branched-chain amino acids as critical switches in health and disease. Hypertension, 72: 1012–1022.
22) Namkung SM, Choi JS, Park JH, Yang MG, Lee MW, Kim SW.(2017). Detection of dopamine and serotonin by competitive enzyme-linked immunosorbent assay. Korean J Clin Lab Sci.;49(3):220-6. [DOI:10.15324/kjcls.2017.49.3.220].
23) Tsai C; Huang S; Kao C; & Hsu P. (2022). Muscle wasting in chronic kidney disease: mechanism and clinical implications—a narrative review. International J. Molecular Sciences, 23(11): 1-25.
24) Ming T; Ou S; Chen H; Hsu H; & Chen T. (2021). Relationship between circulating galectin-3, systemic inflammation, and protein-energy wasting in chronic hemodialysis patients. Nutrients, 13(8): 1-13.
25) Wang Y; Gao L; Yang Z; Chen F; & Zhang Y. (2018). Effects of probiotics on ghrelin and lungs in children with acute lung injury: a double-blind randomized, controlledtrial. PediatricPulmonology, 53(2):197-203. https:/doi.org/10.1002/ppul.23922.
26) Bastings, J; Van Beek S; Van Der Laan S; & Van Marken Lichtenbelt W. (2023). Influence of the gut microbiota on satiety signaling. Trends in Endocrinology & Metabolism, 34(4): 243–255.
27) Lingbo Z; Adjei I; Zhang H; & Wu J. (2023). The WNT/β-catenin system in chronic kidney disease-mineral bone disorder syndrome. International Urology and Nephrology, 55(10): 2527–2538.
28) Ryan L; Qiu C; Zeyaei E; Baxter N; Han D; Wang A; Lock H; Chirikian O; Pruitt B; & Wilson M. Z. (2022). Nucleation of the destruction complex on the centrosome accelerates degradation of β-catenin and regulates Wnt signal transmission. Proceedings of the National Academy of Sciences, 119(36): 1-13. https://doi.org/10.1073/pnas.2204688119.
29) Kuo-Chin H; Yao W; Liu Y; Yang H; Liao M; Chong K; Peng C; & Lu K. (2023). The potential influence of uremic toxins on the homeostasis of bones and muscles in chronic kidney disease. Biomedicines, 11(7): 1-25. https://doi.org/10.3390/biomedicines11072076.
30) Ayesha M; Tauqir H; Ali S; Laiq I; Ali A; & Shakeel M. (2023). Inflammatory process and role of cytokines in inflammation: An overview. Punjab University J. Zoology, 36(2): 235–250.
31) Adaway J; Dobson R; Walsh J; Rees -Smith B; Keevil B; & Coronavirus K. (2015). Serum and plasma 5-hydroxyindoleacetic acid as an alternative to 24-h urine 5-hydroxyindoleacetic acid measurement. Annals of Clinical Biochemistry, 53(5): 554–560. https://doi.org/10.1177/0004563215613109.
32) Noordwest Z; & Piet C. (2006). Platelet activation and serotonin release during treatment with haemodialysis. Nederlands Tijdschrift Voor Klinische Chemie En Laboratoriumgeneeskunde, 31(3): 236–238.
33) Baaten C; Sternkopf M; Henning T; Marx N; Bauwens M; Kuijpers M; Schurgers L; & Dekker L. (2021). Platelet function in CKD: A systematic review and meta-analysis. J. the American Society of Nephrology, 32(7): 1583–1598.
34) Andromeda L; Ochoa-Cortez F; Beyder A; Soghomonyan S; Zuleta-Alarcon A; Coppola V; & Christofi F. (2016). Mechanosensory signaling in enterochromaffin cells and 5-HT release: Potential implications for gut inflammation. Frontiers in Neuroscience, 10: 1-13.
35) Lai W; Rajan S; & Goli U. (2022). Enterochromaffin cells–gut microbiota crosstalk: Underpinning the symptoms, pathogenesis, and pharmacotherapy in disorders of gut-brain interaction. J. Neurogastroenterology and Motility, 28(3): 357–375. https://doi.org/10.5056/jnm22008.

Cite this article

Mohammed, A. H., Aouda, M. A., & Alyasiri, H. M. (2026). Relationship Between Branched Chain Amino Acids, - Catenin and Serotonin in Patients with Chronic Kidney Disease in Thi-Qar Province/ Iraq. INTERNATIONAL JOURNAL OF HEALTH & MEDICAL RESEARCH, 5(5), 493-500. https://doi.org/10.58806/ijhmr.2026.v5i5n22