GABA Agonist Baclofen Increases Beta cell Mass and C Peptide Level in Patients with Type 1 Diabetes
Autor: | Younis, Mahmoud |
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Jazyk: | angličtina |
Rok vydání: | 2019 |
Předmět: | |
ISSN: | 0140-6736 |
DOI: | 10.5281/zenodo.2605019 |
Popis: | Introduction: While diabetes continues to grow as a worldwide major health problem, its cause is obviously simple: β-cell failure. In type 1 diabetes (T1D), β cells are destroyed by autoimmunity, while in type 2 diabetes (T2D), there is a failure of β cells to compensate insulin resistance. Most cases of type 1 diabetes are due to autoimmunity, in the sense that patients often exhibit the features of an immunological contribution to disease (eg, autoantibodies or gene binding with genes that control immune responses). Nevertheless, many patients with type 1 diabetes don't have these features, resulting in proposed classifications for type 1A (autoimmune) diabetes. It is considered that renewal of normal beta cell mass and function could abolish diabetes. GABA is an essential neurotransmitter in the central nervous system. GABA is produced by pancreatic β-cells. It is elucidated that GABA takes part in preserving the β cell mass and in conserving β cells from death. Detects that long-range GABA treatment results in a considerable increase in c peptide levels. Materials and methods: two groups of type 1 diabetes patients had been monitored in a private clinic. In patients who were on baclofen tablets, there were significant differences between c peptide levels before and after treatment with p-value < 0.0001. In patients who were on insulin only, there were no significant differences between c peptide levels. Conclusion: GABA agonist baclofen may increase beta cell mass and c peptide levels in patients with type 1 diabetes. {"references":["Al-Hasani et al., 2013 K. Al-Hasani, A. Pfeifer, M. Courtney, N. Ben-Othman, E. Gjernes, A. Vieira, N.Druelle, F. Avolio, P. Ravassard, G. Leuckx, et al. Dev. Cell, 26 (2013), pp. 86-1001.","Leslie RD. Predicting adult-onset autoimmune diabetes: clarity from complexity. Diabetes. 2010; 59:330–31.","Mark A Atkinson, PhD, Prof, George S Eisenbarth, MD, Prof, and Aaron W Michels, MD.Type 1 diabetes, Lancet. 2014 Jan 4; 383(9911): 69–82.Published online 2013 Jul 26. doi: 10.1016/S0140-6736(13)60591-7.","Petitti DB, Klingensmith GJ, Bell RA, Andrews JS, Dabelea D, Imperatore G, Marcovina S, Pihoker C, Standiford D, Waitzfelder B, Mayer-Davis E. SEARCH for Diabetes in Youth Study Group: Glycemic control in youth with diabetes: The SEARCH for diabetes in Youth Study. J Pediatr. 2009; 155:668–672.","Eisenbarth GS. Update in type 1 diabetes. J Clin Endocrinol Metab. 2007; 92:2403–7.","Gianani R, Campbell-Thompson M, Sarkar SA, et al. Dimorphic histopathology of long-standing childhood-onset diabetes. Diabetologia. 2010; 53:690–98.","Pipeleers D, et al. Restoring a functional beta-cell mass in diabetes. Diabetes Obes Metab. 2008; 10(suppl 4):54–62.","Meier JJ, et al. Direct evidence of attempted beta cell regeneration in an 89-year-old patient with recent-onset type 1 diabetes. Diabetologia. 2006; 49:1838–1844.","Liese, A.D., R.B. D'Agostino, Jr., and R. Hamman, The burden of diabetes mellitus among US youth; prevalence estimates from the SEARCH for diabetes in youth study. Pediatrics, 2006. 118(4): p. 1510-18.","International Diabetes Federation. IDF diabetes atlas. 8th ed. Brussells: International Diabetes Federation; 2017."]} |
Databáze: | OpenAIRE |
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