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Beta cell mass in diabetes: a realistic therapeutic target?
Open accessAbstract
Beta cell deficiency underlies both type 1 and type 2 diabetes, and restoration or replacement of beta cell function is therefore the logical long-term solution to therapy. This review sets out to describe the defects in beta cell mass and function in both forms of diabetes, summarises current understanding of the underlying causes of beta cell death, and the methodological limitations of determining beta cell mass in vivo. Finally, the potential effects of current and future treatment regimens on beta cell mass and turnover are considered.
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“Regeneration of β-cell function in experimental animal models has been widely observed in rodents but remains elusive and controversial in humans (13,14).”
From Adaptive β-Cell Proliferation Is Severely Restricted With Advanced Age (2009) · cites this paper as [14]
Experimental — accuracy not yet measuredIn the citing paper
“Sadly, expansion of bona fide human β-cells has not been convincingly demonstrated (13–15).”
From Adaptive β-Cell Proliferation Is Severely Restricted With Advanced Age (2009) · cites this paper as [14]
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“Discussion Excessive apoptosis of the pancreatic β-cell causing loss of β-cell mass is a major contributor to the initiation and progression of diabetes [12,32,33].”
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“Thus, synthesis and release of chemokines by either islet β-cells, leukocytes, or both cell types contributes to T1DM, T2DM, rejection of transplanted islets, as well as other diseases with inflammatory components (10, 11, 6).”
BackgroundInfluentialRisk Factors Preceding Type 2 Diabetes and Cardiomyopathy
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“5 million Americans with type 1 diabetes mellitus (T1DM),(1) wherein severe insulin deficiency is caused by >95% reduction in β-cell mass.(2,3) Insulin replacement remains standard therapy but does not restore normal glucose homeostasis.”
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“Consequently, potential antidiabetic treatments increasing b-cell mass or preventing b-cell loss are gaining increased interest (Meier, 2008).”
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“However, no therapeutic strategy based on these mechanisms has been successfully developed for treating T2D.”
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BackgroundSelf-citationThe pancreatic beta cell surface proteome
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“In contrast, type 2 diabetes is characterised by beta cell dysfunction that is thought to occur very early in the disease, even preceding insulin resistance [66, 68], and only later by reduced beta cell mass (a loss of up to 63% in long-term type 2 diabetes) [64].”
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InfluentialGuardado‐Mendoza, R., Jiménez-Ceja, L. M., Majluf‐Cruz, A., Kamath, S., Fiorentino, T. V., Casiraghi, F., Velazquez, A. O. C., DeFronzo, R. A., Dick, E. J., Davalli, A. M., et al. (2012) · International Journal of Obesity · doi:10.1038/ijo.2012.205 · Cited by 27
Isolation of genes involved in pancreas regeneration by subtractive hybridization
Choi, J., Lee, M.-Y., Kim, Y., Shim, J.-Y., Han, S.-M., Lee, K., Choi, Y., Jeon, H., & Baek, K. (2010) · Biological Chemistry · doi:10.1515/bc.2010.101 · Cited by 27
“The b cell mass is a crucial factor for both type I and type II DM (Meier, 2008).”
BackgroundBawadi, H. A., Katkhouda, R., Tayyem, R., Kerkadi, A., Raad, S. B., & Subih, H. S. (2019) · Diabetes Metabolic Syndrome and Obesity · doi:10.2147/dmso.s214426 · Cited by 25
Kim, H., Kim, D., Yoon, H., Choi, C. S., Oh, Y. S., & Jun, H. (2020) · Antioxidants · doi:10.3390/antiox9050406 · Cited by 25
Shim, J.-H., Kim, J., Han, J., An, S. Y., Jang, Y. J., Son, J., Woo, D., Kim, S., & Kim, J.-H. (2015) · Cell Transplantation · doi:10.3727/096368914x685438 · Cited by 25
Benefit-Risk Assessment of Exenatide in the Therapy of Type 2 Diabetes Mellitus
Gallwitz, B. (2010) · Drug Safety · doi:10.2165/11319130-000000000-00000 · Cited by 24
Diabetes mellitus: Exploring the challenges in the drug development process
Patnaik, A., & Vaz, J. A. (2012) · Perspectives in Clinical Research · doi:10.4103/2229-3485.100660 · Cited by 23
“Several short to medium term studies have demonstrated the possibility of beta-cell rest but long term studies have yet to emerge to prove this concept.[3] The drug or treatment modality that permits long-term β cell rest (if such a scientific concept is proven) is likely to be the mainstay of therapy for type 2 diabe…”
BackgroundThe treatment of type 1 diabetes mellitus with agents approved for type 2 diabetes mellitus
Munir, K. M., & Davis, S. N. (2015) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2015.1084502 · Cited by 22
“Data now show that some individuals even after many years of T1DM still have preserved C-peptide and ability to regenerate b-cells [15].”
BackgroundKöhler, C. U., Kreuter, A., Rozynkowski, M., Rahmel, T., Uhl, W. H., Tannapfel, A., Schmidt, W. E., & Meier, J. J. (2010) · Regulatory Peptides · doi:10.1016/j.regpep.2009.12.021 · Cited by 22
Self-citationBreuer, T. G. K., Menge, B. A., Banasch, M., Uhl, W., Tannapfel, A., Schmidt, W. E., Nauck, M. A., & Meier, J. J. (2010) · European Journal of Endocrinology · doi:10.1530/eje-10-0330 · Cited by 20
Self-citationKimura, H., Ogawa, Y., Fujimoto, H., Mukai, E., Kawashima, H., Arimitsu, K., Toyoda, K., Fujita, N., Yagi, Y., Hamamatsu, K., et al. (2017) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2017.12.007 · Cited by 18
Emordi, J. E., Agbaje, E. O., Oreagba, I. A., & Iribhogbe, O. I. (2018) · Advances in Pharmacological Sciences · doi:10.1155/2018/1314941 · Cited by 18
“*erefore, logical long-term solution to diabetic therapy is restoration of β-cells since β-cell deficiency underlies both type 1 and type 2 diabetes [16].”
BackgroundBradley, M. D., Arnold, M. E., Biskup, B., Campbell, T. M., Fuhrman, J., Guthrie, G. E., Kelly, J. H., Lacagnina, S., Loomis, J. F., McMacken, M. M., et al. (2022) · Clinical Diabetes · doi:10.2337/cd22-0009 · Cited by 21
“Practitioners also mentioned targeting SFUs first because of potential acceleration of decline in b-cell function, which has been discussed in the literature (38).”
BackgroundEnhancement of β-Cell Regeneration by Islet Transplantation After Partial Pancreatectomy in Mice
Jung, H. S., Ahn, Y., Oh, S.-H., Kim, Y. S., No, H., Lee, M., & Kim, K.-W. (2009) · Transplantation · doi:10.1097/tp.0b013e3181b07a02 · Cited by 17
“Therefore, enhancement of endogenous -cell regeneration for the purpose of insulin replacement is a possible strategy for diabetic therapy (4).”
BackgroundPossible Role of GLP-1 and Its Agonists in the Treatment of Type 1 Diabetes Mellitus
Issa, C. M., & Azar, S. T. (2012) · Current Diabetes Reports · doi:10.1007/s11892-012-0291-6 · Cited by 15
Navaeian, M., Asadian, S., Ahmadpour Yazdi, H., & Gheibi, N. (2021) · Molecular Biology Reports · doi:10.1007/s11033-021-06270-8 · Cited by 14
McGill, J. B. (2009) · Postgraduate Medicine · doi:10.3810/pgm.2009.01.1954 · Cited by 15
“Functional tests of insulin secretion have been developed based on the assumption that the amount of insulin secreted in response to a given antidiabetes agent is proportional to the number of β-cells in the pancreas.(102) The homeostasis model assessment (HOMA)-B is an index used to assess the ability of β-cells to s…”
MethodCyclin D2is sufficient to drive β cell self-renewal and regeneration
Tschen, S.-I., Zeng, C., Field, L. J., Dhawan, S., Bhushan, A., & Georgia, S. K. (2017) · Cell Cycle · doi:10.1080/15384101.2017.1319999 · Cited by 17
“It may be possible to supplement b cell mass as a cellular therapy by stimulating the self-renewal of pre-existing b cells, by differentiating b cells from multipotent progenitor cells, or by stimulating transdifferentiation from other cell types.(4) Self-renewal of pre-existing b cells is the predominant mechanism to…”
BackgroundMoon, J. H., Choe, H. J., & Lim, S. K. (2024) · Journal of Diabetes Investigation · doi:10.1111/jdi.14221 · Cited by 13
Lesch, A., Backes, T. M., Langfermann, D. S., Rößler, O. G., Laschke, M. W., & Thiel, G. (2020) · Pharmacological Research · doi:10.1016/j.phrs.2020.104983 · Cited by 14
Frost, P. A., Chen, S., Mezzles, M. J., Voruganti, V. S., Nava‐González, E. J., Arriaga-Cázares, H. E., Freed, K. A., Comuzzie, A. G., DeFronzo, R. A., Kent, J. W., et al. (2015) · Journal of Medical Primatology · doi:10.1111/jmp.12182 · Cited by 13
Ludwig, B., Barthel, A., Reichel, A., Block, N. L., Ludwig, S., Schally, A. V., & Bornstein, S. R. (2014) · Vitamins and hormones · doi:10.1016/b978-0-12-800174-5.00008-9 · Cited by 12
“Early disruption of this morbid process in order to avoid beta cell destruction is the principal goal of prevention in people at high risk, because in the early stages of the disease beta cell regeneration appears to be adequate to allow reversal of the organ damage (Meier, 2008).”
BackgroundInfluentialNittala, A., & Wang, X. (2008) · Theoretical Biology and Medical Modelling · doi:10.1186/1742-4682-5-17 · Cited by 13
Human Multipotent Stromal Cell Secreted Effectors Accelerate Islet Regeneration
Kuljanin, M., Elgamal, R. M., Bell, G. I., Xenocostas, A., Lajoie, G., & Hess, D. A. (2019) · Stem Cells · doi:10.1002/stem.2976 · Cited by 11
Differential expression of cell-cycle regulators in human beta-cells derived from insulinoma tissue
Ueberberg, S., Tannapfel, A., Schenker, P., Viebahn, R., Uhl, W. H., Schneider, S., & Meier, J. J. (2016) · Metabolism · doi:10.1016/j.metabol.2016.02.007 · Cited by 10
Self-citationFeng, X., Gao, X., Jia, Y., & Xu, Y. (2017) · Diabetes Therapy · doi:10.1007/s13300-017-0257-4 · Cited by 10
Covington, B. A., & Chen, W. (2024) · Biomedicines · doi:10.3390/biomedicines12030473 · Cited by 11
“The expansion of beta cell mass is infrequent in adult humans, with an estimated rate of 0.1–0.5% proliferating cells versus a 4% peak in fetal development [83–85].”
BackgroundInfluentialKinetics of functional beta cell mass decay in a diphtheria toxin receptor mouse model of diabetes
van Krieken, P. P., Dicker, A., Eriksson, M., Herrera, P. L., Ahlgren, U., Berggren, P., & Ilegems, E. (2017) · Scientific Reports · doi:10.1038/s41598-017-12124-w · Cited by 9
Altered autonomic inputs as a cause of pancreatic β-cell amyloid
Watve, M., Bodas, A., & Diwekar-Joshi, M. (2013) · Medical Hypotheses · doi:10.1016/j.mehy.2013.11.002 · Cited by 8
Noninvasive Monitoring of β-Cell Mass and Fetal β-Cell Genesis in Mice Using Bioluminescence Imaging
Sekiguchi, Y., Owada, J., Oishi, H., Katsumata, T., Ikeda, K., Kudo, T., & Takahashi, S. (2012) · EXPERIMENTAL ANIMALS · doi:10.1538/expanim.61.445 · Cited by 9
“a number of human studies have shown that both type 1 and type 2 diabetes are associated with a significant deficit in β-cell mass [11].”
BackgroundLeung, P. S. (2010) · Advances in experimental medicine and biology · doi:10.1007/978-90-481-9060-7_3 · Cited by 8
“Ideally, T1DM treatment should be focused on β-cell regeneration and early intervention (Meier, 2008).”
BackgroundLi, X., Jois, S., & Cui, H. (2022) · BMC Complementary Medicine and Therapies · doi:10.1186/s12906-022-03674-2 · Cited by 8
Suzuki, Y., Inoue, S., Shimizu, H., Ishizuka, N., Kasahara, Y., Takahashi, T., Arai, K., Kobayashi, Y., Kishi, M., Imazeki, N., et al. (2011) · Endocrine Journal · doi:10.1507/endocrj.k10e-408 · Cited by 8
Metadata
- Authors
- Meier, J. J.
- Affiliations
- St. Josef-Hospital (DE)
- Corresponding author
- Meier, J. J.
- ORCID
- Meier, J. J.
- Venue
- Diabetologia
- Published
- 2008-03-04
- Volume
- 51
- Issue
- 5
- Pages
- 703-713
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2166312550
- Cited by
- 155
- References
- 104
- Citations by year
- 2025: 3 · 2024: 5 · 2023: 6 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 7 · 2018: 4 · 2017: 7 · 2016: 7 · 2015: 13 · 2014: 11 · 2013: 11 · 2012: 13
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- beta-cell mass, type 1 diabetes, type 2 diabetes, beta-cell death, diabetes treatment
- MeSH terms
- Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Humans, Hypoglycemic Agents, Insulin Resistance, Regeneration, Apoptosis, Insulin-Secreting Cells
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