Pancreatic islet dysfunction in type 2 diabetes mellitus

References

• Alvarez, A.E., et al., 2004. Cystic fibrosis at a Brazilian center of excellence: clinical and laboratory characteristics of 104 patients and their association with genotype and disease severity]. Jornal de pediatria, 80 (5), 371–379.
   PubMedGoogle Scholar
• Alves, C.A., et al., 2007. Diabetes mellitus in patients with cystic fibrosis. Jornal Brasileiro De Pneumologia:Publicacao Oficial Da Sociedade Brasileira De Pneumologia e Tisilogia, 33 (2), 213–221.
   PubMedGoogle Scholar
• Arkan, M.C., et al., 2005. IKK-beta links inflammation to obesity-induced insulin resistance. Nature medicine, 11 (2), 191–198.
   PubMed Web of Science ®Google Scholar
• Biswas, S., et al., 2017. Insight into the binding of a non-toxic, self-assembling aromatic tripeptide with ct-DNA: spectroscopic and viscositic studies. Biochemistry and biophysics reports, 11, 112–118.
   PubMedGoogle Scholar
• Blüher, M., 2009. Adipose tissue dysfunction in obesity. Experimental and clinical endocrinology & diabetes: Official journal, German society of endocrinology [and] German diabetes association, 117 (6), 241–250.
   PubMed Web of Science ®Google Scholar
• Brennan, A.L., et al., 2004. Clinical importance of cystic fibrosis-related diabetes. Journal of cystic fibrosis: Official journal of the European cystic fibrosis society, 3 (4), 209–222.
   PubMedGoogle Scholar
• Butler, P.C., et al., 1990. Effects of meal ingestion on plasma amylin concentration in NIDDM and nondiabetic humans. Diabetes, 39 (6), 752–756.
   PubMed Web of Science ®Google Scholar
• Cardozo, A.K., et al., 2001. A comprehensive analysis of cytokine-induced and nuclear factor-kappa B-dependent genes in primary rat pancreatic beta-cells. The journal of biological chemistry, 276 (52), 48879–48886.
   PubMed Web of Science ®Google Scholar
• Cawood, T.J., et al., 2006. Cystic fibrosis-related diabetes in adults. Irish medical journal, 99 (3), 83–86.
   PubMedGoogle Scholar
• Cildir, G., Akıncılar, S.C., and Tergaonkar, V. 2013. Chronic adipose tissue inflammation: all immune cells on the stage. Trends in molecular medicine, 19 (8), 487–500.
   PubMed Web of Science ®Google Scholar
• Clark, A., et al., 1990. Islet amyloid polypeptide in diabetic and non-diabetic Pima Indians. Diabetologia, 33 (5), 285–289.
   PubMed Web of Science ®Google Scholar
• Cystic Fibrosis Genotype-Phenotype Consortium.Correlation between genotype and phenotype in patients with cystic fibrosis. New England journal of medicine, 329 (18), 1308–1313.
   PubMed Web of Science ®Google Scholar
• Costa, M., et al.,, 2005. Diabetes: a major co-morbidity of cystic fibrosis. Diabetes & metabolism, 31 (3 Pt 1), 221–232.
   PubMed Web of Science ®Google Scholar
• DeFronzo, R.A. 2004. Pathogenesis of type 2 diabetes mellitus. The medical clinics of North America, 88 (4), 787–835.
   PubMed Web of Science ®Google Scholar
• Dinarello, C.A., 2009. Immunological and inflammatory functions of the interleukin-1 family. Annual review of immunology, 27, 519–550.
   PubMed Web of Science ®Google Scholar
• Donath, M.Y., et al., 2003. Inflammatory mediators and islet beta-cell failure: a link between type 1 and type 2 diabetes. Journal of molecular medicine (Berlin, Germany), 81 (8), 455–470.
   PubMed Web of Science ®Google Scholar
• Donath, M.Y., et al., 2005. Mechanisms of beta-cell death in type 2 diabetes. Diabetes, 54 (Suppl 2), S108–S113.
   PubMed Web of Science ®Google Scholar
• Donath, M.Y., et al., 2008. Islet inflammation in type 2 diabetes: from metabolic stress to therapy. Diabetes care, 31 (Suppl 2), S161–S164.
   PubMed Web of Science ®Google Scholar
• Ehses, J.A., et al., 2007. Increased number of islet-associated macrophages in type 2 diabetes. Diabetes, 56 (9), 2356–2370.
   PubMed Web of Science ®Google Scholar
• Ehses, J.A., et al., 2009. IL-1 antagonism reduces hyperglycemia and tissue inflammation in the type 2 diabetic GK rat. Proceedings of the National academy of sciences of the United States of America, 106 (33), 13998–14003.
   PubMed Web of Science ®Google Scholar
• Eizirik, D.L., and Mandrup-Poulsen, T., 2001 . A choice of death-the signal-transduction of immune-mediated beta-cell apoptosis. Diabetologia, 44 (12), 2115–2133.
   PubMed Web of Science ®Google Scholar
• Eizirik, D.L., et al., 2012. The human pancreatic islet transcriptome: expression of candidate genes for type 1 diabetes and the impact of pro-inflammatory cytokines. PLoS genetics, 8 (3), e1002552.
   PubMed Web of Science ®Google Scholar
• Enoki, S., et al., 1992. Plasma islet amyloid polypeptide levels in obesity, impaired glucose tolerance and non-insulin-dependent diabetes mellitus. Diabetes research and clinical practice, 15 (1), 97–102.
   PubMed Web of Science ®Google Scholar
• Fadista, J., et al., 2014. Global genomic and transcriptomic analysis of human pancreatic islets reveals novel genes influencing glucose metabolism. Proceedings of the National academy of sciences of the United States of America, 111 (38), 13924–13929.
   PubMed Web of Science ®Google Scholar
• Finkelstein, S.M., et al., 1988. Diabetes mellitus associated with cystic fibrosis. The journal of pediatrics, 112 (3), 373–377.
   PubMed Web of Science ®Google Scholar
• Flynn, J.L., et al.,, 1993. An essential role for interferon gamma in resistance to Mycobacterium tuberculosis infection. The journal of experimental medicine, 178 (6), 2249–2254.
   PubMed Web of Science ®Google Scholar
• Fowler, M.J., et al., 1998. Induction of bone morphogenetic protein-2 by interleukin-1 in human fibroblasts. Biochemical and biophysical research communications, 248 (3), 450–453.
   PubMed Web of Science ®Google Scholar
• Fukui, N., et al.,, 2003. Stimulation of BMP-2 expression by pro-inflammatory cytokines IL-1 and TNF-alpha in normal and osteoarthritic chondrocytes. The journal of bone and joint surgery. American volume., 85-A (Suppl 3), 59–66.
   PubMed Web of Science ®Google Scholar
• Gannon, M., 2007. BuMP-ing up insulin secretion by pancreatic beta cells. Cell metabolism, 5 (3), 157–159.
   PubMed Web of Science ®Google Scholar
• Gaskin, K.J., et al., 1982. Evidence for a primary defect of pancreatic HCO3-secretion in cystic fibrosis. Pediatric research, 16 (7), 554–557.
   PubMed Web of Science ®Google Scholar
• German, M.S., et al.,, 1992. The insulin and islet amyloid polypeptide genes contain similar cell-specific promoter elements that bind identical beta-cell nuclear complexes. Molecular and cellular biology, 12 (4), 1777–1788.
   PubMed Web of Science ®Google Scholar
• Goulley, J., et al., 2007. BMP4-BMPR1A signaling in beta cells is required for and augments glucose-stimulated insulin secretion. Cell metabolism, 5 (3), 207–219.
   PubMed Web of Science ®Google Scholar
• Gurlo, T., et al., 2010. Evidence for proteotoxicity in beta cells in type 2 diabetes: toxic islet amyloid polypeptide oligomers form intracellularly in the secretory pathway. The American journal of pathology, 176 (2), 861–869.
   PubMed Web of Science ®Google Scholar
• Hartter, E., et al., 1991. Basal and stimulated plasma levels of pancreatic amylin indicate its co-secretion with insulin in humans. Diabetologia, 34 (1), 52–54.
   PubMed Web of Science ®Google Scholar
• Heimberg, H., et al., 2001. Inhibition of cytokine-induced NF-kappaB activation by adenovirus-mediated expression of a NF-kappaB super-repressor prevents beta-cell apoptosis. Diabetes, 50 (10), 2219–2224.
   PubMed Web of Science ®Google Scholar
• Hinds, A., et al., 1991. Postprandial hyperglycemia and pancreatic function in cystic fibrosis patients. Diabetes research (Edinburgh, Scotland), 18 (2), 69–78.
   PubMedGoogle Scholar
• Hua, H., et al., 2006. BMP4 regulates pancreatic progenitor cell expansion through Id2. The journal of biological chemistry, 281 (19), 13574–13580.
   PubMed Web of Science ®Google Scholar
• Hussein, K.A., et al., 2014. Bone morphogenetic protein 2: a potential new player in the pathogenesis of diabetic retinopathy. Experimental eye research, 125, 79–88.
   PubMed Web of Science ®Google Scholar
• Iannucci, A., et al., 1984. Endocrine pancreas in cystic fibrosis: an immunohistochemical study. Human pathology, 15 (3), 278–284.
   PubMed Web of Science ®Google Scholar
• Ibarra, U.A., et al., 2016. Inflammatory Cytokines Stimulate Bone Morphogenetic Protein-2 Expression and Release from Pancreatic Beta Cells. Journal of interferon cytokine research, 36 (1), 20–29.
   PubMed Web of Science ®Google Scholar
• Johnson, K.H., et al., 1988. Immunolocalization of islet amyloid polypeptide (IAPP) in pancreatic beta cells by means of peroxidase-antiperoxidase (PAP) and protein A-gold techniques. American journal of pathology, 130 (1), 1–8.
   PubMed Web of Science ®Google Scholar
• Kahn, S.E., 2003. The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes. Diabetologia, 46 (1), 3–19.
   PubMed Web of Science ®Google Scholar
• Kahn, S.E., Andrikopoulos, S., and Verchere, C.B. 1999. Islet amyloid: a long-recognized but underappreciated pathological feature of type 2 diabetes. Diabetes, 48 (2), 241–253.
   PubMed Web of Science ®Google Scholar
• Kahn, S.E., et al., 1991. Glucose stimulates and potentiates islet amyloid polypeptide secretion by the B-cell. Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme, 23 (12), 577–580.
   PubMed Web of Science ®Google Scholar
• Kamata, K., et al., 2014. Islet amyloid with macrophage migration correlates with augmented β-cell deficits in type 2 diabetic patients. Amyloid: The international journal of experimental and clinical investigation: The official journal of the international society of amyloidosis, 21 (3), 191–201.
   PubMed Web of Science ®Google Scholar
• Kautzky-Willer, A., et al., 1994. Role of islet amyloid polypeptide secretion in insulin-resistant humans. Diabetologia, 37 (2), 188–194.
   PubMed Web of Science ®Google Scholar
• Kautzky-Willer, A., et al., 1997. Elevated islet amyloid pancreatic polypeptide and proinsulin in lean gestational diabetes. Diabetes, 46 (4), 607–614.
   PubMed Web of Science ®Google Scholar
• Kishigami, S., et al., 2004. BMP signaling through ACVRI is required for left-right patterning in the early mouse embryo. Developmental biology, 276 (1), 185–193.
   PubMed Web of Science ®Google Scholar
• Knowles, N.G., et al., 2002. Insulin and amylin release are both diminished in first-degree relatives of subjects with type 2 diabetes. Diabetes care, 25 (2), 292–297.
   PubMed Web of Science ®Google Scholar
• Koga, M., et al.,, 2013. The bone morphogenic protein inhibitor, noggin, reduces glycemia and vascular inflammation in db/db mice. American journal of physiology. heart and circulatory physiology, 305 (5), H747–H755.
   PubMed Web of Science ®Google Scholar
• Kolb, H., and Mandrup-Poulsen, T., 2005. An immune origin of type 2 diabetes. Diabetologia, 48 (6), 1038–1050.
   PubMed Web of Science ®Google Scholar
• Kopelman, H., et al., 1988. Impaired chloride secretion, as well as bicarbonate secretion, underlies the fluid secretory defect in the cystic fibrosis pancreas. Gastroenterology, 95 (2), 349–355.
   PubMed Web of Science ®Google Scholar
• Kopito, R.R., 1999. Biosynthesis and degradation of CFTR. Physiological reviews, 79 (1 Suppl), S167–S173.
   PubMedGoogle Scholar
• Lanng, S., et al., 1992. Influence of the development of diabetes mellitus on clinical status in patients with cystic fibrosis. European journal of pediatrics, 151 (9), 684–687.
   PubMed Web of Science ®Google Scholar
• Larsen, C.M., et al. 2007. Interleukin-1-receptor antagonist in type 2 diabetes mellitus. The New England journal of medicine, 356 (15), 1517–1526.
   PubMed Web of Science ®Google Scholar
• Leighton, B., and Cooper, G.J., 1988. Pancreatic amylin and calcitonin gene-related peptide cause resistance to insulin in skeletal muscle in vitro. Nature, 335 (6191), 632–635.
   PubMed Web of Science ®Google Scholar
• Lek, N., and Acerini, C.L. 2010. Cystic fibrosis related diabetes mellitus - diagnostic and management challenges. Current diabetes reviews, 6 (1), 9–16.
   PubMedGoogle Scholar
• Li, L., et al., 2005. Glucagon-like peptide-1 protects beta cells from cytokine-induced apoptosis and necrosis: role of protein kinase B. Diabetologia, 48 (7), 1339–1349.
   PubMed Web of Science ®Google Scholar
• Lizotte, F., et al. 2016. Persistent insulin resistance in podocytes caused by epigenetic changes of shp-1 in diabetes. Diabetes, 65 (12), 3705–3717.
   PubMed Web of Science ®Google Scholar
• Lombardo, F., et al., 2003. Natural history of glucose tolerance, beta-cell function and peripheral insulin sensitivity in cystic fibrosis patients with fasting euglycemia. European journal of endocrinology, 149 (1), 53–59.
   PubMed Web of Science ®Google Scholar
• Lukinius, A., et al., 1989. Co-localization of islet amyloid polypeptide and insulin in the B cell secretory granules of the human pancreatic islets. Diabetologia, 32 (4), 240–244.
   PubMed Web of Science ®Google Scholar
• Mackie, A.D., Thornton, S.J., and Edenborough, F.P. 2003. Cystic fibrosis-related diabetes. Diabetic medicine: a journal of the British diabetic association, 20 (6), 425–436.
   PubMed Web of Science ®Google Scholar
• Maedler, K., et al., 2002. Glucose-induced beta cell production of IL-1beta contributes to glucotoxicity in human pancreatic islets. The journal of clinical investigation, 110 (6), 851–860.
   PubMed Web of Science ®Google Scholar
• Mäkimattila, S., Fineman, M.S., and Yki-Järvinen, H., 2000. Deficiency of total and nonglycosylated amylin in plasma characterizes subjects with impaired glucose tolerance and type 2 diabetes. The journal of clinical endocrinology and metabolism, 85 (8), 2822–2827.
   PubMed Web of Science ®Google Scholar
• Masters, S.L., et al., 2010. Activation of the NLRP3 inflammasome by islet amyloid polypeptide provides a mechanism for enhanced IL-1β in type 2 diabetes. Nature immunology, 11 (10), 897–904.
   PubMed Web of Science ®Google Scholar
• May, P.C., Boggs, L.N., and Fuson, K.S. 1993. Neurotoxicity of human amylin in rat primary hippocampal cultures: similarity to Alzheimer's disease amyloid-beta neurotoxicity. Journal of neurochemistry, 61 (6), 2330–2333.
   PubMed Web of Science ®Google Scholar
• Meier, D.T., et al., 2014. Islet amyloid formation is an important determinant for inducing islet inflammation in high-fat-fed human IAPP transgenic mice. Diabetologia, 57 (9), 1884–1888.
   PubMed Web of Science ®Google Scholar
• Mercurio, F., and Manning, A.M., 1999. NF-kappaB as a primary regulator of the stress response. Oncogene, 18 (45), 6163–6171.
   PubMed Web of Science ®Google Scholar
• Moran, A., 2002. Diagnosis, screening, and management of cystic fibrosis-related diabetes. Current diabetes reports, 2 (2), 111–115.
   PubMedGoogle Scholar
• Moran, A., et al., 1991. Pancreatic endocrine function in cystic fibrosis. The journal of pediatrics, 118 (5), 715–723.
   PubMed Web of Science ®Google Scholar
• Moran, A., et al., 1998. Abnormal glucose metabolism in cystic fibrosis. The journal of pediatrics, 133 (1), 10–17.
   PubMed Web of Science ®Google Scholar
• Moran, A., et al., 1999. Diagnosis, screening and management of cystic fibrosis related diabetes mellitus: a consensus conference report. Diabetes research and clinical practice, 45 (1), 61–73.
   PubMedGoogle Scholar
• Morris, P.E., et al., 2012. A placebo-controlled, double-blind, dose-escalation study to assess the safety, tolerability and pharmacokinetics/pharmacodynamics of single and multiple intravenous infusions of AZD9773 in patients with severe sepsis and septic shock. Critical care (London, England), 16 (1), R31.
   PubMed Web of Science ®Google Scholar
• Mulder, H., Ahrén, B., and Sundler, F., 1996. Islet amyloid polypeptide and insulin gene expression are regulated in parallel by glucose in vivo in rats. The American journal of physiology, 271 (6 Pt 1), E1008–E1014.
   PubMedGoogle Scholar
• Opie, E.L., 1901. On the relation of chronic interstitial pancreatitis to the islands of langerhans and to diabetes melutus. The journal of experimental medicine, 5 (4), 397–428.
   PubMedGoogle Scholar
• Ortis, F., et al., 2006. Cytokine-induced proapoptotic gene expression in insulin-producing cells is related to rapid, sustained, and nonoscillatory nuclear factor-kappaB activation. Molecular endocrinology (Baltimore, Md.), 20 (8), 1867–1879.
   PubMedGoogle Scholar
• Pickup, J.C., et al., 1997. NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X. Diabetologia, 40 (11), 1286–1292.
   PubMed Web of Science ®Google Scholar
• Poitout, V., and Robertson, R.P. 2002 . Minireview: Secondary beta-cell failure in type 2 diabetes-a convergence of glucotoxicity and lipotoxicity. Endocrinology, 143 (2), 339–342.
   PubMed Web of Science ®Google Scholar
• Riordan, J.R., et al., 1989. Identification of the cystic fibrosis gene: cloning and characterization of complementary DNA. Science (New York, N.Y.), 245 (4922), 1066–1073.
   PubMed Web of Science ®Google Scholar
• Ritzel, R.A., and Butler, P.C. 2003. Replication increases beta-cell vulnerability to human islet amyloid polypeptide-induced apoptosis. Diabetes, 52 (7), 1701–1708.
   PubMed Web of Science ®Google Scholar
• Roberts, A.B., and Sporn, M.B. 1985. Transforming growth factors. Cancer surveys, 4 (4), 683–705.
   PubMedGoogle Scholar
• Roesch, E.A., Nichols, D.P., and Chmiel, J.F. 2018. Inflammation in cystic fibrosis: an update. Pediatric pulmonology. doi:10.1002/ppul.24129
   PubMedGoogle Scholar
• Saafi, E.L., et al., 2001. Ultrastructural evidence that apoptosis is the mechanism by which human amylin evokes death in RINm5F pancreatic islet beta-cells. Cell biology international, 25 (4), 339–350.
   PubMed Web of Science ®Google Scholar
• Sarvetnick, N., et al., 1988. Insulin-dependent diabetes mellitus induced in transgenic mice by ectopic expression of class II MHC and interferon-gamma. Cell, 52 (5), 773–782.
   PubMed Web of Science ®Google Scholar
• Schubert, D., et al., 1995. Amyloid peptides are toxic via a common oxidative mechanism. Proceedings of the National academy of sciences of the United States of America, 92 (6), 1989–1993.
   PubMed Web of Science ®Google Scholar
• Sheppard, D.N., and Welsh, M.J. 1999. Structure and function of the CFTR chloride channel. Physiological reviews, 79 (1 Suppl), S23–S45.
   PubMedGoogle Scholar
• Silvestre, R.A., et al., 1990. Inhibitory effect of rat amylin on the insulin responses to glucose and arginine in the perfused rat pancreas. Regulatory peptides, 31 (1), 23–31.
   PubMedGoogle Scholar
• Soejima, K., and Landing, B.H. 1986. Pancreatic islets in older patients with cystic fibrosis with and without diabetes mellitus: morphometric and immunocytologic studies. Pediatric pathology, 6 (1), 25–46.
   PubMedGoogle Scholar
• Spence, C. 2005. Cystic fibrosis-related diabetes: practice challenges. Paediatric nursing, 17 (2), 23–26.
   PubMedGoogle Scholar
• Stumvoll, M., Goldstein, B.J., and van Haeften, T.W. 2005. Type 2 diabetes: principles of pathogenesis and therapy. Lancet (London, England), 365 (9467), 1333–1346.
   PubMed Web of Science ®Google Scholar
• Suk, K., et al., 2001. IFN-gamma/TNF-alpha synergism as the final effector in autoimmune diabetes: a key role for STAT1/IFN regulatory factor-1 pathway in pancreatic beta cell death. Journal of immunology, 166 (7), 4481–4489.
   PubMed Web of Science ®Google Scholar
• Tarantino, G., and Caputi, A. 2011. JNKs, insulin resistance and inflammation: A possible link between NAFLD and coronary artery disease. World journal of gastroenterology, 17 (33), 3785–3794.
   PubMed Web of Science ®Google Scholar
• Tominaga, T., et al., 2011. Activation of bone morphogenetic protein 4 signaling leads to glomerulosclerosis that mimics diabetic nephropathy. The journal of biological chemistry, 286 (22), 20109–20116.
   PubMed Web of Science ®Google Scholar
• Tucker, H.M., et al., 1998. Human amylin induces "apoptotic" pattern of gene expression concomitant with cortical neuronal apoptosis. Journal of neurochemistry, 71 (2), 506–516.
   PubMed Web of Science ®Google Scholar
• Urist, M.R., and Peltier, L.F. 2002. Bone: formation by autoinduction. Clinical orthopaedics and related research, 395 (1965), 4–10.
   Google Scholar
• Wascher, T.C., et al., 2011. Chronic TNF-α neutralization does not improve insulin resistance or endothelial function in "healthy" men with metabolic syndrome. Molecular medicine (Cambridge, Mass.), 17 (3-4), 189–193.
   PubMed Web of Science ®Google Scholar
• Weisberg, S.P., et al., 2003. Obesity is associated with macrophage accumulation in adipose tissue. The journal of clinical investigation, 112 (12), 1796–1808.
   PubMed Web of Science ®Google Scholar
• Wellen, K.E., and Hotamisligil, G.S. 2005. Inflammation, stress, and diabetes. The journal of clinical investigation, 115 (5), 1111–1119.
   PubMed Web of Science ®Google Scholar
• Westermark, P. 1972. Quantitative studies on amyloid in the islets of Langerhans. Upsala journal of medical sciences, 77 (2), 91–94.
   PubMed Web of Science ®Google Scholar
• Westermark, P. 1992. Polypeptide hormones in amyloid. Journal of internal medicine, 232 (6), 529–530.
   PubMed Web of Science ®Google Scholar
• Westermark, P., et al., 1987. Islet amyloid in type 2 human diabetes mellitus and adult diabetic cats contains a novel putative polypeptide hormone. American journal of pathology, 127 (3), 414–417.
   PubMed Web of Science ®Google Scholar
• Yamanaka, Y., et al., 1993. Synthesis and expression of transforming growth factor beta-1, beta-2, and beta-3 in the endocrine and exocrine pancreas. Diabetes, 42 (5), 746–756.
   PubMed Web of Science ®Google Scholar
• Yamaoka, T., et al., 1998. Hypoplasia of pancreatic islets in transgenic mice expressing activin receptor mutants. The journal of clinical investigation, 102 (2), 294–301.
   PubMed Web of Science ®Google Scholar
• Yankner, B.A., Duffy, L.K., and Kirschner, D.A. 1990. Neurotrophic and neurotoxic effects of amyloid beta protein: reversal by tachykinin neuropeptides. Science (New York, N.Y.), 250 (4978), 279–282.
   PubMed Web of Science ®Google Scholar
• Yew, K.H., et al., 2005. Cross-talk between bone morphogenetic protein and transforming growth factor-beta signaling is essential for exendin-4-induced insulin-positive differentiation of AR42J cells. Journal of biological chemistry, 280 (37), 32209–32217.
   PubMed Web of Science ®Google Scholar
• Yung, B., et al., 2002. Cystic fibrosis-related diabetes: the role of peripheral insulin resistance and beta-cell dysfunction. Diabetic medicine, 19 (3), 221–226.
   PubMed Web of Science ®Google Scholar
• Zhang, Y.Q., et al., 2004. Inhibition of activin signaling induces pancreatic epithelial cell expansion and diminishes terminal differentiation of pancreatic beta-cells. Diabetes, 53 (8), 2024–2033.
   PubMed Web of Science ®Google Scholar