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Review

Pancreatic Gene Variants Potentially Associated with Dipeptidyl Peptidase-4 Inhibitor Treatment Response in Type 2 Diabetes

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Pages 235-249 | Published online: 21 Jan 2014

References

  • Liu Y , ZhouDZ, ZhangDet al. Variants in KCNQ1 are associated with susceptibility to Type 2 diabetes in the population of mainland China. Diabetologia 52 , 1315–1321 (2006).
  • Brun T , FranklinI, St-OngeLet al. The diabetes-linked transcription factor PAX4 promotes β-cell proliferation and survival in rat and human islets. J. Cell Biol. 167 , 1123–1135 (2004).
  • Inzucchi SE , BergenstalRM, BuseJBet al. Management of hyperglycemia in Type 2 diabetes: a patient-centered approach. Position statement of the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetes Care 35(6) , 1364–1379 (2012).
  • Gautier JF , FetitaS, SobngwiE, MartinCS. Biological actions of the incretins GIP and GLP-1 and therapeutic perspectives in patients with Type 2 diabetes. Diabetes Metab.31(3 Pt 1) , 233–242 (2005).
  • Nauck MA , HombergerE, SiegelEGet al. Incretin effects of increasing glucose loads in man calculated from venous insulin and C-peptide responses. J. Clin. Endocrinol. Metab. 63(2) , 492–498 (1986).
  • Tolhurst G , ReimannF, GribbleFM. Nutritional regulation of glucagon-like peptide-1 secretion. J. Physiol.587(1) , 27–32 (2009).
  • Mussig K , StaigerH, MachicaoF, HaringHU, FritscheA. Genetic variants affecting incretin sensitivity and incretin secretion. Diabetologia53 , 2289–2297 (2010).
  • Drucker DJ , NauckMA. The incretin system: glucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors in Type 2 diabetes. Lancet368 , 1696–1705 (2006).
  • Meier JJ , GallwitzB, SchmidtWE, NauckMA. Glucagon-like peptide 1 as a regulator of food intake and body weight: therapeutic perspectives. Eur. J. Pharmacol.440 , 269–279 (2002).
  • Gautier JF , ChoukemSP, GirardJ. Physiology of incretins (GIP and GLP-1) and abnormalities in Type 2 diabetes. Diabetes Metab.34 , S65–S72 (2008).
  • Lamont BJ , LiY, KwanE, BrownTJ, GaisanoH, DruckerDJ. Pancreatic GLP-1 receptor activation is sufficient for incretin control of glucose metabolism in mice. J. Clin. Invest.122(1) , 388–402 (2012).
  • Sathananthan A , ManCD, MichelettoFet al. Common genetic variation in GLP1R and insulin secretion in response to exogenous GLP-1 in non-diabetic subjects. Diabetes Care 33 , 2074–2076 (2010).
  • Stolerman ES , FlorezJC. Genomics of Type 2 diabetes mellitus: implications for the clinician. Nat. Rev. Endocrinol.5 , 429–436 (2009).
  • Foukas LC , OkkenhaugK. Gene-targeting reveals physiological roles and complex regulation of the phosphoinositide 3-kinases. Arch. Biochem. Biophys.414 , 13–18 (2003).
  • Lyssenko V , EliassonL, KotovaOet al. Pleiotropic effects of GIP on islet function involve osteopontin. Diabetes 60 , 2424–2433 (2011).
  • Charbonnel B , CariouB. Pharmacological management of Type 2 diabetes: the potential of incretin-based therapies. Diabetes Obes. Metab.13(2) , 99–117 (2011).
  • Addison D , AguilarD. Diabetes and cardiovascular disease: the potential benefit of incretin-based therapies. Curr. Atheroscler. Rep.13 , 115–122 (2011).
  • Baggio LL , DruckerDJ. Biology of incretins: GLP-1 and GIP. Gastroenterology132 , 2131–2157 (2009).
  • Lacy CF . Drug Information Handbook (18th Edition). Armstrong LL, Goldman MP, Lance LL (Eds). Lexi-Comp Inc., OH, USA , 1375–1376 (2009).
  • Ye Y , KeyesKT, ZhangC, Perez-PoloJR, LinY, BirnbaumY. The myocardial infarct size-limiting effect of sitagliptin is PKA-dependent, whereas the protective effect of pioglitazone is partially dependent on PKA. Am. J. Physiol. Heart Circ. Physiol.298 , H1454–H1465 (2010).
  • Nauck MA . Incretin-based therapies for Type 2 diabetes mellitus: properties, functions, and clinical implications. Am. J. Med.124 , S3–S18 (2011).
  • Kwon O , ChoeEY, ChoiYet al. Discovery of dipeptidyl peptidase-4 gene variants and the associations with efficacy of vildagliptin in patients with Type 2 diabetes – a pilot study. J. Diabetes Metab. 2013 , S13–006 (2013).
  • Nathan DM , BuseJB, DavidsonMBet al. Medical management of hyperglycemia in Type 2 diabetes: a consensus algorithm for the initiation and adjustment of therapy. Diabetes Care 32 , 193–203 (2009).
  • Duez H , CariouB, StaelsB. DPP-4 inhibitors in the treatment of Type 2 diabetes. Biochem. Pharmacol.83 , 823–832 (2012).
  • American Diabetes Association. Standards of medical care in diabetes. Diabetes Care36 , S11–S66 (2013).
  • Kaneko K , UekiK, TakahashiNet al. Class IA phosphatidylinositol 3-kinase in pancreatic β cells controls insulin secretion by multiple mechanisms. Cell Metab. 12 , 619–632 (2010).
  • Fonseca SG , FukumaM, LipsonKLet al. WFS1 is a novel component of the unfolded protein response and maintains homeostasis of the endoplasmic reticulum in pancreatic β-cells. J. Biol. Chem. 280 , 39609–39615 (2005).
  • Ishihara H , TakedaS, TamuraAet al. Disruption of the WFS1 gene in mice causes progressive β-cell loss and impaired stimulus-secretion coupling in insulin secretion. Hum. Mol. Genet. 13 , 1159–1170 (2004).
  • Masana MI , DubocovichML. Melatonin receptor signaling: finding the path through the dark. Sci. STKE2001(107) , pe39 (2001).
  • Miki T , SeinoS. Roles of KATP channels as metabolic sensors in acute metabolic changes. J. Mol. Cell. Cardiol.38 , 917–925 (2005).
  • Gloyn AL , WeedonMN, OwenKRet al. Large-scale association studies of variants in genes encoding the pancreatic β-cell KATP channel subunit Kir6.2 (KCNJ11) and SUR1 (ABCC8) confirm that the KCNJ11 E23K variant is associated with Type 2 diabetes. Diabetes 52 , 568–572 (2003).
  • Wang J , ElghaziL, ParkerSEet al. The concerted activities of Pax4 and Nkx2.2 are essential to initiate pancreatic β-cell differentiation. Dev. Biol. 266(1) , 178–189 (2004).
  • Damcott CM , PollinTI, ReinhartLJet al. Polymorphisms in the transcription factor 7-like 2 (TCF7L2) gene are associated with Type 2 diabetes in the Amish: replication and evidence for a role in both insulin secretion and insulin resistance. Diabetes 55 , 2654–2659 (2006).
  • Nelson WJ , NusseR. Convergence of Wnt, β-catenin, and cadherin pathways. Science303 , 1483–1487 (2004).
  • Chandak GR , JanipalliCS, BhaskarSet al. Common variants in the TCF7L2 gene are strongly associated with Type 2 diabetes mellitus in the Indian population. Diabetologia 50 , 63–67 (2007).
  • Horikoshi M , HaraK, ItoC, NagaiR, FroguelP, KadowakiT. A genetic variation of the transcription factor 7-like 2 gene is associated with risk of Type 2 diabetes in the Japanese population. Diabetologia50 , 747–751 (2007).
  • Lehman DM , HuntKJ, LeachRJet al. Haplotypes of transcription factor 7-like 2 (TCF7L2) gene and its upstream region are associated with Type 2 diabetes and age of onset in Mexican Americans. Diabetes 56 , 389–393 (2007).
  • Villareal DT , RobertsonH, BellGIet al. TCF7L2 variant rs7903146 affects the risk of Type 2 diabetes by modulating incretin action. Diabetes59 , 479–485 (2010).
  • Reya T , CleverH. Wnt signalling in stem cells and cancer. Nature434 , 843–850 (2005).
  • Taniguchi CM , KondoT, SajanMet al. Divergent regulation of hepatic glucose and lipid metabolism by phosphoinositide 3-kinase via Akt and PKCλ/ζ. Cell Metab. 3 , 343–353 (2006).
  • Zhang X , GanL, PanHet al. Phosphorylation of serine 256 suppresses transactivation by FKHR (FOXO1) by multiple mechanisms. J. Biol. Chem. 277(47) , 45276–45284 (2002).
  • Mussig K , StaigerH, MachicaoFet al. Association of Type 2 diabetes candidate polymorphisms in KCNQ1 with incretin and insulin secretion. Diabetes 57 , 1715–1720 (2009).
  • Shimajiri Y , SankeT, FurutaHet al. A missense mutation of Pax4 gene (R121W) is associated with Type 2 diabetes in Japanese. Diabetes 50 , 2864–2869 (2001).
  • Mellado-Gil JM , Cobo-VuilleumierN, GauthierBR. Islet β-cell mass preservation and regeneration in diabetes mellitus: four factors with potential therapeutic interest. J. Transplant.10 , 1155–1164 (2012).
  • Dohrmann C , GrussP, LemaireL. Pax genes and the differentiation of hormone-producing endocrine cells in the pancreas. Mech. Dev.92 , 47–54 (2000).
  • Sosa-Pineda B , ChowdhuryK, TorresM, OliverG, GrussP. The Pax4 gene is essential for differentiation of insulin-producing β cells in the mammalian pancreas. Nature386(6623) , 399–402 (1997).
  • Greenwood AL , LiS, JonesK, MeltonDA. Notch signalling reveals developmental plasticity of Pax4+ pancreatic endocrine progenitors and shunts them to a duct fate. Mech. Dev.124(2) , 97–107 (2007).
  • Larsson LI , St Onge L, Hougaard DM, Sosa Pineda B, Gruss P. Pax4 and 6 regulate gastrointestinal endocrine cell development. Mech. Dev.79 , 153–159 (1998).
  • Salehi M , AulingerBA, D‘AlessioDA. Targeting β-cell mass in Type 2 diabetes: promise and limitations of new drugs based on incretins. Endocr. Rev.20(3) , 367–379 (2008).
  • Brun T , Hu He KH, Lupi R et al. The diabetes-linked transcription factor Pax4 is expressed in human pancreatic islets and is activated by mitogens and GLP-1. Hum. Mol. Genet.17(4) , 478–489 (2008).
  • Vasavada RC , Gonzalez-PertusaJA, FujinakaY, Fiaschi-TaeschN, Cozar-CastellanoI, Garcia-OcanaA. Growth factors and beta cell replication. Int. J. Biochem. Cell Biol.38 , 931–950 (2006).
  • Johnson JD , Bernal-MizrachiE, Alejandro et al. Insulin protects islets from apoptosis via PDX1 and specific changes in the human islet proteome. Proc. Natl Acad. Sci. USA103 , 19575–19580 (2006).
  • Tan JT , NurbayaS, GardnerD, YeS, TaiES, NgDP. Genetic variation in KCNQ1 associates with fasting glucose and β-cell function: a study of 3,734 subjects comprising three ethnicities living in Singapore. Diabetes58 , 1445–1449 (2009).
  • Yasuda K , MiyakeK, HorikawaYet al. Variants in KCNQ1 are associated with susceptibility to Type 2 diabetes mellitus. Nat. Genet. 40 , 1092–1097 (2008).
  • Unoki H , TakahashiA, KawaguchiTet al. SNPs in KCNQ1 are associated with susceptibility to Type 2 diabetes in east Asian and European populations. Nat. Genet. 40 , 1098–1102 (2008).
  • Bleich M , WarthR. The very small-conductance K+ channel KvLQT1 and epithelial function. Eur. J. Physiol.440 , 202–206 (2000).
  • Vallon V , GrahammerF, VolklHet al. KCNQ1-dependent transport in renal and gastrointestinal epithelia. Proc. Natl Acad. Sci. USA102(49) , 17864–17869 (2005).
  • Schafer SA , MussigK, StaigerHet al. A common genetic variant in WFS1 determines impaired glucagon-like peptide-1-induced insulin secretion. Diabetologia 52 , 1075–1082 (2009).
  • Heni M , KettererC, ThamerCet al. Glycemia determines the effect of Type 2 diabetes risk genes on insulin secretion. Diabetes 59 , 3247–3252 (2010).
  • Fawcett KA , WheelerE, MorrisAPet al. Detailed investigation of the role of common and low-frequency WFS1 variants in Type 2 diabetes risk. Diabetes 59 , 741–746 (2010).
  • Florez JC , JablonskiKA, BayleyNet al. TCF7L2 polymorphisms and progression to diabetes in the diabetes prevention program. N. Engl. J. Med.355 , 241–250 (2006).
  • Lyssenko V . The transcription factor 7-like 2 gene and increased risk of Type 2 diabetes: an update. Curr. Opin. Clin. Nutr. Metab. Care11 , 385–392 (2008).
  • Kim H , ChoeSA, KuSY, KimSH, KimJG. Association between Wnt signalling pathway gene polymorphism and bone response to hormone therapy in postmenopausal Korean women. Menopause18(7) , 808–813 (2011).
  • Shu L , MatveyenkoAV, Kerr-ConteJ, ChoJH, McIntoshCH, MaedlerK. Decreased TCF7L2 protein levels in Type 2 diabetes mellitus correlate with downregulation of GIP- and GLP-1 receptors and impaired beta-cell function. Hum. Mol. Genet.18(13) , 2388–2399 (2009).
  • Bloomgarden ZT . Incretin concepts. Diabetes Care33(2) , e20–e25 (2010).
  • Schafer SA , TschritterO, MachicaoFet al. Impaired glucagon-like peptide-1-induced insulin secretion in carriers of transcription factor 7-like 2 (TCF7L2) gene polymorphisms. Diabetologia 50 , 2443–2450 (2007).
  • Nestorowicz A , GlaserB, WilsonBAet al. Genetic heterogeneity in familial hyperinsulinism. Hum. Mol. Genet. 7 , 1119–1128 (1998).
  • Cartier EA , ContiLR, VandenbergCA, ShyngSL. Defective trafficking and function of KATP channels caused by a sulfonylurea receptor 1 mutation associated with persistent hyperinsulinemic hypoglycemia of infancy. Proc. Natl Acad. Sci. USA98 , 2882–2887 (2001).
  • Koster JC , PermuttMA, NicholsCG. Perspectives in diabetes. Diabetes and insulin secretion. The ATP-sensitive K+ channel (KATP) connection. Diabetes54 , 3065–3072 (2005).
  • Gerdin MJ , MseehF, DubocovichML. Mutagenesis studies of the human MT2 melatonin receptor. Biochem. Pharmacol.66 , 315–320 (2003).
  • Dubocovich ML . Melatonin receptors: role on sleep and circadian rhythm regulation. Sleep Med.8 , S34–S42 (2007).
  • Lyssenko V , NagornyCL, ErdosMRet al. Common variant in MTNR1B associated with increased risk of Type 2 diabetes and impaired early insulin secretion. Nat. Genet. 41(1) , 82–88 (2009).
  • Liu C , WuY, LiHet al. MTNR1B rs10830963 is associated with fasting plasma glucose, HbA1c and impaired beta-cell function in Chinese Hans from Shanghai. BMC Med. Genet.11 , 59 (2010).
  • Spars⊘ T , BonnefondA, AndersonEet al. G-allele of intronic rs10830963 in MTNR1B confers increased risk of impaired fasting glycemia and Type 2 diabetes through an impaired glucose-stimulated insulin release. Diabetes 58 , 1450–1456 (2009).
  • Simonis-Bik AM , NijpelsG, van Haeften TW et al. Gene variants in the novel Type 2 diabetes loci CDC123/CAMK1D, THADA, ADAMTS9, BCL11A, and MTNR1B affect different aspects of pancreatic β-cell function. Diabetes59 , 293–301 (2010).
  • Shimajiri Y , ShimabukuroM, TomoyoseTet al. Pax4 mutation (R121W) as a prodiabetic variant in Okinawans. Biochem. Biophys. Res. Commun.302(2) , 342–344 (2003).
  • Chambers JC , ZhangW, ZabanehDet al. Common genetic variation near melatonin receptor MTNR1B contributes to raised plasma glucose and increased risk of Type 2 diabetes aming Indian Asians and European Caucasians. Diabetes 58 , 2703–2708 (2009).

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