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+{
+  "titles": [
+    "2010 - Neural tube defect genes and maternal diabetes during pregnancy.pdf",
+    "2018 - Genetic variants of gestational diabetes mellitus a study of 112 SNPs among 8722 women in two independent populations.pdf",
+    "2017 - Genome-wide DNA methylation variation in maternal and cord blood of gestational diabetes population.pdf",
+    "2010 - Autism Spectrum Disorders and Epigenetics.pdf",
+    "2017 - Genome-wide DNA methylation variation in maternal and cord blood of gestational diabetes population.pdf",
+    "2015 - Type 2 diabetes mellitus.pdf",
+    "2015 - Maternal diabetes, gestational diabetes and the role of epigenetics in their long term effects on offspring.pdf",
+    "2005  - Animal models of diabetes mellitus.pdf",
+    "2004 - Impaired glucose homeostasis in transgenic mice expressing the human transient neonatal diabetes mellitus locus.pdf",
+    "2010 - Neural tube defect genes and maternal diabetes during pregnancy.pdf"
+  ],
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+    "maternal diabetes reduces the precision of gene regulation in exposed individuals. Loss of precision in embry-onic gene regulation may include changes to the epigenome via deregulated expression of chromatin-modify-ing factors. Unraveling the mechanisms underlying such epigenetic modications in diabetic pregnancies willhelp to understand how teratogenic insults compromise embryonic development and possibly provide ave-nues for therapeutic intervention. Birth Defects Research (Part A) 88:601611, 2010.",
+    "and metabolic imprinting: the ongoing effects of maternal hyper-glycemia. Diabetes Care 30:2287 2292 9. Clausen TD, Mathiesen ER, Hansen T et al (2008) High prevalence of type 2 diabetes and pre-diabetes in adult offspring of women withgestational diabetes mellitus or type 1 diabetes: the role of intrauter- ine hyperglycemia. Diabetes Care 31:340 346 10. Solomon CG, Willett WC, Carey VJ et al (1997) A prospective study of pregravid determinants of gestational diabetes mellitus. JAMA 278:1078 1083",
+    "M. Gestational diabetes alters offspring DNA methylation profiles in human and rat: Identification of key  pathways involved in endocrine system disorders, insulin signaling, diabetes signaling, and ILK signaling.  Endocriniology 2015;156:2222 -38.  [33] Murphy SK, Huang Z, Hoyo  C. Differentially methylated regions of imprinted genes in prenatal,  perinatal and postnatal human tissues. PLOS ONE 2012;7:e40924.",
+    "12. Kim JK, Samaranayake M, Pradhan S. Epigenetic mechanisms in mammals. Cell Mol Life Sci. 2009;66:596-612. 13. Horsthemke B, Buiting K. Genomic imprinting and imprinting defects in humans. Adv Genet. 2008;61:225-246. 14. Iacobuzio-Donahue CA. Epigenetic Changes in Cancer. Annu Rev Pathol. 2009;4:229-249. 15. Temple IK. Imprinting in human disease with special reference to transient neonatal diabetes and Beckwith-Wiedemann syn- drome. Endocr Dev. 2007;12:113-123.",
+    "and Knowler W C. Intrauterine exposure to diabetes conveys risks for type 2 diabetes and obesity: A study  of discordant sibships. Diabetes 2000;49:2208 -11.  [11] Feil R and Fraga  MF. Epigenetics and the environment: Emerging patterns and implications. Nature   Reviews Genetics 2012;13:97 -109.  [12] Recillas -Targa F. DNA Methylation, Chromatin boundaries, and mechanisms of genomic imprinting.  Archives of Medical Research 2002;33:428 -38.",
+    "53. T ravers,M.E. etal.  Insights into the molecular  mechanism for type2 diabetes susceptibility at the  KCNQ1  locus from temporal changes in imprinting  status in human islets. Diabetes 62, 987992 (2013). 54. Gulli,G., Ferrannini,E., Stern,M., Haffner,S.  &DeFronzo,R.A. The metabolic profile of NIDDM  isfully established in glucose-tolerant offspring of  twoMexican-American NIDDM parents. Diabetes 41,  15751586 (1992). PRIMER NATURE REVIEWS | DISEASE PRIMERS   VOLUME 1 | 2015  | 17",
+    "Gaudet, D., Hivert, M.F., Brisson, D., Bouchard, L., 2013 Sep. Gestational diabetesmellitus epigenetically affects genes predominantly involved in metabolic dis- eases. Epigenetics 8 (9), 935 e943. Salbaum, J.M., Kappen, C., 2012 Oct. Responses of the embryonic epigenome to maternal diabetes. Birth Defects Res. A Clin. Mol. Teratol. 94 (10), 770 e781. Salbe, A.D., Lindsay, R.S., Collins, C.B., Tataranni, P.A., Krakoff, J., Bunt, J.C., 2007 Feb.",
+    "environment are probably mediated by a permanent program-ming of the developing offspring, e.g. by the mechanism ofimprinting. Of interest, the increased risk of diabetes continuesinto subsequent generations, suggesting the changes also affectthe germ cell line [143].  Conclusions  There is little doubt that some animal models of diabetes have",
+    "tal diabetes and later onset diabetes: a case of inher - ited insulin resistance. Arch. Dis. Child.  72:5657.  6. Temple, I.K., et al. 1995. An imprinted gene(s) for  diabetes? Nat. Genet.  9:110112.  7. Temple, I.K., et al. 1996. Further evidence for an  imprinted gene for neonatal diabetes localised to chro -",
+    "1994; Martinez-Frias et al., 1998). The underlying mecha-nisms are not well understood, but are thought to involve various responses of the embryonic genome to the adverse intrauterine environment (Greene, 2001;Loeken, 2008). To explore how conditions of maternal diabetes affect gene expression in the embryo, we recently conducted expression proling experiments on embryos from dia-betic dams compared to embryos from normal dams(Pavlinkova et al., 2009). We were able to demonstrate"
+  ],
+  "answer": "Genomic imprinting has a significant impact on the susceptibility and progression of diabetes. Imprinting can influence the expression of genes involved in metabolic processes, which are crucial in the development of diabetes. For instance, changes in imprinting status at specific loci, such as the KCNQ1 locus, have been linked to type 2 diabetes susceptibility, indicating that temporal changes in imprinting can affect the function of pancreatic islets and contribute to diabetes risk [6]. Additionally, imprinting defects have been associated with specific forms of diabetes, such as transient neonatal diabetes, suggesting that imprinted genes play a role in the disease's onset and progression [4]. Furthermore, the effects of maternal diabetes on the offspring's epigenome, including alterations in DNA methylation profiles, highlight the role of imprinting in the intergenerational transmission of diabetes risk [3], [7]. These epigenetic changes can lead to a permanent programming of the developing offspring, increasing the risk of diabetes in subsequent generations [8]. Overall, genomic imprinting is a critical factor in understanding the genetic and epigenetic mechanisms underlying diabetes susceptibility and progression.",
+  "question": "What is the impact of genomic imprinting on the susceptibility and progression of diabetes?,"
+}
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