This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.The purpose of this study is to investigate the determinants of diabetes and cardiovascular disease (CVD) risk in young people diagnosed with diabetes before age 18 and their family members. Recent increases in childhood diabetes herald a substantial jump in the CVD- and diabetes-related public health burden in years to come, unless effective prevention efforts are mounted. It is therefore essential to understand the mechanisms underlying the current epidemic among children and adolescents. The following hypotheses frame the research project: Hypothesis 1. Diabetes can develop in various ways, from autoimmunity leading to type 1, to obesity-related, insulin-resistant type 2 diabetes. A subset of children develop diabetes through a combination of the 2 major pathways, with autoimmune -cell destruction aggravated by the presence of insulin resistance related to genetic susceptibility, obesity and/or physical inactivity.Hypothesis 2. A complex interplay of heritable, behavioral, and treatment factors can accelerate or delay the development of CVD and chronic diabetes complications. Familial clustering of these factors may itself play a role in determining risk for people with diabetes. It is particularly compelling to understand this process in young patients, those with the most years of productive life at stake.Data collection is carried out primarily during home visits, or for those who prefer, outpatient visits to the GCRC. Families gather, fasting, for glucose challenge tests, biochemical measures, anthropometrics, blood pressure and questionnaire administration. Samples are processed through the GCRC core laboratory. We estimate that up to 400 families will take part.
| Rosenfield, Robert L; Ehrmann, David A (2016) The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev 37:467-520 |
| Garyu, Justin W; Meffre, Eric; Cotsapas, Chris et al. (2016) Progress and challenges for treating Type 1 diabetes. J Autoimmun 71:1-9 |
| Rosenfield, Robert L (2015) The Polycystic Ovary Morphology-Polycystic Ovary Syndrome Spectrum. J Pediatr Adolesc Gynecol 28:412-9 |
| Maitland, Michael L; Xu, Chun-Fang; Cheng, Yu-Ching et al. (2015) Identification of a variant in KDR associated with serum VEGFR2 and pharmacodynamics of Pazopanib. Clin Cancer Res 21:365-72 |
| Bershad, Anya K; Jaffe, Jerome H; Childs, Emma et al. (2015) Opioid partial agonist buprenorphine dampens responses to psychosocial stress in humans. Psychoneuroendocrinology 52:281-8 |
| Fleming, Gini F; Schumm, Philip; Friberg, Greg et al. (2015) Circadian variation in plasma 5-fluorouracil concentrations during a 24 hour constant-rate infusion. BMC Cancer 15:69 |
| Refetoff, Samuel; Bassett, J H Duncan; Beck-Peccoz, Paolo et al. (2014) Classification and proposed nomenclature for inherited defects of thyroid hormone action, cell transport, and metabolism. J Clin Endocrinol Metab 99:768-70 |
| Kirkpatrick, Matthew G; Francis, Sunday M; Lee, Royce et al. (2014) Plasma oxytocin concentrations following MDMA or intranasal oxytocin in humans. Psychoneuroendocrinology 46:23-31 |
| Copinschi, Georges; Leproult, Rachel; Spiegel, Karine (2014) The important role of sleep in metabolism. Front Horm Res 42:59-72 |
| Müller, Peter; Quintana, Fernando A; Rosner, Gary L et al. (2014) Bayesian inference for longitudinal data with non-parametric treatment effects. Biostatistics 15:341-52 |
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