Rochelle N. Naylor

ORCID: 0000-0003-1753-8328
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About
Contact & Profiles
Research Areas
  • Pancreatic function and diabetes
  • Diabetes Management and Research
  • Diabetes and associated disorders
  • Diabetes Treatment and Management
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Genomics and Rare Diseases
  • Gestational Diabetes Research and Management
  • Diet and metabolism studies
  • Bariatric Surgery and Outcomes
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Congenital heart defects research
  • Genetics and Neurodevelopmental Disorders
  • Nutrition, Genetics, and Disease
  • BRCA gene mutations in cancer
  • Metabolism, Diabetes, and Cancer
  • Ethics in Clinical Research
  • Cardiovascular Function and Risk Factors
  • Cancer-related gene regulation
  • Endoplasmic Reticulum Stress and Disease
  • Epigenetics and DNA Methylation
  • CRISPR and Genetic Engineering
  • Obesity, Physical Activity, Diet
  • Pregnancy and preeclampsia studies
  • Biomedical Ethics and Regulation
  • Obesity and Health Practices

University of Chicago
2015-2025

University of Ibadan
2024

University College Hospital, Ibadan
2024

Diabetes Australia
2020

Phillips Exeter Academy
2018

OBJECTIVE To evaluate the cost-effectiveness of a genetic testing policy for HNF1A-, HNF4A-, and GCK-MODY in hypothetical cohort type 2 diabetic patients 25-40 years old with MODY prevalence 2%. RESEARCH DESIGN AND METHODS We used simulation model diabetes complications based on UK Prospective Diabetes Study data, modified to account natural history disease by subtype compare at diagnosis versus no testing. Under screening policy, successful sulfonylurea treatment HNF1A-MODY HNF4A-MODY was...

10.2337/dc13-0410 article EN cc-by-nc-nd Diabetes Care 2013-09-12

Maturity-onset diabetes of the young (MODY) is a clinically heterogeneous group monogenic disorders characterized by autosomal dominant inheritance young-onset, non-insulin-dependent diabetes. The genes involved are important in beta cell development, function and regulation lead to glucose sensing insulin secretion. Heterozygous GCK mutations cause impaired glucokinase activity resulting stable, mild hyperglycaemia that rarely requires treatment. HNF1A progressive secretory defect sensitive...

10.1111/j.1365-2265.2011.04049.x article EN Clinical Endocrinology 2011-03-19

Context: Diabetes in neonates nearly always has a monogenic etiology. Earlier sulfonylurea therapy can improve glycemic control and potential neurodevelopmental outcomes children with KCNJ11 or ABCC8 mutations, the most common gene causes. Objective: Assess risks benefits of initiating before genetic testing results become available. Design, Setting, Patients: Observational retrospective study subjects neonatal diabetes within University Chicago Monogenic Registry. Main Outcome Measures:...

10.1210/jc.2014-2494 article EN The Journal of Clinical Endocrinology & Metabolism 2014-09-19

Although insulin resistance consistently occurs with type 1 diabetes, its predominant driver is uncertain. We therefore determined the relative contributions of hyperglycemia and iatrogenic hyperinsulinemia to using hyperinsulinemic-euglycemic clamps in three participant groups (n = 10/group) differing insulinemia glycemia: healthy control subjects (euinsulinemia euglycemia), glucokinase–maturity-onset diabetes young (GCK-MODY; euinsulinemia hyperglycemia), (hyperinsulinemia matching...

10.2337/db19-0324 article EN Diabetes 2019-05-15
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