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151. Replication of Genome-Wide Association Signals in UK Samples Reveals Risk Loci for Type 2 Diabetes

152. A Common Variant in the FTO Gene Is Associated with Body Mass Index and Predisposes to Childhood and Adult Obesity

153. Fetal alleles predisposing to metabolically favorable adiposity are associated with higher birth weight

154. Systematic genetic testing for recessively inherited monogenic diabetes: a cross-sectional study in paediatric diabetes clinics

156. Association of birthweight and penetrance of diabetes in individuals with HNF4A-MODY: a cohort study

158. Genetic Evidence for Causal Relationships Between Maternal Obesity-Related Traits and Birth Weight

159. Routine Islet Autoantibody Testing in Clinically Diagnosed Adult-Onset Type 1 Diabetes Can Help Identify Misclassification and the Possibility of Successful Insulin Cessation.

163. Reappearance of C-Peptide During the Third Trimester of Pregnancy in Type 1 Diabetes: Pancreatic Regeneration or Fetal Hyperinsulinism?

165. Inferring causal pathways between metabolic processes and liver fat accumulation: an IMI DIRECT study

166. HbA1c performs well in monitoring glucose control even in populations with high prevalence of medical conditions that may alter its reliability: the OPTIMAL observational multicenter study

167. The penetrance of age-related monogenic disease depends on ascertainment context

168. Genetic scores to stratify risk of developing multiple islet autoantibodies and type 1 diabetes: A prospective study in children

171. Association Analysis of 29,956 Individuals Confirms That a Low-Frequency Variant at CCND2 Halves the Risk of Type 2 Diabetes by Enhancing Insulin Secretion

172. Genetic studies of body mass index yield new insights for obesity biology

173. New genetic loci link adipose and insulin biology to body fat distribution

176. Evaluating associations between the benefits and risks of drug therapy in type 2 diabetes: a joint modeling approach

177. Additional file 5 of Choice of HbA1c threshold for identifying individuals at high risk of type 2 diabetes and implications for diabetes prevention programmes: a cohort study

178. Additional file 3 of Choice of HbA1c threshold for identifying individuals at high risk of type 2 diabetes and implications for diabetes prevention programmes: a cohort study

180. The power of genetic diversity in genome-wide association studies of lipids

181. Extended data Wellcome Open Research 16097.pdf

182. Loss of MANF causes childhood-onset syndromic diabetes due to increased endoplasmic reticulum stress

183. Additional file 4 of Choice of HbA1c threshold for identifying individuals at high risk of type 2 diabetes and implications for diabetes prevention programmes: a cohort study

184. Phenotypic severity of homozygous GCK mutations causing neonatal or childhood-onset diabetes is primarily mediated through effects on protein stability

191. Monogenic Diabetes and Integrated Stress Response Genes Display Altered Gene Expression in Type 1 Diabetes

192. Neonatal diabetes mutations disrupt a chromatin pioneering function that activates the human insulin gene

196. GATA4 Mutations Are a Cause of Neonatal and Childhood-Onset Diabetes

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