281-OR: Type 2 Diabetes Diagnosed between 16-30 Years in South Asian and White Individuals Is Phenotypically Similar

Abstract

Aim: The incidence of type 2 diabetes is increasing rapidly in young adults. Older south Asian people (SA) develop type 2 diabetes at leaner BMI compared to white and are less likely to be obese. We hypothesised that obesity may be a bigger driver of young-onset type 2 diabetes in SA people and studied the BMI difference in white and SA people with young adult-onset type 2 diabetes. Methods: Data from two UK cross-sectional cohorts were examined to identify adults diagnosed with any type of diabetes <30 years. We defined type 2 diabetes as a fasting C-peptide level >600pmol/L and negativity to GAD-antibodies (YDX study) and GAD, IA-2 and ZnT8 antibodies (MY DIABETES study). We studied phenotypic differences between SA and white ethnicity. Results: Sixty white and 71 SA people with type 2 diabetes diagnosed <30 years were identified, of which 92% (n= 55) white and 83% (n=59) SA were diagnosed 16-30 years. Median age-at-diagnosis (25 vs. 24 years, p=0.6) and duration (8.8 vs. 9.5 years, p=0.8) were similar between white and SA ethnicity. BMI, though lower in SAs than white (29 vs. 32 kg/m2, p=0.0007), was consistent with ethnic-specific obesity. HbA1c (68 vs. 60 mmol/mol, p=0.1), HDL (1.0 vs. 1.1mmol/L) and triglycerides (2.2 mmol/L vs. 1.7) were similar in white vs. SA. Fasting C-peptide was no different between ethnicities 847 pmol/L white vs. 1018 SA, p=0.1. Percentage insulin-treated was similar between both groups: white 54%, SA 66% p=0.2. Conclusion: Type 2 diabetes diagnosed between 16-30 years is associated significantly with the presence of obesity in both ethnicities. The similarity observed in glycaemia, lipid profiles and fasting C-peptide along with similar durations, suggest the degree of insulin resistance to be equal across ethnic groups. This young-onset south Asian phenotype may contrast older-onset cases where SA people are observed to be significantly leaner and more insulin resistant than white counterparts. Disclosure S. Misra: None. I.F. Godsland: None. N. Bhardwaj: None. N. Oliver: Advisory Panel; Self; Medtronic, Roche Diabetes Care, UNEEG. Research Support; Self; Dexcom, Inc., Roche Diabetes Care. K.R. Owen: None. D.G. Johnston: None. Funding Diabetes Research & Wellness Foundation; European Foundation for the Study of Diabetes