Abstract
IntroductionPremature atherosclerosis is a significant cause of morbidity and mortality in type 2 diabetes mellitus. Maturity onset diabetes of the young (MODY) accounts for approximately 2% of all diabetes, with mutations in the transcription factor; hepatocyte nuclear factor 1 alpha (HNF1A) accounting for the majority of MODY cases. There is somewhat limited data available on the prevalence of macrovascular disease in HNF1A-MODY carriers with diabetes. Marked insulin resistance and the associated dyslipidaemia are not clinical features of HNF1A-MODY carriers. The scavenger protein CD36 has been shown to play a substantial role in the pathogenesis of atherosclerosis, largely through its interaction with oxidised LDL. Higher levels of monocyte CD36 and plasma CD36(sCD36) are seen to cluster with insulin resistance and diabetes. The aim of this study was to determine levels of sCD36 in participants with HNF1A-MODY diabetes and to compare them with unaffected normoglycaemic family members and participants with type 2 diabetes mellitus.MethodsWe recruited 37 participants with HNF1A-MODY diabetes and compared levels of sCD36 with BMI-matched participants with type 2 diabetes mellitus and normoglycaemic HNF1A-MODY negative family controls. Levels of sCD36 were correlated with phenotypic and biochemical parameters.ResultsHNF1A-MODY participants were lean, normotensive, with higher HDL and lower triglyceride levels when compared to controls and participants with type 2 diabetes mellitus. sCD36 was also significantly lower in HNF1A-MODY participants when compared to both the normoglycaemic family controls and to lean participants with type 2 diabetes mellitus.ConclusionIn conclusion, sCD36 is significantly lower in lean participants with HNF1A-MODY diabetes when compared to weight-matched normoglycaemic familial HNF1A-MODY negative controls and to lean participants with type 2 diabetes mellitus. Lower levels of this pro-atherogenic marker may result from the higher HDL component in the lipid profile of HNF1A-MODY participants.
Highlights
Premature atherosclerosis is a significant cause of morbidity and mortality in type 2 diabetes mellitus
When multivariate analysis was performed accounting for age and duration of diabetes status the levels of sCD36 remain significantly different between hepatocyte nuclear factor 1 alpha (HNF1A)-Maturity onset diabetes of the young (MODY) participants and normoglycaemic HNF1A-MODY negative controls
HNF1A-MODY patients have been shown in this current study to have a better metabolic profile compared to BMImatched type 2 diabetes mellitus (T2DM) controls
Summary
Premature atherosclerosis is a significant cause of morbidity and mortality in type 2 diabetes mellitus. Results: HNF1A-MODY participants were lean, normotensive, with higher HDL and lower triglyceride levels when compared to controls and participants with type 2 diabetes mellitus. SCD36 was significantly lower in HNF1AMODY participants when compared to both the normoglycaemic family controls and to lean participants with type 2 diabetes mellitus. Conclusion: In conclusion, sCD36 is significantly lower in lean participants with HNF1A-MODY diabetes when compared to weight-matched normoglycaemic familial HNF1A-MODY negative controls and to lean participants with type 2 diabetes mellitus. Lower levels of this pro-atherogenic marker may result from the higher HDL component in the lipid profile of HNF1A-MODY participants. Previous studies assessing the lipid profiles of HNF1A-MODY patients have demonstrated a favourable profile from a cardiovascular aspect with lower fasting triglyceride levels and comparable HDL levels to normoglycaemic controls [4,5]
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