G.P.104 Liver insulin resistance and insulin secretion abnormality in myotonic dystrophy type 1

Abstract

<h2>Abstract</h2> Insulin resistance (IR) is a characteristic feature of glucose intolerance in myotonic dystrophy type 1 (DM1). The mechanism of IR is still unknown. The aim of this study was to investigate IR in DM1 by means of some indexes derived from oral glucose tolerance test (OGTT Seventy-seven non-diabetic patients with DM1 (the median value: age, 47years; body mass index (BMI), 22.4) were classified into the normal glucose response group (NGTDM1) and the impaired glucose tolerance group (IGTDM1) by 75g OGTT. For age and BMI matched controls, 100 normal glucose response subjects (NGTCT) and 130 impaired glucose tolerance cases (IGTCT) were picked up from our diabetic database. Liver and muscle insulin resistance indexes derived from OGTT supposed by Abdul-Ghani et al. were calculated: AUCgi30 for liver, glucose0–30[AUC]×insulin0–30[AUC]; dG/dt/I for muscle, the rate of decay of plasma glucose concentration from its peak value to its nadir during OGTT divided by the mean plasma insulin concentration; AUC, area under curve. AUCgi30, dG/dt/I, fasting plasma glucose (FPG) and insulin (FIRI), plasma glucose (PG120) and insulin (IRI120) level at 120min after oral glucose load, and Insulinogenic-Index (I-I) were analyzed. There was no significant difference between NGTDM1 and NGTCT for AUCgi30 or dG/dt/I. I-I in NGTDM1 was significantly lower than that in NGTCT. FPG and PG120 in NGTDM1 were significantly lower than those in NGTCT, whereas there was no significant difference in FIRI and IRI120. AUCgi30 in IGTDM1 was significantly higher than that in IGTCT, and dG/dt/I in IGTDM1 was significantly lower. I-I in IGTDM1 was also significantly lower than that in IGTCT. FPG in IGTDM1 was significantly lower than that in IGTCT. DM1 patients with dysglycaemia showed liver IR as well as muscle IR. Lower I-I in DM1 could represent abnormality of insulin secretion. Our data suggested IR in DM1 might result in multiple metabolic defects.