Why have we carried out this study?

Prevalence of overweight and obesity among individuals with type 1 diabetes (T1D) is increasing. Obesity is an independent risk factor for cardiovascular diseases (CVD) which are the dominant cause of mortality in diabetic patients. There is data implying that insulin resistance (IR) develops in patients with T1D as well as in patients with T2D, but little attention is paid to this problem in clinical practice and clinical research; it is thought it might be related to diabetes complications, CVD, testosterone (T), and sex hormone-binding globulin (SHBG) levels. There is inconsistency in data regarding how IR might be diagnosed in T1D

We aimed to determine the estimated glucose disposal rate (eGDR) level (cutoff) that reflects IR and to evaluate the association of IR with micro- and macrovascular complications, sex hormones, and other clinical data

We decided to examine the relation between IR and weight and sex hormones in T1D as the relation between of SHBG and T1D is not clear; little is known about the interaction between T, SHBG levels, and insulin sensitivity in T1D

What was learned from the study?

Our study is the first one that assessed CVD risk according to eGDR. We found that IR expressed as eGDR cutoff  less than 6.4 mg kg−1 min−1 was significant for all diabetes vascular complication progression and less than 2.3 mg kg−1 min−1 for CVD. Moreover, eGDR was significantly lower in the obese, smokers, men, subjects aged over 50 years, and in those with long-standing T1D

Positive linear correlation was observed between men’s T and eGDR level, i.e., men with higher T level had better insulin sensitivity. Other parameters such as T in women, estrogens, and SHBG did not show any significant association with eGDR. Our results contradict the results of other studies and point to the need for additional research

We found that obese patients with T1D were significantly more insulin resistant and the prevalence of metabolic syndrome tended to be higher in obese than in lean patients with T1D, with a tendency to significant difference. This is in line with previous results of other studies and has reasonably understood pathogenic mechanisms