The following is a summary of “Women Have Greater Endothelin-B Receptor Function and Lower Mitochondrial Capacity Compared to Men With Type 1 Diabetes,” published in the October 2023 issue of Endocrinology by Derella, et al.
In the realm of type 1 diabetes (T1D), the negative impact on both the endothelin system and muscle oxidative capacity is a recognized phenomenon. The endothelin pathway, a crucial regulator of microcirculatory function, may exhibit a sexual dichotomy, with healthy premenopausal women showcasing greater endothelin-B receptor (ETBR) function compared to men. Additionally, T1D has been observed to affect muscle oxidative capacity in men and women differentially. However, the specific investigation into whether ETBR function is impaired in women compared to men with T1D, and its potential correlation with muscle oxidative capacity has yet to be explored.
For a study, researchers sought to ascertain whether ETBR-mediated dilation is compromised in women compared to men with T1D and if such impairment is linked to their skeletal muscle oxidative capacity. The study recruited men (n = 9; glycated hemoglobin A1c [HbA1c] = 7.8 ± 1.0%) and women (N = 10; HbA1c = 8.4 ± 1.3%) with uncomplicated T1D. Near-infrared spectroscopy (NIRS) and intradermal microdialysis with 750 nM BQ-123 + ET-1 [10-20–10-8 mol/L] were employed to assess skeletal muscle oxidative capacity and ETBR-mediated vasodilation, respectively.
The findings revealed that women with T1D exhibited significantly lower skeletal muscle oxidative capacity than their male counterparts. Contrarily, ETBR-mediated dilation induced a significantly greater vasodilatory response in women with T1D than in men with T1D. Importantly, the area under the curve for ETBR-mediated vasodilation was inversely associated with skeletal muscle oxidative capacity, indicating a potential compensatory mechanism in women with T1D to preserve microvascular blood flow.