Whilst altered arterial stiffness is a hallmark of diabetes, the causative mechanisms and molecular targets remain poorly defined. Using a streptozotocin (STZ)-induced rat model of type 1 diabetes we have: i) mapped the relative micromechanical changes in the elastic lamellae (EL) and inter-lamellar regions (ILR) of the aorta and ii) characterised the effects of diabetes on the structure fibrillin microfibrils (long lived elastic fibre components which sequester TGF-β and hence play a key role in tissue homeostasis).

Diabetes was induced in five adult rats by STZ injection. These rats and five age-matched controls were killed after 8 weeks. Aortic cryosections were imaged by scanning acoustic microscopy to map variations in speed of sound (a measure of tissue stiffness). Fibrillin microfibrils were isolated by bacterial collagenase digestion and imaged by atomic force microscopy.

Exposure to a diabetic mileu affected the mechanical properties of aortic EL and ILR. In diabetic animals mean speed of sound was significantly reduced in EL (control, 1766±13 ms⁻¹; diabetic, 1722±11 ms⁻¹, p<0.05) and in the ILR (control, 1902±8 ms⁻¹; diabetic, 1868±11 ms⁻¹, p<0.001). Fibrillin microfibril periodicity was also profoundly affected in diabetic animals (control, uni-modal distribution centred at 56nm; diabetic, bi-modal distributions centred at 52 and 78nm).

These observations suggest that profound micro-mechanical changes occur in diabetic blood vessels, in both the EL and collagen-rich ILR, and that pathological changes in the nano-structure of homeostatic components may play a role in driving localised remodelling in these tissues.