As insulin is required for glucose uptake, hyperglycemia in diabetes mellitus does not result in a net increase in intracellular glucose in most cells. However, chronic dysregulated blood glucose in diabetes is toxic to cells of the vascular endothelium which passively assimilate glucose. That is, cells in which insulin is not required for intercellular transport of glucose, most-notably the pericytes of the microvasculature. In addition to direct glucose-induced damage by (e.g.) glycation, pericytes, express enzymes which convert glucose into osmotically-active metabolites such as sorbitol leading to hypertonic cell lysis. The enzyme, namely aldose reductase, is also expressed in the endothelial and Schwann cells of the peripheral nervous system, contributing to<unk>  neuropathy. Over time, pericyte death may result in reduced capillary integrity; subsequently, there is leaking of albumin and other proteins into fluid compartments. The glomeruli of the kidneys are especially sensitive – see<unk>  nephropathy – where protein leakage caused by late-stage<unk>  results in diagnostic proteinuria and eventually kidney failure. In<unk>  retinopathy the end-result is often blindness due to irreversible retinal damage.
Diabetic angiopathy
Chorangiosis
Arteriolosclerosis
Microangiopathy
Arterial tortuosity syndrome
Angiolathyrism
Macrovascular disease
Monckeberg's arteriosclerosis