Blood Viscosity, Glycaemic Control and Retinopathy in Insulin-Dependent Diabetes

Poon, P. Y. W.; Dornan, Timothy; Orde-Peckar, C.; Mullins, Richard E.; Bron, A. J.; Turner, R. C.

doi:10.1042/cs0630211

Cited by 18 publications

(1 citation statement)

References 1 publication

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Raised plasma viscosity associated with increased fibrinogen and globulin levels has been observed in diabetes by many (241,(244)(245)(246)(247) but not all (248)(249)(250) investigators, and has been invoked as a cause for increased susceptibility to thrombosis in diabetes. Whole-blood viscosity appears to be increased in diabetes (245, 251), and it has been attributed to increased circulating fibrinogen levels (251)(252)(253), decreased erythrocyte deformability (245,253,254) (a finding disputed by some [249,255,256]), and/or leukocytosis (247,249,256) (which may occur in diabetes without infection [241,257]). Hyperviscosity in diabetes appears to reflect the degree of metabolic control (258).…”

Section: Contribution Of Abnormal Rheology To Diabetic Neuropathymentioning

confidence: 99%

Complications: Neuropathy, Pathogenetic Considerations

et al. 1992

View full text Add to dashboard Cite

The most common form of neuropathy associated with diabetes mellitus is distal symmetric sensorimotor polyneuropathy, often accompanied by autonomic neuropathy. This disorder is characterized by striking atrophy and loss of myelinated and unmyelinated fibers accompanied by Wallerian degeneration, segmental, and paranodal demyelination and blunted nerve fiber regeneration. In both humans and laboratory animals, this progressive nerve fiber damage and loss parallels the degree and/or duration of hyperglycemia. Several metabolic mechanisms have been proposed to explain the relationship between the extent and severity of hyperglycemia and the development of diabetic neuropathy. One mechanism, activation of the polyol pathway by glucose via AR, is a prominent metabolic feature of diabetic rat peripheral nerve, where it promotes sorbitol and fructose accumulation, myo-inositol depletion, and slowing of nerve conduction by alteration of neural Na(+)-K(+)-ATPase activity or perturbation of normal physiological osmoregulatory mechanisms. ARIs, which normalize nerve myo-inositol and nerve conduction slowing, are currently the focus of clinical trials. Other specific metabolic abnormalities that may play a role in the pathogenesis of diabetic neuropathy include abnormal lipid or amino acid metabolism, superoxide radical formation, protein glycation, or potential blunting of normal neurotrophic responses. Metabolic dysfunction in diabetic nerve is accompanied by vascular insufficiency and nerve hypoxia that may contribute to nerve fiber loss and damage. Although major questions about the pathogenesis of diabetic neuropathy remain unanswered and require further intense investigation, significant recent progress is pushing us into the future and likely constitutes only the first of many therapies directed against one or more elements of the complex pathogenetic process responsible for diabetic neuropathy.

show abstract