The development of electroretinogram abnormalities and the possible role of polyol pathway activity in diabetic hyperglycemia and galactosemia

Segawa, Mitsuru; Hirata, Yoshihiro; Fujimori, Shizuyoshi; Okada, Kodo

doi:10.1016/0026-0495(88)90046-7

Cited by 38 publications

(17 citation statements)

References 26 publications

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“…ERGs were obtained at 6,8,16,24, and 32 weeks of age using the method of Segawa et al [18], with minor modification. Rats adapted to darkness for at least 60 min, then anaesthetized with an intraperitoneal injection of 50 mg/kg ketamine (Sankyo, Tokyo, Japan).…”

Section: Electroretinogram (Erg)mentioning

confidence: 99%

Diabetes-Associated Complications in Spontaneously Diabetic Torii Fatty Rats

et al. 2008

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Section: Electroretinogram (Erg)mentioning

confidence: 99%

Diabetes-Associated Complications in Spontaneously Diabetic Torii Fatty Rats

et al. 2008

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“…69 In addition to its welldocumented glucose metabolism role, the polyol pathway has been found to cause a loss of retinal capillary cells and that this involves aldose reductase, a rate-limiting enzyme of the polyol pathway that reduces glucose to sorbitol. 70,71 Aldose reductase inhibitor has been reported to inhibit the high glucoseinduced death of retinal capillary cells. 72,73 Sorbitol, a common organic osmolyte in many cells, accumulates in retinal capillary cells in response to hyperglycaemia and causes hyperosmolality of the cells.…”

Section: Retinal Capillary Cell Deathmentioning

confidence: 99%

The pathogenesis of diabetic retinopathy: old concepts and new questions

Cai

Boulton

2002

Eye

294

196

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Hyperglycaemia appears to be a critical factor in the aetiology of diabetic retinopathy and initiates downstream events including: basement membrane thickening, pericyte drop out and retinal capillary non-perfusion. More recently, focus has been directed to the molecular basis of the disease process in diabetic retinopathy. Of particular importance in the development and progression of diabetic retinopathy is the role of growth factors (eg vascular endothelial growth factor, placenta growth factor and pigment epithelium-derived factor) together with specific receptors and obligate components of the signal transduction pathway needed to support them. Despite these advances there are still a number of important questions that remain to be answered before we can confidently target pathological signals. How does hyperglycaemia regulate retinal vessels? Which growth factors are most important and at what stage of retinopathy do they operate? What is the preferred point in the growth factor signalling cascade for therapeutic intervention? Answers to these questions will provide the basis for new therapeutic interventions in a debilitating ocular condition.

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“…These changes include accelerated apoptosis of retinal inner neurons [48, 49, 50], altered expression of glial fibrillary acidic protein (GFAP) in two macroglial cells (astrocytes and Müller cells) [51, 52, 53, 54], activated microglia [50], and impaired glutamate metabolism [52, 55, 56, 57]. These altered neuroglial functions, in fact, have been clinically acknowledged by prolonged latencies of oscillatory potentials on the ERG b wave [58, 59, 60, 61, 62, 63, 64, 65, 66, 67], deficits in contrast sensitivity [68, 69, 70, 71]and color vision [72, 73, 74, 75, 76], and nerve fiber layer defects, which were observed by green filter photography in earlier studies [77, 78]and recently by scanning laser polarimetry [79]. Histologically, as early as the 1960s, Wolter [80]and Bloodworth [81]found pyknotic configurations of neuronal cells in retinas of postmortem eyes from patients with diabetes.…”

Section: Research Observations Showing Evidence That Diabetes May Incmentioning

confidence: 99%

Diabetes mellitus as a Risk Factor for Glaucomatous Optic Neuropathy

Nakamura

Kanamori

Negi³

2005

Ophthalmologica

100

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Open-angle glaucoma (OAG) is an optic neuropathy characterized by progressive retinal ganglion cell (RGC) death and optic disk excavation. Evidence is accumulating that RGC apoptosis is the fundamental pathology of OAG. Among several risk factors for development and progression of OAG, inclusion of comorbid diabetes has been controversial. Some large population-based prevalence and incidence studies found a positive association between diabetes and OAG, whereas others did not. This inconsistency is derived from selection-, recall-, or survival-bias or misclassification due to low incidence of the two diseases. On the other hand, recent basic studies have shown that diabetes not only affects vascular tissues but also compromises neuronal and glial functions and metabolism in the retina, which ultimately gives rise to apoptotic death of retinal neurons including RGCs. The impaired metabolism of neurons and glia by diabetes may render RGCs susceptible to additional stresses related to OAG such as elevated intraocular pressure. In fact, our latest data demonstrate that retinas taken from rats with streptozotocin-induced diabetes, which underwent cauterization of three episcleral veins to become a chronic glaucoma model, had significantly more apoptotic cells than those from rats with diabetes alone or with chronic glaucoma alone. In this regard, diabetes is a ‘risk factor’ for glaucomatous optic neuropathy. Additionally, prospective studies are needed to determine if OAG patients with diabetes have a more aggressive course than those without diabetes.

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The development of electroretinogram abnormalities and the possible role of polyol pathway activity in diabetic hyperglycemia and galactosemia

Cited by 38 publications

References 26 publications

Diabetes-Associated Complications in Spontaneously Diabetic Torii Fatty Rats

Diabetes-Associated Complications in Spontaneously Diabetic Torii Fatty Rats

The pathogenesis of diabetic retinopathy: old concepts and new questions

Diabetes mellitus as a Risk Factor for Glaucomatous Optic Neuropathy

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