Cataract Prevention in Diabetic Octodon Degus with Pfizer's Sorbinil

Datiles, Manuel B.; Fukui, Henry N.

doi:10.3109/02713688908997564

Cited by 34 publications

(29 citation statements)

References 2 publications

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“…This is in accord with literature reports in other rodents e.g. degus 7 , sand rats 31 , and in rats with streptozotocin induced diabetes 38 . Other etiologies are possible for cataract, such as inheritance, toxins or medication, injury of the lens or inflammation of the eye.…”

Section: Discussionsupporting

confidence: 82%

“…4 Cataract formation in plains viscachas might be accelerated by an increased aldosereductase activity in the lens similar to degus with type 2 diabetes mellitus. 7 Diabetic cataract is always bilateral. In the animal with unilateral cataract, a trauma-related etiology was suspected.…”

Section: Discussionmentioning

confidence: 99%

“…For example, nutritionally induced type 2 diabetes with possible cataract formation was described in the fat sand rat (Psammomys obesus); 31 a genetic component seems to be involved because different genetic lines of Psammomys obesus can be generated that differ in their proneness to dietinduced diabetes. 16,18 A diet-induced diabetes mellitus with cataract formation is described also in degus (Octodon degus) 7 , while a genetic etiology is suspected in Chinese hamsters (Cricetulus griseus) 12 and chinchillas (Chinchilla lanigera) 10 . Additionally, viruses associated with a type 1 diabetes-like syndrome have been described in several rodent species e.g.…”

Section: Introductionmentioning

confidence: 99%

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Occurrence of Cataract and Fatty Liver in Captive Plains Viscachas (Lagostomus maximus) in Relation to Diet

Gull¹,

Steinmetz²,

Clauß

et al. 2009

Journal of Zoo and Wildlife Medicine

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Occurrence of cataract and fatty liver in captive plains viscachas (Lagostomus maximus) in relation to diet Abstract An increased incidence of cataract and fatty liver in plains viscachas (Lagostomus maximus) was noted for many years at the Zurich Zoo. Based on elevated serum fructosamine and glucose, diabetes mellitus was diagnosed, and these parameters normalized when the diet of the animals was changed from a low-fiber to a high-fiber diet. Here, we evaluate 177 necropsy reports from before and after the diet change for the incidence of cataracts and fatty liver. Sixteen of 56 animals (29%) that were born before the diet change developed cataract. In contrast, only two of 121 animals (1.65%) that were born after the diet change developed cataracts. The prevalence of cataract and fatty liver in animals born after the diet change (1% and 0%, respectively) was significantly lower than in animals born before (9% and 6%, respectively) the diet change. The results suggest that the plains viscachas at Zurich Zoo were affected by an alimentary induced diabetes mellitus (type 2) before the diet was changed. Clauss (e-mail: mclauss@vetclinics.uzh.ch) CATARACTS IN VISCACHASAbstract: An increased incidence of cataract and fatty liver in plains viscachas (Lagostomus maximus) was noted for many years at the Zurich Zoo. Based on elevated serum fructosamine and glucose, diabetes mellitus was diagnosed, and these parameters normalized when the diet of the animals was changed from a low-fiber to a high-fiber diet. Here, we evaluate 177 necropsy reports from before and after the diet change for the incidence of cataracts and fatty liver. Sixteen of 56 animals (29%) that were born before the diet change developed cataract.In contrast, only two of 121 animals (1.65%) that were born after the diet change developed cataracts. The prevalence of cataract and fatty liver in animals born after the diet change (1% and 0%, respectively) was significantly lower than in animals born before (9% and 6%, respectively) the diet change. The results suggest that the plains viscachas at Zurich Zoo were affected by an alimentary induced diabetes mellitus (type 2) before the diet was changed.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Occurrence of Cataract and Fatty Liver in Captive Plains Viscachas (Lagostomus maximus) in Relation to Diet

Gull¹,

Steinmetz²,

Clauß

et al. 2009

Journal of Zoo and Wildlife Medicine

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“…Using this animal model and indirect ophthalmoscopy and portable slit lamp examination, we demonstrated that the ARI fidarestat, completely blocked slow-developing diabetic cataract formation. The important role of AR in diabetic cataractogenesis is in line with studies in other diabetic animal models including, i) the South American rodent, Octodon degus, which has a very high AR expression in the lens, and rapidly develops cataracts after spontaneously becoming diabetic in a laboratory environment (37,38), and ii) transgenic mice selectively expressing human AR in the lens, which, in contrast to wild-type diabetic mice that do not accumulate sorbitol in the lens and do not develop cataracts, display clearly manifest lens sorbitol accumulation and opacification (39).…”

Section: Discussionmentioning

confidence: 50%

Aldose reductase inhibitor fidarestat counteracts diabetes-associated cataract formation, retinal oxidative-nitrosative stress, glial activation, and apoptosis

Drel

Pacher²,

Ali³

et al. 2008

Int J Mol Med

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Abstract. This study was aimed at evaluating the potent and specific aldose reductase inhibitor fidarestat, on diabetesassociated cataract formation, and retinal oxidative-nitrosative stress, glial activation, and apoptosis. Control and streptozotocin-diabetic rats were treated with or without fidarestat (16 mg kg -1 d -1 ) for 10 weeks after an initial 2-week period without treatment. Lens changes were evaluated by indirect ophthalmoscopy and portable slit lamp. Nitrotyrosine, poly(ADP-ribose), and glial fibrillary acidic protein expression were assessed by immunohistochemistry. The rate of apoptosis was quantified in flat-mounted retinas by TUNEL assay with immunoperoxidase staining. To dissect the effects of high glucose exposure in retinal microvascular cells, primary bovine retinal pericytes and endothelial cells were cultured in 5 or 30 mM glucose, with or without fidarestat (10 μM) for 3-14 days. Apoptosis was assessed by TUNEL assay, nitrotyrosine and poly(ADP-ribose) by immunocytochemistry, and Bax and Bcl-2 expression by Western blot analyses. Fidarestat treatment prevented diabetic cataract formation and counteracted retinal nitrosative stress, and poly(ADP-ribose) polymerase activation, as well as glial activation. The number of TUNEL-positive nuclei (mean ± SEM) was increased approximately 4-fold in diabetic rats vs. controls (207±33 vs. 49±4, p<0.01), and this increase was partially prevented by fidarestat (106±34, p<0.05 vs. untreated diabetic group). The apoptotic cell number increased with the prolongation of exposure of both pericytes and endothelial cells to high glucose levels. Fidarestat counteracted nitrotyrosine and poly(ADP-ribose) accumulation and apoptosis in both cell types. Antiapoptotic effect of fidarestat in high glucose-exposed retinal pericytes was not associated with the inhibition of Bax or increase in Bcl-2 expression. In conclusion, the findings, i) support an important role for aldose reductase in diabetes-associated cataract formation, and retinal oxidative-nitrosative stress, glial activation, and apoptosis, and ii) provide a rationale for the development of aldose reductase inhibitors, and, in particular, fidarestat, for the prevention and treatment of diabetic ocular complications.

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“…This transgenic data is complemented by prevention studies with aldose reductase inhibitors. Administration of aldose reductase inhibitors at the onset of diabetes or galactosemia have been observed to result in dose dependent inhibition of sugar cataract formation in rats, Octodon degus and dogs (Kador and Kinoshita, 1984 ;Datiles and Fukui, 1989 ;Sato et al, 1998). Age-dependent studies also illustrate the importance of lenticular aldose reductase levels on sugar cataract formation.…”

Section: Discussionmentioning

confidence: 84%

Effect of Sorbitol Dehydrogenase Inhibition on Sugar Cataract Formation in Galactose-fed and Diabetic Rats

Kador

Inoue

Secchi

et al. 1998

Experimental Eye Research

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Cataract Prevention in Diabetic Octodon Degus with Pfizer's Sorbinil

Cited by 34 publications

References 2 publications

Occurrence of Cataract and Fatty Liver in Captive Plains Viscachas (Lagostomus maximus) in Relation to Diet

Occurrence of Cataract and Fatty Liver in Captive Plains Viscachas (Lagostomus maximus) in Relation to Diet

Aldose reductase inhibitor fidarestat counteracts diabetes-associated cataract formation, retinal oxidative-nitrosative stress, glial activation, and apoptosis

Effect of Sorbitol Dehydrogenase Inhibition on Sugar Cataract Formation in Galactose-fed and Diabetic Rats

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