Diabetic Cataract—Pathogenesis, Epidemiology and Treatment

Pollreisz, Andreas; Schmidt‐Erfurth, Ursula

doi:10.1155/2010/608751

Cited by 318 publications

(280 citation statements)

References 90 publications

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“…The use of insulin or oral hypoglycemic agents (OHA) is reported to be associated with increased risk of incidence of cataract, 50 more specifically CC 51 in subjects with diabetes. However, we did not examine for the influence of insulin or diet or oral hypoglycemic agents on the incidence and progression of cataract.…”

Section: Discussionmentioning

confidence: 99%

Incidence, Progression, and Risk Factors for Cataract in Type 2 Diabetes

Srinivasan¹,

Raman²,

Swaminathan³

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PURPOSE.We report the 4-year incidence, progression, and risk factors of cataract subtypes in type 2 diabetes. METHODS.A total of 779 subjects completed baseline and 4-year follow-up.RESULTS. The incidences of nuclear opalescence (NO), nuclear color (NC), cortical cataract (CC), and posterior subcapsular cataract (PSC) were 70%, 55.2%, 25.7%, and 7.3%, respectively. One-step progressions of NO, NC, CC, and PSC were 14.3%, 16.1%, 8.8%, and 8.1%, respectively, and two-step or more progressions were 5.0%, 6.0%, 0.8%, and 6.0%, respectively. Incident NO was seen in patients 50 to 59 (odds ratio [OR] ¼ 3.3), NC in those 50 to 59 (OR ¼ 2.7) and 60 to 69 (OR ¼ 3.9), and CC in those 60 to 69 (OR ¼ 3.3) years old. A lower hemoglobin A 1c (HbA 1c ; OR ¼ 0.7), longer diabetes duration (OR ¼ 1.1), and hyperopia (OR ¼ 4.0) were associated with incident PSC. Women (OR ¼ 1.7) and patients with higher total cholesterol (OR ¼ 1.3) at baseline showed one-step NO progression. Patients 60 to 69 (OR ¼ 2.8) and ‡70 (OR ¼ 3.8) years old showed one-step NC progression, while those 60 to 69 years old showed one-step CC progression (OR ¼ 6.3). A lower HbA 1c (OR ¼ 0.3) was associated with one-step PSC progression. A higher low-density lipoprotein (OR ¼ 1.6) was associated with two-step or more NO progression. Patients 60 to 69 years old (OR ¼ 6.7) had a greater risk, while those with hyperopia at baseline (OR ¼ 0.2) had lower risk of two-step or more NC progression. Patients 40 to 49 years old constituted the reference group for all.CONCLUSIONS. The 4-year cumulative incidence of cataract is higher than that of progression. Greater age is a risk factor for incidence and progression of most types of cataract.

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Section: Discussionmentioning

confidence: 99%

Incidence, Progression, and Risk Factors for Cataract in Type 2 Diabetes

Srinivasan¹,

Raman²,

Swaminathan³

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…83 The lens does not depend on insulin for its glucose uptake and the intracellular glucose concentration reflects the extracellular environment. The crystallin proteins of the lens may be glycosylated both in vivo and in vitro, in response to the high glucose concentrations.…”

Section: Discussionmentioning

confidence: 99%

Featured Article: Inhibition of diabetic cataract by glucose tolerance factor extracted from yeast

Mirsky

Cohen

Eliaz

et al. 2016

Exp Biol Med (Maywood)

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Diabetes leads to many complications; among them is the development of cataract. Hyperglycemia brings to increased polyol concentration in the lens, to glycation of lens proteins, and to elevated level of ROS (Reactive Oxygen Species) causing oxidative stress. The glucose tolerance factor (GTF) was found by several groups to decrease hyperglycemia and oxidative stress both in diabetic animals and humans. The aim of our study was to explore the damages induced by high glucose to the eye lens and to assess the protective effects of GTF both in vivo and in vitro. The in vivo study included control healthy rats, streptozotocin (STZ) diabetic untreated rats, and STZ diabetic rats orally treated with 15 doses of GTF. The diabetic untreated rats developed cataracts, whereas the development of cataract was totally or partially prevented in GTF treated animals. In vitro studies were done on bovine lenses incubated for 14 days. Half of the lenses were incubated in normal glucose conditions, and half in high glucose conditions (450 mg%). To one group of the normal or high glucose condition GTF was added. The optical quality of all the lenses was measured daily by an automated scanning laser system. The control lenses, whether with or without GTF addition, did not show any reduction in their quality. High glucose conditions induced optical damage to the lenses. Addition of GTF to high glucose conditions prevented this damage. High glucose conditions affected the activity of aldose reductase and sodium potassium ATPase in lens epithelial cell. Addition of GTF decreased the destructive changes induced by high glucose conditions. The amount of soluble cortical lens proteins was decreased and structural changes were detected in lenses incubated in high glucose medium. These changes could be prevented when GTF was added to high glucose medium. Our findings demonstrate the anticataractogenic potential of GTF.

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“…In the polyol pathway, the excess glucose changes to sorbitol via aldose reductase and the excessive accumulation of sorbitol in the crystalline lens produces a high osmotic gradient, and causes the collapse and liquefaction of lens fibers, resulting in cataract formation (14,15). Furthermore, enhanced osmotic stress leads to the production of reactive oxygen species (ROS) in the crystalline lens (16)(17)(18). In addition, sorbitol is metabolized to fructose.…”

Section: Introductionmentioning

confidence: 99%

Proteomic profile of the lens in a streptozotocin-induced diabetic rat model using shotgun proteomics

et al. 2017

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Abstract. Streptozotocin (STZ)-induced diabetic rats (STZ rats) were used to investigate diabetic cataracts. In the current study, a shotgun liquid chromatography (LC)/mass spectrometry (MS)-based global proteomic analysis method was used to examine the mechanism of lens opacification as a result of hyperglycemia in STZ rats. The 6-week old Wistar rats were injected with STZ for 2 days (100 mg/kg/day, i.p.) and housed for 3 weeks. The plasma glucose levels were identified to be significantly higher when compared with the normal rats and insulin was not detected in the STZ rats. Furthermore, opacification of the cortical epithelium was observed in the lenses of STZ rats. A total of 235 proteins were identified in the lenses of the STZ rats and 229 in the lenses of the normal rats. A label-free semi-quantitative method, based on spectral counting, identified 52 proteins that were differentially expressed in the lenses of STZ rats compared with normal rats. In particular, superoxide dismutase, which is a critical antioxidant enzyme that detoxifies superoxide through redox cycling, was downregulated when analyzed by the semi-quantitative method. In addition, phosphorylated-p38, which is important in the signaling pathway involved in the oxidative stress response, was significantly increased in the lenses of STZ rats when compared with normal rats (P<0.05). Thus, the changes in protein expression were evaluated in the lenses of STZ rats using a shotgun LC/MS-based global proteomic analysis approach, and a decrease in antioxidant enzymes and an increase in oxidative stress were identified in the lenses of STZ rats. Further studies are required to examine the role of these proteins in the onset or progression of diabetic cataracts. IntroductionDiabetes mellitus is one of the most severe types of metabolic disorder in humans globally, and is characterized by insulin resistance and impaired insulin secretion (1). Long-term hyperglycemia in diabetics leads to many complications with tissues that require insulin for glucose entrance or with insulin-independent organs (2), and cataracts are one of the most common complications of exposure to uncontrolled chronic hyperglycemia in diabetes. It has been reported that the onset of cataracts in diabetic patients is 20 years earlier than in non-diabetic subjects (3).Activation of the polyol pathway (4), non-enzymatic glycation of lens proteins (5-8) and increased oxidative stress (9-13) were reported as pathogenetic mechanisms of diabetic cataracts. In the polyol pathway, the excess glucose changes to sorbitol via aldose reductase and the excessive accumulation of sorbitol in the crystalline lens produces a high osmotic gradient, and causes the collapse and liquefaction of lens fibers, resulting in cataract formation (14,15). Furthermore, enhanced osmotic stress leads to the production of reactive oxygen species (ROS) in the crystalline lens (16)(17)(18). In addition, sorbitol is metabolized to fructose. The fructose is metabolized into fructose-3-phospate and 3-deoxyglucosone (p...

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Diabetic Cataract—Pathogenesis, Epidemiology and Treatment

Cited by 318 publications

References 90 publications

Incidence, Progression, and Risk Factors for Cataract in Type 2 Diabetes

Incidence, Progression, and Risk Factors for Cataract in Type 2 Diabetes

Featured Article: Inhibition of diabetic cataract by glucose tolerance factor extracted from yeast

Proteomic profile of the lens in a streptozotocin-induced diabetic rat model using shotgun proteomics

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