A Role for Omega-3 Polyunsaturated Fatty Acid Supplements in Diabetic Neuropathy

Yee, Peter; Weymouth, Anne; Fletcher, Erica L.; Vingrys, Algis J.

doi:10.1167/iovs.09-3792

Cited by 40 publications

(44 citation statements)

References 50 publications

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“…It is likely that other metabolic abnormalities may also contribute. Alterations in timing and amplitude of the b-wave and OPs associated with diabetes have been shown to be reversible by pharmacological treatments including docosahexaenoic acid (DHA)/lutein (Arnal et al, 2009; Yee et al, 2010) and acetyl- l -carnitine (Lowitt et al, 1993). Other treatments such as lipoic acid (Johnsen-Soriano et al, 2008), topical ciliary neurotrophic factor (CNTF) (Aizu et al, 2003), propionyl- l -carnitine (Hotta et al, 1996), angiotensin-converting-enzyme (ACE) inhibition (Bui et al, 2003), protein kinase C (PKC) inhibitors (Nakamura et al, 1999), and induction of heat shock proteins (Biro et al, 1998; Nanasi & Jednakovits, 2001) have each also been shown to prevent delays and reductions in the OPs but not the b-wave.…”

Section: Discussionmentioning

confidence: 99%

Exclusion of aldose reductase as a mediator of ERG deficits in a mouse model of diabetic eye disease

et al. 2012

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Streptozotocin (STZ)-induced diabetes is associated with reductions in the electrical response of the outer retina and retinal pigment epithelium (RPE) to light. Aldose reductase (AR) is the first enzyme required in the polyol-mediated metabolism of glucose, and AR inhibitors have been shown to improve diabetes-induced electroretinogram (ERG) defects. Here, we used control and AR−/− mice to determine if genetic inactivation of this enzyme likewise inhibits retinal electrophysiological defects observed in a mouse model of type 1 diabetes. STZ was used to induce hyperglycemia and type 1 diabetes. Diabetic and age-matched nondiabetic controls of each genotype were maintained for 22 weeks, after which ERGs were used to measure the light-evoked components of the RPE (dc-ERG) and the neural retina (a-wave, b-wave). In comparison to their nondiabetic controls, wildtype (WT) and AR−/− diabetic mice displayed significant decreases in the c-wave, fast oscillation, and off response components of the dc-ERG but not in the light peak response. Nondiabetic AR−/− mice displayed larger ERG component amplitudes than did nondiabetic WT mice; however, the amplitude of dc-ERG components in diabetic AR−/− animals were similar to WT diabetics. ERG a-wave amplitudes were not reduced in either diabetic group, but b-wave amplitudes were lower in WT and AR−/− diabetic mice. These findings demonstrate that the light-induced responses of the RPE and outer retina are disrupted in diabetic mice, but these defects are not due to photoreceptor dysfunction, nor are they ameliorated by deletion of AR. This latter finding suggests that benefits observed in other studies utilizing pharmacological inhibitors of AR might have been secondary to off-target effects of the drugs.

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Section: Discussionmentioning

confidence: 99%

Exclusion of aldose reductase as a mediator of ERG deficits in a mouse model of diabetic eye disease

et al. 2012

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“…Yee et al investigated the role for omega-3 polyunsaturated fatty acid supplements in rats with diabetic retinopathy [66]. A partial improvement was evident in the oscillatory potentials at electroretinogram, most likely secondary to the larger photoreceptor output.…”

Section: Protective Role Of Dha In the Retinamentioning

confidence: 99%

Retina and Omega-3

Querques

Forte

2011

Journal of Nutrition and Metabolism

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Over the last decade, several epidemiological studies based on food frequency questionnaires suggest that omega-3 polyunsaturated fatty acids could have a protective role in reducing the onset and progression of retinal diseases. The retina has a high concentration of omega-3, particularly DHA, which optimizes fluidity of photoreceptor membranes, retinal integrity, and visual function. Furthermore, many studies demonstrated that DHA has a protective, for example antiapoptotic, role in the retina. From a nutritional point of view, it is known that western populations, particularly aged individuals, have a higher than optimal omega-6/omega-3 ratio and should enrich their diet with more fish consumption or have DHA supplementation. This paper underscores the potential beneficial effect of omega-3 fatty acids on retinal diseases.

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“…In this regard we have focused on examining the use of a combination of dietary supplements and drugs (enalapril, α-lipoic acid and menhaden [fish] oil) for treatment of diabetic peripheral neuropathy in rodent models (Davidson et al, 2014). The reason for selecting these three compounds is that we have demonstrated that each of these treatments individually had beneficial effects on diabetic peripheral neuropathy and each have also been shown to be safe for use in humans (Coppey et al, 2001; 2006; 2012; 2015; Davidson et al, 2011; Gopinath et al, 2012; Mcllduff and Rutkove, 2011; Papanas and Ziegler, 2014; Rudkowska, 2010; Shevalye et al, 2015; Yee et al, 2010; Ziegler et al, 2011). The primary mechanism of action of these three compounds is oxidative and inflammatory stress.…”

Section: Introductionmentioning

confidence: 99%

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

et al. 2017

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We have previously demonstrated that enalapril, α-lipoic acid and menhaden (fish) oil has potential as a treatment for diabetic peripheral neuropathy. In this study we sought to determine the efficacy of these treatments individually or in combination on multiple neuropathic endpoints in a high fat fed low dose streptozotocin treated mouse, a model of type 2 diabetes, following early or late intervention. Four or twelve weeks after the onset of hyperglycemia, diabetic mice were treated with enalapril, α-lipoic acid, menhaden oil or their combination for 12 weeks. Afterwards, endpoints including glucose tolerance, motor and sensory nerve conduction velocity, thermal nociception, and intraepidermal and cornea nerve fiber density was determined. Glucose clearance was impaired in diabetic mice and significantly improved only with combination treatment and early intervention. Diabetes caused steatosis, slowing of motor and sensory nerve conduction velocity, thermal hypoalgesia and reduction in intraepidermal and cornea nerve fiber density. Treating diabetic mice with enalapril, α-lipoic acid or menhaden oil partially protected diabetic mice from these deficits, whereas the combination of these three treatments was more efficacious following early or late intervention. These studies suggest that a combination therapy may be more effective for treating neural complications of type 2 diabetes.

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A Role for Omega-3 Polyunsaturated Fatty Acid Supplements in Diabetic Neuropathy

Abstract: A diet balanced in long-chain PUFAs modifies retinal lipid membranes in diabetes and prevents rod dysfunction. Dietary modification was not found in the cone or glial response but a partial improvement was evident in the OPs, most likely secondary to the larger photoreceptor output.

Cited by 40 publications

References 50 publications

Exclusion of aldose reductase as a mediator of ERG deficits in a mouse model of diabetic eye disease

Exclusion of aldose reductase as a mediator of ERG deficits in a mouse model of diabetic eye disease

Retina and Omega-3

Early vs. late intervention of high fat/low dose streptozotocin treated C57Bl/6J mice with enalapril, α-lipoic acid, menhaden oil or their combination: Effect on diabetic neuropathy related endpoints

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