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Omega 3 And Diabetes Pdf

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Published: 16.05.2021

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Omega-3 fats don’t reduce the risk of diabetes or improve blood sugar control

Peter Yee, Anne E. Weymouth, Erica L. Fletcher, Algis J. This study considers the role that this lipid change has on retinal function. Key metabolic indices were assayed at 19 weeks, and retinal function was determined by electroretinogram ERG at 20 weeks. Retinal anatomy and lipid assays of week-old animals were used to identify structural changes and tissue PUFA content. Lipid composition of retinal membranes reflected the dietary manipulation, and diabetes amplified some fatty acid changes consistent with reduced desaturase activity.

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. Purchase this article with an account.

Jump To Peter Yee ; Anne E. Weymouth ; Erica L. Fletcher ; Algis J. Corresponding author: Algis J. Alerts User Alerts. You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account. This feature is available to authenticated users only. Get Citation Citation. Get Permissions. Diabetic retinopathy is a major complication for long-term management of diabetes mellitus.

Current treatments target vascular changes, but there is growing evidence that neuronal changes take place either before or in conjunction with vascular abnormalities 2 — 4 and may require an alternative approach to treating early diabetic retinopathy.

Neural dysfunction in the diabetic retina is well recognized in humans and animals. Apart from these functional changes, the effect of diabetes on lipid metabolism and its implication for neural function has received little attention. The diabetic insulin deficiency results in reduced desaturase activity, 15 , 16 an important enzyme in forming long-chain polyunsaturated fatty acid PUFA metabolites, of which docosahexaenoic acid DHA, Fig. Given that low levels of DHA are known to promote retinal dysfunction, 17 , 18 it might be expected that the lower desaturase activity in diabetes would lead to retinal dysfunction in diets lacking long-chain substrates.

Indeed, studies have shown that DHA supplementation of STZ-treated rats can have beneficial effects on sciatic nerve function 19 , 20 and can reduce oxidative damage to the heart and liver. The findings of Hammes et al.

Later, we will argue that the lack of antioxidant cover used in that study see the Discussion section influences the interpretation of these findings. That intakes of these PUFAs and adequate antioxidant cover can reduce oxidative damage 21 and modify retinal angiogenesis 26 implies that these substrates could be of some benefit in the management of diabetes and that this issue should to be revisited, given the negative finding of Hammes et al.

In this article, we consider the role that balanced diets high in PUFA and adequate antioxidants can have in modulating the retinal function of diabetic animals. We propose that the lipid changes associated with diabetes reduced DHA might partially explain the reported neural dysfunction. The purpose of our study was to evaluate this possibility. This latter diet, was called FO because of its fish oil content, but it provides a well-balanced PUFA intake of both short- and long-chain omega-6 and -3 substrates.

The diet macronutrient composition, oil additive, and independent lipid assay outcomes are listed in Supplementary Table S1. Moreover, it has been argued that it is not the diet composition per se but the tissue effects that have to be considered in determining health outcomes. As in past studies, 12 STZ animals were given insulin infrequently 1 unit protophane , depending on their condition, and returned high HbA 1c levels Table 2 consistent with a poorly controlled diabetic state.

Twelve weeks after diabetogenesis age 19 weeks , the animals were housed in metabolic cages 24 hours to measure urine and fecal output and water intake. The ERG was used to assess retinal function. The initial ms of a typical rod waveform after a bright flash is shown in Figure 2. The first, negative-going potential is known as the a-wave Fig. The subsequent positive-going potential is called the b-wave Fig.

The small ripples seen on the leading edge of the b-wave Fig 2 are known as oscillatory potentials OPs. These wavelets reflect the activity of inner retinal neurons, particularly amacrine and ganglion cells. The recording procedures and our step-wise analysis allows extraction of the neural generators PIII, PII of these waveforms a- and b-wave in terms of different retinal populations as will be described later and detailed elsewhere. A twin-flash paradigm was used to identify the cone contribution to the waveform.

Corneal anesthesia and mydriasis were induced with 1 drop of 0. Calibrated neutral-density filters were used to attenuate the flash. Chlorided silver wire formed the active cornea and inactive incisor electrodes. These were referenced to a ground gauge needle; Terumo Corp. The rate of oscillation can be specified by its frequency h , in hertz and phase p , in degrees. Parameter optimization was achieved for each intensity, as detailed earlier.

The small magnitude of cone waveforms allowed only b-wave extraction. The animals were decapitated before enucleation, and the eye cup formed by careful dissection of the cornea and lens. The eye cups were rinsed with 0.

The resin blocks were sectioned vertically 1 mm within 5 mm of the optic nerve head and the sections etched in a sodium ethoxide-ethanol solution , rinsed in a graded series of methanol, and washed in 0. Sections where applied with toluidine blue for 30 seconds, washed with dH 2 O, and coverslipped.

Thickness was measured for specific retinal layers and for the total retina distance from the inner limiting membrane to photoreceptor outer segments from the digital images. Oblique sections were excluded from the analysis. Phospholipids were separated from the neutral lipids by thin-layer chromatography. In the presence of a significant interaction or main effect, simple comparisons were performed with a Holm-Sidak test.

Correlations were determined by nonparametric Spearman correlation coefficient r s. The central purpose of this study was to evaluate whether dietary consumption of PUFAs affects retinal function during diabetes. It was necessary to confirm that dietary consumption of omega-3 or -6 PUFA over 12 weeks of diabetes had led to changes in phospholipid profiles in retinal membranes. Table 1 lists retinal concentrations of selected long-chain PUFA for all experimental groups. Diabetes resulted in a reduction in retinal DHA in the absence of fish oil.

A complete lipid analysis is listed in Supplementary Table S2. Table 1. View Table. Data are the percentage total phospholipids. More details on retinal fat content are given in Supplementary Table S2. Figure 1. View Original Download Slide. PUFA metabolic pathways. Competition is involved in the desaturation of both n-3 and n-6 PUFAs. Note that the HbA 1c data were collected 1 week later 13 weeks.

Table 2. BG, blood glucose. Having established that lipid composition of retinal membranes was altered by dietary intake of PUFA, we evaluated the effect that diet and diabetes had on retinal function. Representative rod ERG waveforms are shown in Figure 2. They indicate a general reduction in rod amplitudes in STZ-treated animals fed SO, which was particularly evident in signals obtained at higher exposures Fig.

In contrast, minimal change was found between rod responses in FO-fed animals Fig. Figure 2. Top left : a- and b-wave and OPs. An implicit time analysis of these experimental groups is given in Table 3. In contrast, diabetes produced a significant timing t d delay of Table 3. Figure 3. Raw data were modeled with a delayed Gaussian over an ensemble of three flash energies 0. Middle : postreceptoral PII components 1.

Bottom : oscillatory potentials 1. The b-wave was significantly reduced and delayed by both experimental manipulations Figs. Implicit time showed significant diet This lack of correlation for PII is consistent with the previous observation of a significant diabetes effect, as Figure 3 J shows that most of this group effect was driven by the low amplitudes in the SO group.

Representative cone waveforms are shown in Figure 4 , where a reduction in cone amplitude is evident in STZ animals, irrespective of diet Figs. Figure 4. The b-wave A , arrow , with group size as per Figure 3. Unfilled symbols : control; filled symbols : STZ treated. The implicit time analysis for these experimental groups is given in Table 3.

Acceleration of experimental diabetic retinopathy in the rat by omega-3 fatty acids

Peter Yee, Anne E. Weymouth, Erica L. Fletcher, Algis J. This study considers the role that this lipid change has on retinal function. Key metabolic indices were assayed at 19 weeks, and retinal function was determined by electroretinogram ERG at 20 weeks.

Akadiri Yessoufou, Magloire P. Omega-3 polyunsaturated fatty acids PUFAs are increasingly being used to prevent cardiovascular diseases, including diabetes and obesity. In this paper, we report data on the observed effects of omega-3 PUFA on major metabolic disorders and immune system disruption during gestational diabetes and their consequences on macrosomia. While controversies still exist about omega-3 PUFA effects on antioxidant status regarding the level of omega-3 PUFA in diet supplementation, their lipid-lowering effects are unanimously recognized by researchers. Based on the available evidence, international nutritional and food agencies recommend administration of omega-3 PUFA as triglyceride-lowering agents, for the prevention of cardiovascular disease risk and during human pregnancy and lactation.

To evaluate the effects of omega-3 long-chain polyunsaturated fatty acids on proteinuria, estimated glomerular filtration rate eGFR and metabolic biomarkers among patients with diabetes. Ten RCTs with participants were included in our meta-analysis. Omega-3 fatty acids reduced the amount of proteinuria among type 2 diabetes mellitus type 2 DM and type 1 diabetes mellitus type 1 DM.

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