A low glycemic diet protects disease-prone Nrf2-deficient mice against age-related macular degeneration

Rowan, Sheldon; Jiang, Shiqin; Chang, Min-Lee; Volkin, Jonathan; Cassalman, Christa; Smith, Kelsey; Streeter, Matthew D.; Spiegel, David A.; Neto, Carlos A. Moreira; Rabbani, Naila; Thornalley, Paul J.; Smith, Donald E.; Waheed, Nadia K.; Taylor, Allen

doi:10.1016/j.freeradbiomed.2020.02.010

Cited by 25 publications

(20 citation statements)

References 96 publications

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“…Downregulation of NRF2 signaling is linked to decreased expression of Glo1 and reduction of NRF2-antioxidant pathway signaling is associated with inflammation [108,157]. Nevertheless, even in Nrf2-knockout mice, GLO1 protein is still present in the retina and can even be moderately increased through dietary treatment, suggesting that NRF2 is just one of many different regulatory nodes for Glo1, at least in this specific ocular tissue [164]. The molecular mechanisms behind the increased retinal GLO1 stability in mice lacking NRF2 remain unknown.…”

Section: Protective Role Of Nrf2 Against Glycation-derived Damage and Modulation Of Glo1mentioning

confidence: 99%

Glyoxalase System as a Therapeutic Target against Diabetic Retinopathy

et al. 2020

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Hyperglycemia, a defining characteristic of diabetes, combined with oxidative stress, results in the formation of advanced glycation end products (AGEs). AGEs are toxic compounds that have adverse effects on many tissues including the retina and lens. AGEs promote the formation of reactive oxygen species (ROS), which, in turn, boost the production of AGEs, resulting in positive feedback loops, a vicious cycle that compromises tissue fitness. Oxidative stress and the accumulation of AGEs are etiologically associated with the pathogenesis of multiple diseases including diabetic retinopathy (DR). DR is a devastating microvascular complication of diabetes mellitus and the leading cause of blindness in working-age adults. The onset and development of DR is multifactorial. Lowering AGEs accumulation may represent a potential therapeutic approach to slow this sight-threatening diabetic complication. To set DR in a physiological context, in this review we first describe relations between oxidative stress, formation of AGEs, and aging in several tissues of the eye, each of which is associated with a major age-related eye pathology. We summarize mechanisms of AGEs generation and anti-AGEs detoxifying systems. We specifically feature the potential of the glyoxalase system in the retina in the prevention of AGEs-associated damage linked to DR. We provide a comparative analysis of glyoxalase activity in different tissues from wild-type mice, supporting a major role for the glyoxalase system in the detoxification of AGEs in the retina, and present the manipulation of this system as a therapeutic strategy to prevent the onset of DR.

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Section: Protective Role Of Nrf2 Against Glycation-derived Damage and Modulation Of Glo1mentioning

confidence: 99%

Glyoxalase System as a Therapeutic Target against Diabetic Retinopathy

et al. 2020

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“…Starting at twelve months of age, mice were divided into three isocaloric dietary groups ( n = 16/group, 48 total) with different dietary starch composition as follows: high glycemic (HG, 100% amylopectin (Amioca starch, Ingredion Inc., Bridgewater, NJ)), low glycemic (LG, 30% amylopectin/70% amylose (Hylon VII starch, Ingredion Inc., Bridgewater, NJ)), or low glycemic containing antibiotics shown to modify gut microbiome composition (LG Amp + Neo, 320 mg ampicillin /kg chow +640 mg neomycin /kg chow (Goldbio, St. Louis, MO, USA)). Diet composition was 542 g/kg starch, 200 g/kg casein, 85 g/kg sucrose, 56 g/kg soybean oil, 50 g/kg wheat bran, 2 g/kg DL methionine, 10 g/kg vitamin mix, and 35 g/kg mineral mix ( Rowan et al, 2020 ). Macronutrient energy percentages were 65% carbohydrate, 21% protein, and 14% fat for both HG and LG diets.…”

Section: Methodsmentioning

confidence: 99%

Alterations to the gut microbiome impair bone tissue strength in aged mice

et al. 2021

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Whole bone strength and resistance to fracture are determined by a combination of bone quantity and bone quality – key factors in determining risk for osteoporosis and age-related fractures. Recent preclinical studies have shown that alterations to the gut microbiome can influence bone quantity as well as bone tissue quality. Prior work on the gut microbiome and bone has been limited to young animals, and it is unknown if the gut microbiome can alter bone tissue strength in aged animals. Here we ask if alterations to the constituents of the gut microbiome influence bone strength in older mice (12–24 months of age). Male C57BL/6J mice raised on a standard chow diet until 12 months of age were assigned to one of three diets: high glycemic, low glycemic, or low glycemic diet containing antibiotics (ampicillin and neomycin) to modify the constituents of the gut microbiome. The group fed the low glycemic diet containing antibiotics showed reductions in whole bone strength that could not be explained by geometry, indicating reduced bone tissue strength ( p < 0.007). The high glycemic diet group had larger bone cross-sectional area and moment of inertia and a corresponding greater bone strength as compared to the low glycemic groups, however tissue strength did not noticeably differ from that of the low glycemic group. These findings demonstrate that modifying the gut microbiome in aged mice can alter bone tissue quality.

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“…Replacing rapidly digested starch with resistant starches, which humans have limited capacity to digest, has been shown to attenuate the rise in blood glucose following the meal and prevent the long-term negative health outcomes of a high carbohydrate diet [ 50 ]. Research from our group has found that replacing a rapidly digested starch with resistant starch can arrest or reverse the development of retinal lesions and photoreceptor layer thinning in the eyes of aged mice [ 44 , 51 , 52 ].…”

Section: Physiological Effects Of Dietary Carbohydratesmentioning

confidence: 99%

“…The diet used in this study was an extreme model of unhealthy eating, the equivalent of consuming “fast food” with high fat content paired with high sugar, soda-like drinks. In the Nrf2 knockout mouse, a model of age-related macular degeneration, HG diet induced more severe AMD features that were ameliorated with LG diet, underscoring the strong effects of diet over a genetic factor in disease progression [ 51 ].…”

Section: Physiological Effects Of Dietary Carbohydratesmentioning

confidence: 99%

Dietary Patterns, Carbohydrates, and Age-Related Eye Diseases

et al. 2020

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Over a third of older adults in the U.S. experience significant vision loss, which decreases independence and is a biomarker of decreased health span. As the global aging population is expanding, it is imperative to uncover strategies to increase health span and reduce the economic burden of this age-related disease. While there are some treatments available for age-related vision loss, such as surgical removal of cataracts, many causes of vision loss, such as dry age-related macular degeneration (AMD), remain poorly understood and no treatments are currently available. Therefore, it is necessary to better understand the factors that contribute to disease progression for age-related vision loss and to uncover methods for disease prevention. One such factor is the effect of diet on ocular diseases. There are many reviews regarding micronutrients and their effect on eye health. Here, we discuss the impact of dietary patterns on the incidence and progression of age-related eye diseases, namely AMD, cataracts, diabetic retinopathy, and glaucoma. Then, we focus on the specific role of dietary carbohydrates, first by outlining the physiological effects of carbohydrates on the body and then how these changes translate into eye and age-related ocular diseases. Finally, we discuss future directions of nutrition research as it relates to aging and vision loss, with a discussion of caloric restriction, intermittent fasting, drug interventions, and emerging randomized clinical trials. This is a rich field with the capacity to improve life quality for millions of people so they may live with clear vision for longer and avoid the high cost of vision-saving surgeries.

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A low glycemic diet protects disease-prone Nrf2-deficient mice against age-related macular degeneration

Cited by 25 publications

References 96 publications

Glyoxalase System as a Therapeutic Target against Diabetic Retinopathy

Glyoxalase System as a Therapeutic Target against Diabetic Retinopathy

Alterations to the gut microbiome impair bone tissue strength in aged mice

Dietary Patterns, Carbohydrates, and Age-Related Eye Diseases

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