Is Diabetes a Model for Aging?

Shagan, Bernard P.

doi:10.1016/s0025-7125(16)31876-4

Cited by 18 publications

(6 citation statements)

References 11 publications

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“…Theories of aging center around models relating free-radical formation, immune dysfunction, and cumulative DNA damage [2]. Several diseases commonly considered as models for aging [diabetes, atherosclerosis, rheumatoid arthritis, osteoporosis, and the progeroid syndromes] are also characterized by pathophysiology involving imbalances of reactive oxidation species formation, innate and adaptive immunity, and DNA damage/repair processes [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]. Furthermore, chronic immune dysfunction and reactive oxidation species (ROS) inhibit genetic and cellular repair, contributing to a synergistic and cumulative decline in cellular and physiological function [18].…”

Section: Resultsmentioning

confidence: 99%

“…The end result of these pathways is an imbalance of oxidative free radicals with resultant DNA damage and increased expression of proliferation genes and inflammatory cytokines, which can lead to aging and age related diseases such as cancer and atherosclerosis [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17]. Inhibiting angiotensin II or the AGTR1 receptor has been demonstrated to block these ROS generating pathways.…”

Section: Skin Agingmentioning

confidence: 99%

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Psychological Stress and skin aging: A review of possible mechanisms and potential therapies

Dunn

Koo²

2013

Dermatology Online Journal

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The link between psychological stress and aging is intuitive although the underlying mechanisms are not well defined. Evidence suggests that chronic psychological stress stimulates the autonomic nervous system, renin-angiotensin system, and the hypothalamic-pituitary-adrenal axis when the body attempts to resolve perceived threats to homeostasis. Prolonged activation of these pathways can result in chronic immune dysfunction, increased production of reactive oxygen species, and DNA damage, which are known to contribute to the again of skin and other tissues.Despite the lack of conclusive evidence directly linking psychological stress to skin aging, mechanisms by which stress leads to immune dysfunction, oxidative radicals, and ultimately DNA damage via neuronal, endocrine, and immune modulation may present a possible intervention for skin aging. In addition to the wide array of anti-oxidant therapies being developed to combat aging, the topical use of beta-blockers such as timolol, angiotensin receptor blockers such as valsartan, glucocorticoid blockers such as mifepristone, and cholinergic modulators including botulinum toxin, might be potential therapeutic strategies to prevent skin aging. Given the current understanding of these pathways, it would be premature to utilize such modalities for prevention of skin aging at this time, but future research into this type of topical pharmacologic anti-aging intervention may be promising.

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Section: Resultsmentioning

confidence: 99%

Section: Skin Agingmentioning

confidence: 99%

Psychological Stress and skin aging: A review of possible mechanisms and potential therapies

Dunn

Koo²

2013

Dermatology Online Journal

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“…Evidence has been obtained from collagenase digestion studies suggesting that collagen from diabetics is prematurely aged (3)(4)(5).…”

Section: Introductionmentioning

confidence: 99%

Effects of age and diabetes mellitus on the solubility and nonenzymatic glucosylation of human skin collagen.

Schnider¹,

Kohn²

1981

J. Clin. Invest.

311

112

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A B S T R A C T Collagen from human skin was fractionated into neutral salt-soluble, acid-soluble, pepsinreleased, and insoluble fractions. No age-related changes were observed in the proportion ofcollagen extracted by neutral salt. A significant age-related decrease in the proportion of acid-soluble collagen was found. A highly significant (P < 0.001) agerelated decrease in the amount of collagen released by pepsini digestion was observed, with a concomitant age-related increase in the fraction of insoluble collagen. The amount of ketoamine-linked glucose bound to this insoluble collagen also increased significantly with age.Skin collagen from three juvenile onset diabetics (JOD) and one young maturity onset diabetic (MOD) appeared to have undergone accelerated aging. JOD and the young MOD had significantly less collagen released by pepsin digestion and significantly more insoluble collagen than would be predicted by their ages. The collagen released by pepsin digestion of the diabetic samples had more high molecular weight components than similar fractions obtained from agematched nondiabetic controls. There was also more ketoamine-linked glucose bound to the insoluble collagen of JOD than to that fraction from comparably aged control subjects. The apparent acceleration of collagen aging in diabetes mellitus may play a role in complications of diabetes that occur in collagenrich tissues.

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“…Diabetes mellitus, on the other hand, is a common disease and a variety of animal models of diabetes is available. Based on biochemical and physiological similarities between aged animals and humans and diabetic patients, it has been suggested that diabetes mellitus may be an appropriate model of premature aging 2,3 . There are significant discordances, however, between the phenotypic changes in diabetes and aging.…”

mentioning

confidence: 99%

Tissue Specificity of Premature Aging in Diabetes Mellitus The Role of Cellular Replicative Capacity

Mooradian

1988

J American Geriatrics Society

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Is Diabetes a Model for Aging?

Cited by 18 publications

References 11 publications

Psychological Stress and skin aging: A review of possible mechanisms and potential therapies

Psychological Stress and skin aging: A review of possible mechanisms and potential therapies

Effects of age and diabetes mellitus on the solubility and nonenzymatic glucosylation of human skin collagen.

Tissue Specificity of Premature Aging in Diabetes Mellitus The Role of Cellular Replicative Capacity

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