Nonenzymatic glycosylation of basement membranes: in vitro studies

Cohen, Morrel H.; Urdanivia, E.; Surma, Maria Linda; Ciborowski, C. J.

doi:10.2337/diabetes.30.5.367

Cited by 25 publications

(7 citation statements)

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“…18,19 Thickening of the basement membrane may impede the transfer of nutrients from the circulation, rendering surrounding areas more vulnerable to insult and perhaps interfering with the movement of leucocytes to damaged or infected areas. 20,21 Autoimmune diseases and auto-antibodies are frequently associated with T1D. The risk of developing several coexisting autoimmune diseases and conditions is especially high in 'autoimmune families' where the probands may manifest an additional autoimmune disease.…”

Section: Physiopathologymentioning

confidence: 99%

Juvenile, insulin‐dependent diabetes mellitus, type 1‐related dermatoses

Sehgal¹,

Bhattacharya²,

Verma³

2010

Acad Dermatol Venereol

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Juvenile insulin-dependent diabetes mellitus type 1 (IDDM) is a well-recognized worldwide entity, the significance of which has increased because of its recent upsurging trends, warranting attention on variety of its clinical expressions, in particular, pertaining to skin, an aspect seldom taken cognizance of. Hence an endeavour to recap the related dermatoses, such as limited joint mobility syndrome including sclerodermoid (scleroderma-like) changes, xerosis, necrobiosis lipoidica diabeticorum, granuloma annulare, diabetic foot syndrome, has been made. Complexities relating to the recently explored issues of atopic dermatitis and drug hypersensitivity syndrome have also been covered adequately. In addition, the current concepts of the physiopathology of type 1 diabetes-related dermatoses are briefly recapitulated for clarity.

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Section: Physiopathologymentioning

confidence: 99%

Juvenile, insulin‐dependent diabetes mellitus, type 1‐related dermatoses

Sehgal¹,

Bhattacharya²,

Verma³

2010

Acad Dermatol Venereol

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“…(1985) in diabetic dogs, and their in uiuo studies revealed impaired fibronectinheparin binding in uitro, which they considered could imply abnormal BL component interaction. Cohen et al (1981) demonstrated the non-enzymatic glycosylation of glomerular BL in diabetes and a review of the literature by Sternberg et aE. (1985) summarizes the effects of diabetes on collagens; of particular interest here is the demonstration of a reduction in glycosoaminoglycans and accumulation of overglycosylated collagens.…”

Section: A S C U L a R A N D P E R I N E U R I A L B A S A L L A M mentioning

confidence: 99%

Diabetic Neuropathy: Abnormalities of Schwann Cell and Perineurial Basal Laminae. Implications for Diabetic Vasculopathy

King

Llewelyn

Thomas

et al. 1989

Neuropathology Appl Neurobio

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During Wallerian degeneration, the Schwann cell basal laminal ensheathment around myelinated nerve fibres remains after the removal of myelin and axonal debris, forming a corrugated tube within which Schwann cell proliferation takes place. In nerve biopsies from patients with diabetic neuropathy, such residual basal laminal tubes tend to be circular rather than corrugated and appear to be more persistent during regeneration; this suggests increased rigidity and durability. These changes could be the result of increased cross-linkage of type IV collagen or alterations to other components of the basal lamina. A similar mechanism may be responsible for the thickening of perineurial basal laminae and the reduplication of basal laminae around endoneurial capillaries in diabetic patients; such reduplication may lead to reduced compliance of the vessel walls and impaired vascular perfusion.

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“…Any carbohydrate with a reactive carbonyl group can participate in this reaction (13). It is now clear that a number of different proteins are similarly glycosylated, including the collagen of basement membrane (14)(15)(16), skin (15,(17)(18)(19)(20), tendons (17,21,22), and peripheral nerve proteins (22).…”

mentioning

confidence: 99%

“…The basemetjt membranes of glotneruli are glycosylated in experimental diabetes and may be related to diabetic nephropathy. It has been postulated by a number of investigators that thickening of the basement membrane impedes the transfer of nutrients from the circulation, rendering surrounding areas more vulnerable to insult and perhaps interfering with the movement of leukocytes to damaged or infected areas (15,16).…”

mentioning

confidence: 99%

Cutaneous Manifestations of Diabetes Mellitus in Children

Edidin

1985

Pediatric Dermatology

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This article reviews skin changes occurring in diabetic children. Skin changes may be related to metabolic alterations associated with diabetes. Others may be manifestations of macro or microvascular disease. Insulin injections, required for management of most diabetes in the pediatric age group, may also cause cutaneous changes. There remain several cutaneous abnormalities which are observed with increased frequency among diabetics, the significance of which is unknown. The skin is a potentially invaluable tool for understanding certain diabetic complications; however, the value of observations and experimental data relating to cutaneous changes in diabetics depends upon documentation of the type of diabetes mellitus employing the currently accepted classification system.

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Nonenzymatic glycosylation of basement membranes: in vitro studies

Cited by 25 publications

References 0 publications

Juvenile, insulin‐dependent diabetes mellitus, type 1‐related dermatoses

Juvenile, insulin‐dependent diabetes mellitus, type 1‐related dermatoses

Diabetic Neuropathy: Abnormalities of Schwann Cell and Perineurial Basal Laminae. Implications for Diabetic Vasculopathy

Cutaneous Manifestations of Diabetes Mellitus in Children

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