Loss of Receptor for Advanced Glycation End Products (RAGE) Defense: A cause of Charcot neuroarthrop

NewsBot · May 20, 2011

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Loss of Receptor for Advanced Glycation End Products (RAGE) Defense: A cause of Charcot neuroarthropathy?
Witzke KA, Vinik AI, Grant LM, Grant WP, Parson HK, Pittenger GL, Burcus N
Diabetes Care. 2011 May 18;

OBJECTIVE This study investigated the relationship between circulating soluble receptor for advanced glycation end products (sRAGE) and parameters of bone health in patients with Charcot neuroarthropathy (CNA).

RESEARCH DESIGN AND METHODS Eighty men (aged 55.3 ± 9.0 years), including 30 healthy control subjects, 30 type 2 diabetic patients without Charcot, and 20 type 2 diabetic patients with stage 2 (nonacute) CNA, underwent evaluations of peripheral and autonomic neuropathy, nerve conduction, markers of bone turnover, bone mineral density, and bone stiffness of the calcaneus.

RESULTS CNA patients had worse peripheral and autonomic neuropathy and lower bone stiffness index than the diabetic or control individuals (77.1, 103.3, and 105.1, respectively; P < 0.05), but no difference in bone mineral density (P > 0.05). CNA subjects also had lower sRAGE levels than control (162 vs. 1,140 pg/mL; P < 0.01) and diabetic (162 vs. 522 pg/mL; P < 0.05) subjects, and higher circulating osteocalcin levels.

CONCLUSIONS CNA patients had significantly lower circulating sRAGE, with an accompanying increase in serum markers of bone turnover, and reduced bone stiffness in the calcaneus not accompanied by reductions in bone mineral density. These data suggest a failure of RAGE defense mechanisms against oxidative stress in diabetes. Future studies should determine if medications that increase sRAGE activity could be useful in mitigating progression to CNA.
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Admin2 · May 20, 2011

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NewsBot · Sep 24, 2011

Levels of Soluble Advanced Glycation End Product-Receptors and Other Soluble Serum Markers as Indicators of Diabetic Neuropathy in the Foot.
El-Mesallamy HO, Hamdy NM, Ezzat OA, Reda AM.
J Investig Med. 2011 Sep 21. [Epub ahead of print]

OBJECTIVE:
Advanced glycation end products (AGEs) and the interaction with their receptors (RAGE) play an important role in the pathogenesis of diabetic foot (DF) associated with diabetic neuropathy. Our study examined the association between asymmetric dimethyl arginine (ADMA), fructosamine, nitric oxide (NO), and soluble (s) RAGE levels in serum of diabetic patients with and without neuropathy.

METHODS:
Circulating levels of ADMA, fructosamine, NO, and sRAGE, estimated either chemically or by enzyme-linked immunosorbent assay, were examined in 60 type 2 diabetes mellitus (T2DM) overweight/obese (body mass index, 30.5 ± 1.5 kg/m) male patients and 20 age-matched (55 ± 3 years) obese healthy subjects as control group. The T2DM subjects were categorized as patients without DF (n = 30), and the remaining were patients with DF associated with neuropathy.

RESULTS:
First sRAGE levels were significantly increased in T2DM patients without DF in comparison to healthy controls (1656.6 [1198.8-2065.4] vs 1111.7 [909-1605.3] pg/mL, respectively; P < 0.05). However, in the DF group (1049.6 [783.7-1221.8] pg/mL), its level decreased significantly in comparison to both groups (P < 0.05). However, ADMA and fructosamine were significantly higher in diabetic patients with DF than both T2DM without DF and healthy controls. Moreover, NO was significantly lower in DF than in diabetic patients without DF and controls (5 ± 0.4 and 8 ± 0.4 vs 42 ± 2.5 μmol/L, respectively; P < 0.05). Finally, sRAGE levels were significantly correlated with ADMA, fructosamine, and NO.

CONCLUSIONS:
Soluble forms of the receptor for advanced glycation end product could be an endogenous protection factor against occurrence of DF, hence may be of therapeutic value in the treatment of DF.
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NewsBot · Mar 4, 2014

Dietary advanced glycation end-products exacerbate oxidative stress in patients with diabetic foot ulcers
Haiyan M. Maier, Jasminka Z. Ilich, Jeong-Su Kim, Cathy W. Levenson, Bahram H. Arjmandi and Maria T. Spicer
Journal of Diabetes Research & Clinical Metabolism

Background: This study examined the association between advanced glycation end-products (AGE) and serum markers of oxidative stress and inflammation in diabetic patients with or without diabetic foot ulcers.

Methods: Eighty-two adult participants were recruited and assigned to one of three groups: 1) non-diabetic control; 2) diabetic participants without foot ulcers (DM); and 3) diabetic participants with foot ulcers (DFU). Demographical data, 24 hour food recalls, and blood samples were collected from each participant. Both dietary and serum AGE were evaluated as well astumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and thiobarbituric acid reactive substances (TBARS).

Results: The diabetic participants had significantly higher levels of dietary AGE, serum AGE, TNF-α, CRP, and TBARS compared to non-diabetic controls. TBARS were significantly higher in DFU than DM. Serum AGE and TBARS were significantly correlated with dietary AGE. Serum TBARS strongly predicted the duration of DFU (R2=0.52).

Conclusions: Individuals with DFU had the highest levels of both dietary and serum AGE. Because dietary AGE causes a rise in serum AGE concentration, it is important to reduce the intake of foods containing AGE by promoting appropriate dietary choices in this population.
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NewsBot · Jun 9, 2021

DETERMINATION OF ADVANCED OXIDATIVE PROTEIN PRODUCTS
LEVELS AND ITS CORRELATION WITH INFLAMMATION IN DIABETIC
FOOT PATIENTS
Haneen Muhanedalnajer et al
Biochem. Cell. Arch. Vol. 20, No. 2, pp. 000-000, 2020

Advanced oxidation protein products (AOPPs) are the marker of protein oxidation through oxidative stress,
which represents the overall status of the protein in the cell/tissue. Due to their increased levels of AOPPs were reported
during T2DM. The aim of this study was to assess AOPP level in T2DM subjects with foot ulcer (DFU) and explore its
correlation with infection. Type 2 diabetic patients (n=108) and healthy subjects (n=25) were enrolled in this study. The T2DM
group was subdivided to diabetic patients without complications (n=25) and eighty-three (83) of them have diabetic foot. They
were sub- grouped into two groups according to presence Osteomyelitis and abscess, and in reliance on medical analysis of
WBC count and CRP. Group of diabetic without superficial or deep ulcer and no osteomyelitis or abscess G(0,1,2) (n =45),
which consist patients with grades (0,1,2), and group of diabetic with deep ulcer abscess and osteomyelitis G(3,4,5)(n = 38) that
consist patients with grade (3,4,5). Twenty- five (25) non-diabetic apparently healthy subjects serve as control (group C) were
enrolled.The Biochemical analysis was done for all participants such as serum glucose, hemoglobin A1C, insulin, lipid profile,
WBC, and C-reactive protein (CRP). Serum AOPP concentration was determined using an enzyme-linked immunosorbent
assay kit. The oxidative status was assessed by measuring catalase activity, glutathione (GSH), malondialdehyde (MDA) and
total thiol levels. AOPP, MDA, WBC, and CRP, were significantly higher in G (0,1,2) and G (3,4,5) groups in comparison to
control group, while GSH and total thiol levels were significantly lower as compared with control group. The outcomes of this
study reveal the incidence of oxidative stress among DFU patients with higher Wagner grades and the presence of relation
between inflammation state in DFU subjects and oxidative stress.
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NewsBot · Aug 19, 2021

The role of glycation end products in the development and progression of diabetic neuroarthropathy
M M Kalandiya et al
Probl Endokrinol (Mosk). 2021 Jul 4;67(3):4-9

Diabetic neuroarthropathy (DNOAP, Charcot's foot) is a serious complication of diabetes mellitus, the genesis of which is not fully understood. In most cases, this pathology is diagnosed late, which leads to the development of severe deformities of the foot, up to the loss of support ability of the limb. There is no single hypothesis for the formation of Charcot's foot, but there are factors predisposing to its development, as well as a few likely provoking events. Excessive formation and accumulation of end products of glycation may play an important role in the pathogenesis of this complication of diabetes. End products of glycation (AGE) are a variety of compounds formed as a result of a non-enzymatic reaction between carbohydrates and free amino groups of proteins, lipids and nucleic acids. There are various factors that lead to the accumulation of AGE in the human body. Allocate endogenous and exogenous factors. The former include certain diseases, such as diabetes mellitus, renal failure, which accelerate glycation processes. Exogenous factors leading to the formation of lipo-oxidation and glyco-oxidation products include tobacco smoke and prolonged heat treatment of food.This review provides information on the role of glycation end products in the development and progression of complications in patients with diabetes mellitus.
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Loss of Receptor for Advanced Glycation End Products (RAGE) Defense: A cause of Charcot neuroarthrop

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HCPC Podiatrist - Glossop Derbyshire - Self Employed - Fee Sharing

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Loss of Receptor for Advanced Glycation End Products (RAGE) Defense: A cause of Charcot neuroarthrop

NewsBot The Admin that posts the news.

Admin2 Administrator Staff Member

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

NewsBot The Admin that posts the news.

Activity levels in those with limb loss

Semmes Weinstein Monofilament to Test for Loss of Protective Sensation in Diabetic Patients

Weight loss and foot symptoms

HCPC Podiatrist - Glossop Derbyshire - Self Employed - Fee Sharing

Runners perception of loss of rearfoot cushioning in worn running shoes

Elderly with loss of fatty pad and foot pain

Beau's lines, hair loss and fatigue...?

Share This Page

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