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Cooking, AGEs and FMD

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The only difference in the two meals was the cooking

type and temperatue. Everything else was the same.

I have included the description of the 2 meals below.

Jeff

American Journal of Clinical Nutrition, Vol. 85, No.

5, 1236-1243, May 2007

Effects of low- and high-advanced glycation endproduct

meals on macro- and microvascular endothelial function

and oxidative stress in patients with type 2 diabetes

mellitus1,2,3

Negrean, Alin Stirban, Bernd Stratmann,

Gawlowski, Tina Horstmann, Christian Götting, Knut

Kleesiek, a Mueller-Roesel, Theodor Koschinsky,

Uribarri, Helen Vlassara and Diethelm Tschoepe

1 From the Diabetes Clinic, Heart and Diabetes Centre

NRW Bad Oeynhausen (MN, AS, BS, TG, TH, MM-R, and DT),

and Institute for Laboratory and Transfusion Medicine

(CG and KK), Ruhr University Bochum, Germany;

Heinrich-Heine University Duesseldorf, Germany (TK);

and the Division of Diabetes and Aging, Mount Sinai

School of Medicine, New York, NY (JU and HV)

Background: An advanced glycation endproducts

(AGEs)–rich diet induces significant increases in

inflammatory and endothelial dysfunction markers in

type 2 diabetes mellitus (T2DM).

Objective: The aim was to investigate the acute

effects of dietary AGEs on vascular function in T2DM

patients.

Design: Twenty inpatients with T2DM [ (±SEM) age: 55.4

± 2.2 y; glycated hemoglobin: 8.8 ± 0.5%] were

investigated. In a randomized crossover design, the

effects of a low-AGE (LAGE) and high-AGE (HAGE) meal

on macrovascular [by flow-mediated dilatation (FMD)]

and microvascular (by Laser-Doppler flowmetry)

function, serum markers of endothelial dysfunction

(E-selectin, intracellular adhesion molecule 1, and

vascular cell adhesion molecule 1), oxidative stress,

and serum AGE were assessed. The meals had identical

ingredients but different AGE amounts (15.100 compared

with 2.750 kU AGE for the HAGE and LAGE meals,

respectively), which were obtained by varying the

cooking temperature and time. The measurements were

performed at baseline and 2, 4, and 6 h after each

meal.

Results: After the HAGE meal, FMD decreased by 36.2%,

from 5.77 ± 0.65% (baseline) to 3.93 ± 0.48 (2 h),

3.70 ± 0.42 (4 h), and 4.42 ± 0.54% (6 h) (P < 0.01

for all compared with baseline). After the LAGE meal,

FMD decreased by 20.9%, from 6.04 ± 0.68% (baseline)

to 4.75 ± 0.48% (2 h), 4.69 ± 0.51% (4 h), and 5.62 ±

0.63% (6 h), respectively (P < 0.01 for all compared

with baseline; P < 0.001 for all compared with the

HAGE meal). This impairment of macrovascular function

after the HAGE meal was paralleled by an impairment of

microvascular function (–67.2%) and increased

concentrations of serum AGE and markers of endothelial

dysfunction and oxidative stress.

Conclusions: In patients with T2DM, a HAGE meal

induces a more pronounced acute impairment of vascular

function than does an otherwise identical LAGE meal.

Therefore, chemical modifications of food by means of

cooking play a major role in influencing the extent of

postprandial vascular dysfunction.

From the study.....

HAGE and LAGE meals

The 2 meals were isocaloric, had identical

ingredients, and

differed only by the temperature and time of cooking.

Each meal

consisted of 200 g chicken breast, 250 g potatoes, 100

g carrots,

200 g tomatoes, and 15 g vegetable oil and provided

580 kcal,

54 g protein, 17 g fat, 48 g carbohydrates, 60 mg

cholesterol, and

10 g fibers. The HAGE meal (15.100 kU AGE) was

prepared by

frying or broiling at 230 °C for 20 min, whereas the

LAGE meal

(2750 kU AGE) was prepared by steaming or boiling at

100 °C

for 10 min. The subjects were instructed to eat the

test meal

within 30 min.

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