Consumption of a diet low in advanced glycation end products for 4 weeks improves insulin sensitivity in overweight women

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Alicja Budek Mark, Malene Wibe Poulsen, Stine Andersen, Jeanette Marker Andersen, Monika Judyta Bak, Christian Ritz, Jens Juul Holst, John Nielsen, Barbora de Courten, Lars Ove Dragsted, Susanne Gjedsted Bügel

OBJECTIVE High-heat cooking of food induces the formation of advanced glycation end products (AGEs), which are thought to impair glucose metabolism in type 2 diabetic patients. High intake of fructose might additionally affect endogenous formation of AGEs. This parallel intervention study investigated whether the addition of fructose or cooking methods influencing the AGE content of food affect insulin sensitivity in overweight individuals. RESEARCH DESIGN AND METHODS Seventy-four overweight women were randomized to follow either a high- or low-AGE diet for 4 weeks, together with consumption of either fructose or glucose drinks. Glucose and insulin concentrations-after fasting and 2 h after an oral glucose tolerance test-were measured before and after the intervention. Homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity index were calculated. Dietary and urinary AGE concentrations were measured (liquid chromatography tandem mass spectrometry) to estimate AGE intake and excretion. RESULTS When adjusted for changes in anthropometric measures during the intervention, the low-AGE diet decreased urinary AGEs, fasting insulin concentrations, and HOMA-IR, compared with the high-AGE diet. Addition of fructose did not affect any outcomes. CONCLUSIONS Diets with high AGE content may increase the development of insulin resistance. AGEs can be reduced by modulation of cooking methods but is unaffected by moderate fructose intake.
OriginalsprogEngelsk
TidsskriftDiabetes Care
Vol/bind37
Udgave nummer1
Sider (fra-til)88-95
Antal sider8
ISSN0149-5992
DOI
StatusUdgivet - 2014

Bibliografisk note

CURIS 2014 NEXS 020

ID: 96079806