Adiponectin Decreases Postprandially Following a Heat-Processed Meal in Individuals With Type 2 Diabetes

Adiponectin regulates insulin sensitivity (1), reduces the expression of endothelial adhesion molecules (2), and has anti-inflammatory effects (3). Decreased adiponectin levels accompany obesity (4) and type 2 diabetes (5), promoting insulin resistance (5) and cardiovascular disease (6,7). Data on postprandial adiponectin regulation in different populations are controversial, with studies showing no effect (8–11), increases (12,13), or decreases (14,15). Advanced glycation end products (AGEs) (16) play a major role in the development of diabetes complications (17). We have shown that dietary AGEs acutely impair endothelial function (18,19), an effect counteracted by benfotiamine (20), a transketolase activator that blocks several hyperglycemia-induced pathways, including the formation of AGEs (21). AGEs might interact with adipocytes through AGE receptors (22) and induce cellular dysfunction via generation of reactive oxygen species (23), a pathway probably responsible for the AGE-induced downregulation of leptin secretion in vitro (24).Our study aimed at investigating the effects of a high heat–processed meal with high AGE content (HAGE) and a low heat–processed meal with low AGE content (LAGE) on postprandial adiponectin concentration. We postulated a protective effect of benfotiamine.Nineteen inpatients with type 2 diabetes (mean ± SEM age 55.2 ± 1.9 years; diabetes duration 7.3 ± 1.2 years; BMI 29.2 ± 0.8 kg/m2; A1C 8.8 ± 0.4%; 13 male and 6 female; 4 smokers and 15 nonsmokers; 15 on oral diabetes medication alone, 2 on oral diabetes medication plus insulin, and 2 …