Abstract
Studies examining the effects of consumption of diets low in advanced glycation end products (AGEs) on cardiometabolic parameters are conflicting. Hence, we performed a meta-analysis to determine the effect of low AGE diets in reducing cardiometabolic risk factors. Seventeen randomised controlled trials comprising 560 participants were included. Meta-analyses using random effects models were used to analyse the data. Low AGE diets decreased insulin resistance (mean difference [MD] −1.3, 95% CI −2.3, −0.2), total cholesterol (MD −8.5 mg/dl, 95% CI −9.5, −7.4) and low-density lipoprotein (MD −2.4 mg/dl, 95% CI −3.4, −1.3). There were no changes in weight, fasting glucose, 2-h glucose and insulin, haemoglobin A1c, high-density lipoprotein or blood pressure. In a subgroup of patients with type 2 diabetes, a decrease in fasting insulin (MD −7 µU/ml, 95% CI −11.5, −2.5) was observed. Tumour necrosis factor α, vascular cell adhesion molecule-1, 8-isoprostane, leptin, circulating AGEs and receptor for AGEs were reduced after consumption of low AGE diets with increased adiponectin and sirtuin-1. Our findings suggest that diets low in AGEs may be an effective strategy for improving cardiometabolic profiles in individuals with and without type 2 diabetes.
Highlights
Advanced glycation end products (AGEs) are formed endogenously from the non-enzymatic reaction of sugars with proteins or lipids[1]
We showed a significant decrease in tumour necrosis factor (TNFα) in peripheral mononuclear cells (PMNC) (MD −4.7 pg/mg, 95% confidence interval (CI) −7 to −2.3)[17, 20,21,22,23, 29], and leptin (MD −18.6 ng/ml, 95% CI −29.1 to −8.2)[17, 23] (Figure 4) and an increase in adiponectin levels (MD 7 μg/ml, 95% CI 5.6 to 8.4) (Figure 5) after consumption of the low advanced glycation end products (AGEs) diets compared to the high AGE diets[17, 21, 23]
We have demonstrated that consumption of low AGE diets decreased insulin resistance regardless of participants’ T2DM status and reduced fasting insulin levels in patients with T2DM as well as decreased total cholesterol in participants without T2DM
Summary
Advanced glycation end products (AGEs) are formed endogenously from the non-enzymatic reaction of sugars with proteins or lipids[1] These processes are present in healthy individuals but are accelerated in diabetes due to high glucose levels with patients with diabetes having approximately 50% higher levels of serum AGEs than those of healthy, age-matched controls[2,3,4]. A high AGE diet has been shown to enhance chronic inflammation, oxidative stress, endothelial dysfunction, and thereby increase the risk of development of T2DM and its complications[13, 14]. Prior systematic reviews assessing the effect of low AGE and high AGE diets on insulin resistance, markers of inflammation and oxidative stress[13, 14] have not considered other measures of glucose homeostasis and cardiovascular risk factors. The aim of this study was to conduct a meta-analysis on the effects of dietary AGEs (dAGEs) on a broad range of cardiometabolic parameters in individuals with or without T2DM
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