Trial reportThe British journal of nutrition2015
Contribution of dietary advanced glycation end products (AGE) to circulating AGE: role of dietary fat.
Trial report in The British journal of nutrition, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 38 citations in OpenAlex.
- Plant-Based Approaches for Inhibition of Advanced Glycation End Products Formation: Dietary Polyphenols.Molecules (Basel, Switzerland) · 2026Review
- Paeonol Inhibits the MAPK Signaling Pathway by Targeting SIRT1 in AGE-Induced HUVECs Injury.Combinatorial chemistry & high throughput screening · 2026Article
- A One-Month Advanced Glycation End Products-Restricted Diet Improves CML, RAGE, Metabolic and Inflammatory Profile in Patients with End-Stage Renal Disease Undergoing Haemodialysis.International journal of molecular sciences · 2024Article
- Do advanced glycation end products contribute to food allergy?Frontiers in allergy · 2023Review
- Receptor of advanced glycation end-products axis and gallbladder cancer: A forgotten connection that we should reconsider.World journal of gastroenterology · 2022Review
- Article
- Dietary protein intake and circulating advanced glycation end product/receptor for advanced glycation end product concentrations in the Health, Aging, and Body Composition Study.The American journal of clinical nutrition · 2020Article
- The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases.Molecules (Basel, Switzerland) · 2020Review
- Article
- Review
- Iron and Advanced Glycation End Products: Emerging Role of Iron in Androgen Deficiency in Obesity.Antioxidants (Basel, Switzerland) · 2020Article
- Advanced Glycation End Products: Building on the Concept of the "Common Soil" in Metabolic Disease.Endocrinology · 2020Review
- Advanced glycation end products and risk of hypertension in Iranian adults: Tehran lipid and glucose study.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2018Article
- Influence of Varying Dietary Protein Levels on Glycation of Albumin, Tryptophan and Valine in the Plasma of Chickens.The journal of poultry science · 2017Article
- Cellular mechanisms and consequences of glycation in atherosclerosis and obesity.Biochimica et biophysica acta · 2016Review
- Advanced Glycation End Products Induce Obesity and Hepatosteatosis in CD-1 Wild-Type Mice.BioMed research international · 2016Article
- Advanced Glycation End Products and Risks for Chronic Diseases: Intervening Through Lifestyle Modification.American journal of lifestyle medicineArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The purpose of this pilot study was to determine whether macronutrient content (low-fat v. high-fat diet) influences an indicator of advanced glycation end products (AGE), N(ε) carboxymethyl-lysine (CML), in the context of a 1-d, high-AGE diet. The effect of the diets on inflammatory markers was also assessed. A total of nineteen overweight and obese adults (nine men and ten women) without known disease were recruited to participate in a crossover challenge of a high-fat, high-AGE (HFHA) and low-fat, high-AGE (LFHA) diet. In each phase patients had fasting blood drawn, followed by consumption of a high-fat or low-fat breakfast test meal, then three postprandial blood draws at 1, 2 and 3 h after consuming the test meal. After consuming high-AGE meals for the remainder of the day, participants returned the next day for a follow-up analysis. A different pattern in the 3-h post-meal CML and soluble receptor for AGE response to the two diets was observed (P=0·01 and 0·05, respectively). No change in serum CML was observed following consumption of a LFHA breakfast (535 (25th-75th percentile 451-790) to 495 (25th-75th percentile 391-682) ng/ml; P=0·36), whereas a rise in CML occurred after the HFHA breakfast (463 (25th-75th percentile 428-664) to 578 (25th-75th percentile 474-865) ng/ml; P=0·05). High sensitivity C-reactive protein and high molecular weight adiponectin were not affected by either diet. These findings suggest that dietary CML may not be as important in influencing serum CML as other dietary factors. In addition, acute exposure to dietary CML may not influence inflammation in adults without diabetes or kidney disease. This is contrary to previous findings.
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