Soluble receptor for advanced glycation end products (sRAGE) correlates with obesity-related parameters, and it is not easy to be modified by moderate caloric restriction in obese humans.


Journal

Journal of physiology and pharmacology : an official journal of the Polish Physiological Society
ISSN: 1899-1505
Titre abrégé: J Physiol Pharmacol
Pays: Poland
ID NLM: 9114501

Informations de publication

Date de publication:
Aug 2022
Historique:
received: 16 06 2022
accepted: 30 08 2022
entrez: 25 1 2023
pubmed: 26 1 2023
medline: 28 1 2023
Statut: ppublish

Résumé

Deficiency of a soluble form of the advanced glycation end products receptor (sRAGE) is implicated in obesity-induced complications. Serum sRAGE is inclined to be modified by changes in body weight. We analysed serum sRAGE concentrations in patients with obesity undergoing moderate calorie restriction, which mimics the real-life situation and is not harmful to obese humans. Serum sRAGE was measured by immunoassay in 50 patients with obesity who underwent calorie restriction by 300-500 kcal/day for 8 weeks. In effect calorie restriction resulted in an expected decrease in body weight (by 2.1 kg for an 8-week intervention, p<0.0001), as well as reduced systolic blood pressure, modified dyslipidemia (cholesterol, triglycerides), reduced obesity-related inflammation (tumor necrosis factor-alfa, interleukin-6, C-reactive protein), improved insulin sensitivity. However, it was not accompanied by any significant change in sRAGE concentration. There was a strong negative correlation between BMI and the sRAGE level. Accordingly, the levels of sRAGE were the highest in lean control. In conclusion: a modest weight reduction is unlikely to improve decreased sRAGE levels.

Identifiants

pubmed: 36696243
doi: 10.26402/jpp.2022.4.06
doi:

Substances chimiques

Receptor for Advanced Glycation End Products 0
Glycation End Products, Advanced 0
Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Auteurs

D Kanikowska (D)

Department of Pathophysiology, Poznan University of Medical Sciences, Poznan, Poland. dkanikowska@ump.edu.pl.

A Kanikowska (A)

Department of Internal Diseases, Metabolism and Nutrition, Poznan University of Medical Science, Poznan, Poland.

E Swora-Cwynar (E)

Department of Internal Diseases, Metabolism and Nutrition, Poznan University of Medical Science, Poznan, Poland.

M Grzymisławski (M)

Department of Internal Diseases, Metabolism and Nutrition, Poznan University of Medical Science, Poznan, Poland.

M Sato (M)

Institutional Research, Aichi Medical University School of Medicine, Aichi, Japan.

A Breborowicz (A)

Department of Pathophysiology, Poznan University of Medical Sciences, Poznan, Poland.

J Witowski (J)

Department of Pathophysiology, Poznan University of Medical Sciences, Poznan, Poland.

K Korybalska (K)

Department of Pathophysiology, Poznan University of Medical Sciences, Poznan, Poland.

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Classifications MeSH