Dietary glycotoxins affect scavenger receptor expression and the hormonal profile of female rats

J Endocrinol. 2013 Aug 29;218(3):331-7. doi: 10.1530/JOE-13-0175. Print 2013 Sep.


The levels of advanced glycation end products (AGEs) are increased under conditions of impaired glucose metabolism and/or oxidative stress, promoting insulin resistance and other endocrine abnormalities. AGEs play a major role in the pathogenesis of several diseases such as diabetes, atherosclerosis, polycystic ovary syndrome and Alzheimer's disease, contributing to progressive ageing. Receptor-based clearance of AGEs by the receptor for AGE (RAGE) and/or the macrophage scavenger receptor A (SR-A) is considered as a main factor for the regulation of the concentration of AGEs under these conditions. This study aimed to investigate the expression of RAGE (AGER) and SR-A (MSR1) under high/low-dietary AGE conditions in vivo and their potential contribution to the metabolic and sex hormonal profile of female rats. Female Wistar rats were fed a low-AGE or high-AGE diet for 3 months. Serum samples were collected at baseline and at the completion of the 3-month period for the measurements of metabolic and hormonal parameters. Peripheral blood mononuclear cells (PBMCs) were isolated for the determination of the expression of RAGE and SR-A. The high-AGE diet-fed rats exhibited increased glucose, insulin and testosterone levels as well as decreased oestradiol and progesterone levels compared with the low-AGE diet-fed ones, thus indicating a metabolic and hormonal dysregulation attributed to high-AGE dietary exposure. The expression of RAGE was significantly down-regulated in the PBMCs of the high-AGE diet-fed rats (P=0.041), and it was correlated negatively with insulin and testosterone levels and positively with progesterone levels. The expression of SR-A was also decreased in the high-AGE diet-fed rats to marginal significance. Decreased monocytic expression of scavenger receptors such as RAGE and SR-A may result in a higher deposition of AGEs in peripheral endocrine tissues, thus promoting endocrine-related abnormalities and diseases.

Keywords: AGEs; PCOS; RAGE; SR-A; endocrine dysregulation; insulin resistance.

MeSH terms

  • Animals
  • Diet / adverse effects*
  • Estradiol / blood*
  • Female
  • Glucose / metabolism
  • Glycation End Products, Advanced / metabolism*
  • Glycation End Products, Advanced / toxicity
  • Insulin / blood*
  • Leukocytes, Mononuclear / metabolism
  • Progesterone / blood*
  • Rats
  • Rats, Wistar
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / metabolism*
  • Receptors, Scavenger / genetics
  • Receptors, Scavenger / metabolism*
  • Testosterone / blood*


  • Glycation End Products, Advanced
  • Insulin
  • Receptor for Advanced Glycation End Products
  • Receptors, Immunologic
  • Receptors, Scavenger
  • Testosterone
  • Progesterone
  • Estradiol
  • Glucose