The effects of different diets (high fat and high fructose diet) on the development of insulin resistance and tissue advanced glycation end product levels in rats

Demirci T., Orbak Z., Öztürk N., Kaygisiz M. D., Nalcı K. A., Polat Z. B.

HORMONE RESEARCH IN PAEDIATRICS, cilt.91, ss.345-346, 2019 (SCI-Expanded) identifier

  • Yayın Türü: Makale / Özet
  • Cilt numarası: 91
  • Basım Tarihi: 2019
  • Dergi Adı: HORMONE RESEARCH IN PAEDIATRICS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED)
  • Sayfa Sayıları: ss.345-346
  • Atatürk Üniversitesi Adresli: Evet

Özet

bring many metabolic diseases, especially obesity and diabetes. Recent years, more scientific interest in how can diet effect on brain function has emerged. We aimed to investigate the effect of high fructose and high-fat diet on the brain, and whether the presence of relationship with advanced glycation end products histologically, in rat model. Materials & Methods: Twenty-four Sprague Dawley rats were used and divided into 3 groups as control group, high fructose group and high fatty group. During 12 weeks, while the rats in the control group were given standard rat chow, those of in the high fructose and high fatty group were fed with %60 high fructose diet and %45 high fat diet, respectively. At the end of the experiment, their brains were removed. AGE and R-AGE expression were evaluated by immunohistochemistry and biochemically. Results: In the H-E stained sections, the control group rat brains showed healthy histological appearance. The brain sections of the high fructose group showed that histological structure was deteriorated. There was a significant increase in glial cells, especially in the mediobasal hypothalamus. Shrinkage and eosinophilic staining of the neurons were noticed, chromatin condensation in the nucleus was prominent. Also, pericellular edema was present in neurons and glial cells. Similar findings were observed in the high-fat group. Glial cells were increased compared to the control group but were less than the high fructose group. There was dilated blood vessels and pericellular edema. Small eosinophilic neurons with shrunken nuclei and with condensed chromatin were also abundantly observed in the high-fat group. In the control group, no AGE immunostaining was observed in the axonal structures, whereas immunopositive staining was observed in neural cells. When the brain sections of high fructose group were examined, it was observed that AGE immunostaining positivity was more significant than the control and high-fat group. R-AGE immunostaining intensity in hypothalamus of both high fructose and high-fat groups was higher than in the control group. Biochemical results are given in Table 1.

Conclusions: The feeding with both high fructose and highfat diet might cause the deterioration in the brain mainly the hypothalamus, and increased advanced glycation end products may play an essential role in the development of damage. Control Brain High fructose Brain High fat Brain Glucose µmol/L 25,86 25,09 19,42 Insulin ng/mL 17,93 16,25 17,09 R-AGE pg/mL 93,24 169,42 163,78 GEs ng/mL 132,73 86,85 100,36