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Scientific Research of the Union of Scientists in Bulgaria - Plovdiv, series G. Medicine, Pharmacy and Dental medicine, Vol. XVII, ISSN 1311-9427, International Conference of Young Scientists, 11 - 13 June 2015, Plovdiv
ADIPONECTIN AND LEPTIN LEVELS IN RAT METABOLIC
SYNDROME
Petar Hrischev1, Penka Angelova1, Katerina Georgieva1, Nikolay Boydziev1, Dora Terzieva2, Pepa Atanassova3
l. Department of Physiology, 2. Clinical Laboratory, 3. Department of Anatomy, Histology and Embryology; Medical University-Plovdiv, Bulgaria
ABSTRACT The aim of the study was to investigate the adiponectin and leptin levels in metabolic syndrome of male Wistar rats subjected to a high-fat-carbohydrate diets for 16 weeks. The animals were divided into 3 groups: a control group which received standard rat chow (C), a dietary manipulated group which received combined high-fat-sucrose food (D) and dietary resistant group (DR) that had low body mass after 12 weeks after the beginning of the study. The serum levels of fasting leptin and adiponectin were analyzed by the sandwich ELISA method. The results revealed increased leptin levels of D as compared with C group. The leptin levels in DR group were higher as compared with C and lower as compared with D, but the results were not significant (P>0.05). The adiponectin levels of C were not significantly different than that of group D (P>0.05). The adiponectin levels in dietary resistant group were higher as compared with C, and higher as compared with D (P<0.05). In conclusion the results suggest the possible role of leptin and adiponectin in the pathogenesis of the metabolic syndrome.
INTRODUCTION Metabolic syndrome (MetSyn) is a combination of obesity, insulin resistance, impaired fasting glucose, hyperlipidemia, hypertension. Increasing evidence suggests that chronic, low-grade inflammation may be common in the pathogenesis of MetSyn [1]. Adispose tissue is an active immune and endocrine organ that secretes various humoral factors (adipokines) involved in the regulation of energy metabolism and insulin resistance. Alteration of white adispose tissue mass in obesity affects the production of most adipose secreted factor and activates some pro-inflammatory signalling pathways, resulting in the induction of several biological markers of inflammation [2]. MetSyn corresponds to a clinical condition in which white adipose tissue is characterized by an increased production and secretion of inflammatory molecules which may have local effects on adipose tissue physiology but also systemic effects on other organs. A body of evidence suggests the presence of an overall low-grade inflammation in humanobesity and MetSyn with altered levels of several circulating factors such as an increase in the plasma levels of C-reactive protein, tumor necrosis factor, leptin, interleukin-6, transforming growth factor-beta, NGF, adiponectin [3, 4,5,6]. Combined high-fat-carbohydrate diets for the inducement of metabolic syndrome in rats imitate successfully the pathology in humans.
AIM The aim of the study was to investigate the adiponectin and leptin expression in metabolic syndrome in rats induced by high-fat-carbohydrate diet (HFCD).
MATERIAL AND METHODS The duration of the experiment was 16 weeks. Male Wistar
rats (n=80) were divided into two groups: a control group which received standard rat chow (C, n=20), and a dietary manipulated group which received combined high-fat-sucrose food with additional cholesterol (D, n=60). Twelve weeks after the beginning of the study we found that 13.3% (n=8) of the rats from group D had low body mass and were considered a dietary resistant group (DR). HFCD induced MetSyn in the rats as indicated by obesity, dislipidemia, impaired fasting glucose. 12 h after the last intake of food mix blood was collected from each animal. The serum levels of fasting adiponectin and leptin were analyzed by the sandwich ELISA method with a Sirio microplate reader (SEAC, Italy) using mouse/rat leptin ELISA kit (Bio Vendor, EU). The data of the experiments were analyzed with one-way ANOVA. The results are represented as X±SEM.
RESULTS AND DISCUSSION There was a difference between the immunochemical leptin expression of D and C groups. The application of HFSD with additional cholesterol resulted in increased leptin levels of D as compared with the C group. Leptin plasma immunochemical expression was stronger in the dietary manipulated group in comparison to C rats (173.76±71.04 pg/ml vs. 27.63±1.56 pg/ml, P<0.05). The leptin level in dietary resistant group (56.42±11.08 pg/ml) was higher as compared to the C and lower as compared to D, but the results were not significant (C/DR and D/DR, P>0.05). (Table 1) The serum adiponectin levels of C were not significantly different than that of D. The serum adiponectin levels in DR were higher as compared with C and D. (Table 2)
Table 1. Leptin expression (pg/ml)
group X SEM
C 27.625 1.558
D 173.775 71.035
D 5 1
R 6.417 1.076
C vs D, P<0.05 C vs DR, P>0.05 D vs DR, P>0.05 (one-way ANOVA)
Table 2. Adiponectin expression (ng/ml)
group X SEM
C 13.57 4.142
D 37.46 15.291
D 37.46 15.291
R 133.39 23.554
C vs D, P>0.05 C vs DR, P<0.01 D vs DR, P<0.05 (one-way ANOVA)
Our results correlate to a certain degree with data concerning human MetSyn (4,5). In rats MetSyn causes an increase of leptin levels only in that animals which have become obese. Atanassova et al. (2014) like us report about increased leptin expression in the blood and subcutaneous adipose tissue in women with MetSyn. In the same study adiponectin plasma levels were found decreased. We found that MetSyn in rats does not significantly change adiponectin plasma levels.
CONCLUSION The application of HFSD with additional cholesterol in rats is a good experimental model for inducement of metabolic syndrome. It causes an increase in plasma leptin levels. The result suggest the possible role of leptin and adiponectin in the pathogenesis of the metabolic syndrome. Our data encourage further studies on the relationship between adipokines and metabolic syndrome.
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