Objective: The aim of this study was to verify if the exposure to the pulsed electromagnetic field (PEMF) infl uenced the release of proinfl ammatory cytokines from adipose-derived stem cells (ADSCs) of normal and overweight rats of various age and sex. Moreover, we compared body temperatures of normal-weight and overweight rats. Methods: ADSCs of Wistar rats were isolated from the subcutaneous area in females and paratesticular region in males, cultured and exposed to PEMF (7 Hz, 30 mT). Concentrations of proinflammatory cytokines were determined in rat sera and supernatant from ADSCs cultures exposed and non-exposed to PEMF. Body temperature (BT) was measured twice a week, using an infrared and rectal thermometer. Results: Irrespective of age and sex, animals maintained on low-fat (LF) diet had higher BT than those grown on high-fat (HF) diet. Exposure to PEMF reduced the release of TNF-α and enhanced the production of IL-6 in ADSCs cultures from female pups maintained on LF diet. In contrast, a decrease in IL-6 level was observed in PEMF-exposed ADSCs cultures from female pups grown on HF diet. A similar phenomenon, i.e. a post-exposure increase in IL-6 level was also observed in male pups fed with the LF diet. In the case of ADSCs cultures from adult rats maintained on an HF diet, either males or females, PEMF exposure contributed to a dramatic increase in TNF-α production. Conclusion: Our findings suggest that PEMF exposure may affect the production of proinflammatory cytokines in ADSCs cultures. The intergroup diff erences in BT may result from the presence of an underlying inflammation in obese rats.
O b j e c t i v e: The main goal of our studies was to investigate the eff ect exerted by pulsed electromagnetic filed (PEMF) on adipocytokines secretion in cell culture supernatants from rat adipose derived stem cells (ADSCs) grown on varied energy-rich diet. Off spring and adult animals were randomly selected for two types of experimental diets: low (LF) or high fat (HF) diet for 7 weeks. After the diet period, serum glucose level was measured, ADSCs were isolated from adipose tissues from different locations. ADSCs from all experimental groups were exposed to PEMF, supernatants collected and adipokines level was determined. R e s u l t s: HF diet feed in pups/adult animals elevated blood glucose level and increased the level of adiponectin (Apn) and leptin of both genders and age measured in serum. ADSCs cell cultures originated from female pups on LF diet and exposed to PEMF released large amounts of Apn. PEMF effect exerted on Apn release was also observed in ADSCs isolated from male pups HF diet. ADSCs from female pups on LF diet exposed to PEMF released smaller amounts of leptin in comparison to cell cultures without PEMF treatment. PEMF exposure of ADSCs cell cultures originated from female adults on LF diet decreased release of Apn, contrary adult male on LF diet ADSCs under PEMF treatment produced more leptin. PEMF treated male HF diet-originated ADSCs cultures released significantly more leptin than controls. C o n c l u s i o n: Our results suggest that PEMF exposure is responsible for metabolic physiological balance effects obtained in ADSCs cultures originating from adult animals on HF diet.
Background: Anorexia nervosa is a widely prevalent eating disorder that often leads to life-threatening complications. Since it mostly concerns females, many authors have focused on studying the reproductive system in anorexic women. Recently discovered telocytes may give a new insight into the pathophysiology of gynecological complications in these patients. Material and Methods: We adopted an animal model of anorexia nervosa induced by voluntary physical activity. Sixteen female Wistar rats were divided into two groups: control and activity-based anorexia. When the weight loss of activity-based anorexia (ABA) rats reached 25% animals were euthanized. Size and weight measurements as well as histopathological analysis of the reproductive organs were performed. Additionally, we used immunohistochemical staining for detection of telocytes. Results: Telocytes were identified in uteri of anorectic rats but no diff erences were observed when compared to the control group. Nevertheless, in the ABA group the weight of the uteri and the number of follicles in the ovaries decreased significantly. Conclusions: Our rat model of anorexia nervosa mimics the effects of this eating disorder that occur in the female reproductive system since we reported ovarian dysfunction and uterine involution in the experimental animals. It supports its potential role in the further studies of anorexia pathophysiology and treatment possibilities.