Effect of prolactin and estrogen on the serum level of 1,25-dihydroxy vitamin D and FGF23 in female rats.

INTRODUCTION: Estrogen and prolactin affect vitamin D metabolism. In conditions such as pregnancy and lactation, their interaction in regulating vitamin D metabolism and circulating FGF23 is not clearly defined. The aim of this study is to investigate this interaction in female rats. METHOD: This study was performed on 50 female adult rats, which were divided into five groups of Sham, ovariectomized rats (O), and three groups of ovariectomized rats were indicated with prolactin alone (OP), estradiol alone (OE), and a combination of estradiol and prolactin (OEP). Serum levels of 25(OH)D, 1,25(OH)2D3, FGF23, PTH, vitamin D-binding protein, calcium, and phosphorous were evaluated. RESULTS: Serum 1,25(OH)2D3 and PTH in OE were higher than the O group (P < 0.001 and P = 0.003, respectively). Serum FGF23 in the OE group was lower than the O group (P = 0.016). Serum 1,25(OH)2D3 increased in OP compared to the O group (P < 0.001) and OE group (P < 0.001). Serum FGF23 in OP was lower than the O group (P = 0.04). Furthermore, combining estradiol and prolactin showed no extra effect on increasing serum 1,25(OH)2D3. Serum 1,25(OH)2D3 was positively correlated with serum prolactin levels (r = 0.318, P = 0.017) in all five groups. CONCLUSION: It is suggested that estradiol could increase 1,25(OH)2D3 by elevating PTH and decreasing serum FGF23; however, prolactin was able to increase 1,25(OH)2D3 by lowering serum FGF23. Moreover, prolactin was shown to be more potent in augmenting serum 1,25(OH)2D3 than estrogen itself, which is important in maternal and fetal calcium supply during late pregnancy and lactation.

The effect of prolactin itself and in combination with estrogen on bone mineral density in female rats.

Estrogen deficiency induced by hyperprolactinemia can reduce bone mineral density. Hyperprolactinemia through other mechanisms other than estrogen deficiency, with direct effect on the bone might cause bone loss in women. The present study evaluated the effect of prolactin itself and in combination with estrogen on bone mineral density of female rats. This study was performed on 50 adult female rats divided into five groups; included (a) Sham, (b) Ovariectomized rats; and (c-e) included ovariectomized rats were given prolactin alone, prolactin + estradiol and estradiol, respectively. Bone mineral density (BMD) and vitamin D metabolism parameters were checked in all groups before and after the study. There was no significant difference in baseline values of these parameters. Estradiol could increase 1,25(OH)2D3 and PTH levels and decrease serum ALP level. In addition, Prolactin could increase serum 1,25(OH)2D3 and ALP levels and decrease tibia BMD significantly without any change in PTH level. Combination of estradiol and prolactin could increase serum 1,25(OH)2D3 and PTH and tibia BMD compared with OVX group. Combination of estradiol and prolactin could significantly increase tibia BMD, in ovariectomized rats. We hypothesized that this combination could improve bone loss secondary to hyperprolactinemia by elevated PTH.

The effect of testosterone itself and in combination with letrozole on bone mineral density in male rats.

Testosterone is an essential hormone to maintain bone integrity; however, the effect of aromatase enzyme in androgen-induced bone maintenance remains somewhat unclear. The present study evaluated the effect of testosterone itself and combined with letrozole, an aromatase inhibitor, on bone mineral density of male rats. Total of 48 male rats were divided into 4 equal groups (n = 12/group); sham group, O: orchiectomy, O + T: orchiectomized rats treated with testosterone, O + T + L: orchiectomized rats treated with combination of testosterone and letrozole. Bone density (BMD), bone markers, and vitamin D metabolism parameters were checked in all groups before and after the study. There was no significant difference in baseline values of these parameters, but at the end of the study there was a significant decrease in delta BMD at both lumbar and femor in orchiectomized rats in comparison with the sham group (p < 0.001, p < 0.001, respectively). Both testosterone and its combination with letrozole increased lumbar and femoral BMD of orchiectomized rats, with a higher increase in lumbar BMD in O + T group. CTX were higher in O group rats. The present study showed a major role for testosterone on BMD maintenance in male rats. However, testosterone has a potent effect on lumbar BMD, by the aromatization to estradiol.

Hypoglycemic Effect of Aquatic Extract of Stevia in Pancreas of Diabetic Rats: PPARγ-dependent Regulation or Antioxidant Potential.

BACKGROUND: Traditional medicines with anti-diabetic effects are considered suitable supplements to treat diabetes. Among medicinal herbs, Stevia Rebaudiana Bertoni is famous for its sweet taste and beneficial effect in regulation of glucose. However, little is known about the exact mechanism of stevia in pancreatic tissue. Therefore, this study investigated the possible effects of stevia on pancreas in managing hyperglycemia seen in streptozotocin-induced Sprague-Dawley rats. METHODS: Sprague-Dawley rats were divided into four groups including normoglycemic, diabetic and two more diabetic groups in which, one was treated with aquatic extract of stevia (400 mg/kg) and the other with pioglitazone (10 mg/kg) for the period of 28 days. After completion of the experimental duration, rats were dissected; blood samples and pancreas were further used for detecting biochemical and histopathological changes. FBS, TG, cholestrol, HDL, LDL, ALT and AST levels were measured in sera. Moreover, MDA (malondialdehyde) level, catalase activity, levels of insulin and PPARγ mRNA expression were also measured in pancreatic tissue. RESULTS: Aquatic extract of stevia significantly reduced the FBS, triglycerides, MDA, ALT, AST levels and normalized catalase activity in treated rats compared with diabetic rats (p<0.05). In addition to this, stevia surprisingly, increased PPARγ and insulin mRNA levels in treated rats (p<0.05). Furthermore, stevia compensated for the histopathological damage in diabetic rats. CONCLUSION: It is concluded that stevia acts on pancreatic tissue to elevate the insulin level and exerts beneficial anti-hyperglycemic effects through the PPARγ-dependent mechanism and stevia's antioxidant properties.

Effects of essential oil of Satureja khuzestanica on the oxidative stress in experimental hyperthyroid male rat.

This work analyzes the effects of Satureja khuzestanica essential oil (SKEO) on the thyroid and antioxidant system, assessed by measuring levels of tri-iodothyronine (T3), thyroxine (T4), thyroid-stimulating hormone (TSH), malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPx) activity. Forty adult male Sprague Dawley rats (225 ± 25 g) were divided into five equal groups: one control and four hyperthyroid groups that received placebo, 200 mg kg(-1) body weight of vitamin (Vit.) E, 225 mg kg(-1) body weight of SKEO, 200 and 225 mg kg(-1) body weight of Vit. E and SKEO together, respectively. Hyperthyroidism was induced by administering of L-thyroxin in drinking water. After 30 days of L-thyroxin consumption, serum T3 and T4 levels, TSH, and oxidative stress indices were determined. Significant increase in serum T3, T4 and MDA concentrations with a simultaneous significant decrease in TSH, GSH level and GPx activity were observed in hyperthyroid group (p <0.05). In the treatment groups, SKEO and/or Vit. E can compensate serum MDA elevation and GPx activity reduction. Only, SKEO + Vit. E could compensate the decline of GSH levels in response to hyperthyroidism. Supplementation of SKEO, plus Vit. E as antioxidants is useful in attenuating lipid peroxidation and may potentially benefit hyperthyroid patients.

Hepatoprotective effect of satureja khuzestanica essential oil and vitamin e in experimental hyperthyroid rats: evidence for role of antioxidant effect.

BACKGROUND: Hyperthyroidism is associated with liver oxidative stress causing liver dysfunction in many hyperthyroid patients. The hepatoprotective effect of Satureja Khuzestanica Essential Oil (SKEO), as herbal origin antioxidant and anti-inflammatory agent on the hyperthyroidism induced hepatotoxicity and oxidative stress is investigated. METHODS: Adult male sprague dawley rats were divided into categories of; control (group C), hyperthyroid (group H), hyperthyroid with olive oil (group H+O), hyperthyroid with vitamin E (group H+E), hyperthyroid with SKEO (group H+S), combination of hyperthyroid with vitamin E and SKEO (group H+S+E). Hepatoprotective and antioxidant properties of SKEO with or without vitamin E in hyperthyroid rats were then investigated. RESULTS: Serum Aspartate Transaminase (AST) and Alanine Transaminase (ALT) activities reduced significantly in H+O, H+E, H+S and H+S+E groups in comparison with hyperthyroid rats. Enzymes activities returned to normal in H+S+E group. Hepatic Malondialdehyde (MDA) was reduced in H+E, H+S and H+S+E groups in comparison with hyperthyroid rats. The most significant MDA reduction was in the H+S+E group. Glutathione Peroxidase (GPx) and Glutathione Reductase (GR) activities increased in H+E, H+S and H+S+E groups in comparison with group H. The largest increment in GPx and GR activities were in the H+S+E group. Glutathione level did not change in any group in comparison with the control group. CONCLUSION: Administration of SKEO has hepatoprotective effect in hyperthyroid rats and is more effective when used in combination with vitamin E.