ABSTRACT
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 PPARgamma 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 PPARgamma 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 PPARgamma-dependent mechanism and stevia's antioxidant properties
ABSTRACT
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
ABSTRACT
Polycystic ovary syndrome [PCOS] is one of the most common diseases among women associated with various inflammatory reactants such as C-reactive protein [CRP] and ferritin. This study aimed to investigate the effect of metformin on probable reduction of serum ferritin in patients with PCOS. This study was conducted on 45 patients with PCOS who had not other systemic diseases and did not take any medications. Weight, waist and hip circumstances [WHR], body mass index [BMI], metabolic indexes, CRP, ferritin and "Homeostasis Model Assessment of Insulin Resistance [HOMA-IR] ? were measured before the study. Metformin [500 mg/tid] tablets were prescribed for three months and then same above parameters were re-measured. Of 45 patients, 19 [42.2%] were overweight and 14 [31.1%] were obese. After drug therapy, there was a significant reduction in waist circumstance and serum ferritin. This reduction was significant only in the lean and overweight groups but not in the obese group. There was not significant association between serum ferritin and CRP, HOMA-IR, BMI and WHR. There was not significant correlation between CRP and HOMA-IR and also BMI. The effect of metformin on reduction of serum ferritin was not significant just in obese group and was not associated with metabolic and anthropometric indexes
Subject(s)
Humans , Female , Ferritins/blood , MetforminABSTRACT
Diabetes mellitus is the most common cause of renal failure, blindness, non- traumatic amputation and neuropathy. Homocysteine, a sulfurated amino acid, has a close correlation with Methionine and Cysteine. The conversion of Methionine to Homocysteine and Cysteine is required coenzymes like vitamin B6, B12 and Folate. The effect of Metformin on serum Homocysteine level by decreasing vitamin B12 level in patients with type 2 diabetes mellitus was described previously. This is a prospective clinical trail study among patients with type 2 diabetes mellitus in Shiraz. 76 patients were divided into two groups [38 patients in each group]. First group treated with Metformin 500-2000 mg/day and the second group treated with Glibenclamide 5-20 mg/day with follow up period of at least 6 months. Hb and MCV were used in follow up to detect megaloblastic anemia, indicator of B12 and folate deficiency. Fasting plasma Homocysteine level Hb A1C and blood sugar were measured in baseline and at 3 and 6 months follow up periods. There was no significant difference between age, sex, weight, height and BMI and baseline serum profile between the two groups. Homocysteine level increased significantly in Metformin group at 3 and 6 months[P=0.003 and 0.001 respectively]. Mean plasma homocysteine level after 6 months were 10.98 +/- 0.58 micro mol/l in Metformin and 10.0 +/- 0.88 micro mol/l in Glibenclamide group, with significant difference between the two groups [P=0.001]. Metformin increases the plasma Homocysteine level. Metformin will accumulate highly in gastrointestinal wall and cause malabsorption of vitamin B12, therefore we can conclude that the use of Metformin for 6 months can cause vitamin B12 malabsorption and increase in plasma homocysteine level. Increase in plasma homocysteine level was 7.54% in our study that is higher in comparing to the other studies. It can be explained by longer duration of Metformin therapy in our study. Rising in Homocysteine levels may have detrimental effect on vessels that need further study