Introduction: The hypoglycemic effects of the Uritca Dioica (UD) extract, used for treatment of diabetes mellitus for many centuries, have been documented in several studies. The present study was designed to determine the possible mechanisms of hypoglycemic effects of UD on human muscle cells and RIN5F rat pancreatic b cells.Materials and Methods: In the cell culture laboratory of the Drug Applied Research Center, pancreatic b cells and human muscle cells were prepared in multiple flasks containing culture media. Alcoholic extract of UD at concentrations of 50, 100 and 200 mg/mL were added to muscle cell flasks. The same concentrations of extract plus insulin were added to other muscle cell flasks. Glucose levels were measured in the flasks before and after 60, 120 and 180 minutes after adding of extract. Also the same concentrations of UD were added to flask containing RIN5F rat pancreatic b cells, and insulin and C-PEPTIDE level were measured at 0, 60, 120 and 180 minutes.Results: Mean glucose level in the muscle cell media with UD alone and UD plus insulin, at the concentrations and time intervals mentioned, did not change significantly.Insulin levels in pancreatic cells media, before and after applying of UD at different concentrations, and at different times was £0.2 mg/ml. C-PEPTIDE (mg/ml) levels in these medias with a dose of 50 mg/ml of UD and at above mentioned times were 0. 31, 0.33, 0.86 and 0.8; at concentration of 100 mg/mL they were 0.7, 0.2, 0.4 and 0.39, and at concentration of 200 mg/mL were 0.32, 0.33, 0.93, 0.77 respectively (Nonsignificant changes).Conclusion: The results of the present study showed that alcoholic extract of UD was unable to increase insulin sensitivity in muscle cells and/or increase insulin and C-PEPTIDE secretion from RIN5F pancreatic b cells. It seems that hypoglycemic effects of UD were not mediated through the proposed mechanisms of this study.

Background: Tumor-associated hypoglycemia can be caused by non-islet cell tumors including gastrointestinal stromal tumor (GIST) which is a rare paraneoplastic syndrome that leads to the release of insulin-like growth factor-2 (IGF-2). Case Presentation: We report the case of a 45-year old woman who was admitted to our hospital with refractory hypoglycemic episodes. We found normal serum insulin and cpeptide level and abdominal CT-scan showed a small duodenal wall lesion suggesting insulinoma. After tumor resection, hypoglycemia symptoms were recovered, but the pathological findings demonstrated the lesion was GIST. Conclusion: In a small gastrointestinal lesion with hypoglycemic symptoms we should consider IGF-II secreting GIST in addition to insulinoma.

Introduction: Gama amino butyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian nervous system. The concentration of GABA and the number of GABA cell secretion decrease in diabetic patient and experimental diabetes model. The reported effects of GABA activation on insulin secretion from beta cells have been controversial. In this study we investigated if GABA administration in animal diabetes model can change insulin and glucagon secretion and improve some diabetic symptoms.Methods: Twenty fourth-week old NOD mi (Non obese diabetic mice) ce were used. Two months after diabetic induction animals were divided into the two groups. One group received 200 mmol of GABA and the other group received phosphate buffer solution (PBS) for one month.Results: GABA administration could significantly decrease plasma glucose and glucagon level, water consumption and urine volume and body fat distribution in the mesenteric bed and abdominal wall. It also could increase plasma Cpeptide level and it has not effect on food intake.Conclusion: NOD mice is very good genetically model for type one diabetes and GABA administration in this mice could treatment some of diabetic symptom. It seems may be we could use of GABA for treatment of diabetic symptom in future.

Endostatin, the C-terminal fragment of collagen XVIII, is known as an endogenous inhibitor of angiogenesis and is currently used as an anticancer drug. Endostatin fragments can be used as alternatives for full-length molecule, among which a peptide derived from the Cterminal fragment of protein, including residues 123-184 was shown to effectively inhibit angiogenesis and tumor growth. The aim of current study was to design a shortened peptide of the fragment 123-184. For this purpose, the presumably non-functional segments were deleted, including β-hairpin segment, comprising residues 145-163 and C-terminus of the protein, including residues 175-184. The designed 30-amino acid peptide that encompasses random coils in 123-184 (referred to as C-PEPTIDE) was synthesized and characterized. Cpeptide inhibited the proliferation of the Human Umbilical Vein Endothelial Cells (HUVECs) with an IC50 value of 0. 35 μ M. Administration of C-PEPTIDE caused the regression of 4T1 murine mammary carcinoma tumor growth, considerable reduced tumor cell proliferation (Ki67 expression) and angiogenesis (CD31 and CD34 expression), and the induction of apoptosis (increased TUNEL staining). These results confirm that the random coils of the C-terminal domain of endostatin are implicated in its antiangiogenic and antitumor properties.

Background & Aim: Alzheimer disease is characterized by a progressive loss of memory. Its prevalence in diabetic patients is nearly twice in comparison of others. Recent findings suggest that C-PEPTIDE replacement in type 1 diabetes exerts beneficial effects on diabetic rats. We examined the effects of C-PEPTIDE on cognitive dysfunction and neuronal apoptosis caused by Ab 1-42 on working memory in Streptozotocin induced diabetic rats.Methods: In the present experimental study which was carried out in 2009 at Shiraz University of Medical Sciences, 50 male Sprague Dawley rats (230-300 gr) were divided into five groups: control, type 1 diabetic, diabetic groups receiving C-PEPTIDE, diabetic group receiving beta amyloid, diabetic group receiving beta amyloid and C-PEPTIDE. The Neuronal apoptosis were assessed with tunnel staining. Diabetes was induced with IV injection of Streptozotocin (60 mg/kg). Twenty six days after the onset of diabetes, behavioral tests were conducted for three days. For data analysis, the Tukey and One way ANOVA tests were used.Results: In comparison to control group, in all diabetic groups working memory impairments was observed (P<0.05), but Ab 1-42 caused severe deficits in the working memory (P<0.001) and Cpeptide could significantly decrease the impairment (P<0.05). Only the diabetic beta amyloid group showed significant amount of tunnel positive neuron (P<0.05) and C-PEPTIDE replacement significantly decreased the amount of these cells (P<0.05).Conclusion: C-PEPTIDE could significantly decrease memory impairment and neuronal apoptosis among diabetic rats.

Introduction: Some cell culture and animal studies have reported that Conjugated Linoleic Acids (CLAs) have several health related benefits. CLAs have been shown to have antiadipogenic, antiatherogenic, antidiabetogenic and anti-inflammatory properties. While increase in insulin resistance with 10-trans, 12-cis isomer of CLA was reported in some animal studies, there are controversial results about a 50:50 isomer mixture. The object of the present study was to determine the effect of CLAs supplementation (providing equal proportions of c9, t11 and t10, c12 CLA) on plasma glucose, insulin, proinsulin, C-PEPTIDE, insulin sensitivity, insulin resistance, beta cell function and HbA1c in patients with type 2 diabetes mellitus. Materials & Methods: The study was performed as an 8-week randomized double-blind, placebo-controlled parallel intervention. Participants were 39 (19 men and 20 women) type 2 diabetic subjects (35 to 50 Y, BMI >25 and <30), stratified according to sex, age and BMI into two groups. Group one were given 3.0 g CLA/d (3×1g capsules, a 50:50 isomer blend of c9, t11 and t10, c12 CLA) and, group 2 took CLA placebos (soy bean oil) for 8 weeks. Blood sample collection after fasting and 2 hours after a standard breakfast, was done before and after the intervention in order to determine insulin, glucose, pre insulin, cpeptide and HbA1c levels. Results: No significant differences were seen in fasting and postprandial glucose, insulin, proinsulin, C- peptide and HbA1c levels between groups or in insulin resistance, insulin sensitivity, beta cell function and beta cell responsiveness. Conclusion: CLA supplementation has no effects on diabetes glucose level and insulin function and its prescription is not recommended.