effects of ginger on fasting blood sugar, hemoglobin A1c, apolipoprotein B, apolipoprotein A-I and malondialdehyde in type 2 diabetic patients

Diabetes mellitus is the most common endocrine disorder, causes many complications such as micro- and macro-vascular diseases. Anti-diabetic, hypolipidemic and anti-oxidative properties of ginger have been noticed in several researches. The present study was conducted to investigate the effects of ginger on fasting blood sugar, Hemoglobin A1c, apolipoprotein B, apolipoprotein A-I, and malondialdehyde in type 2 diabetic patients. In a randomized, double-blind, placebo-controlled, clinical trial, a total of 41 type 2 diabetic patients randomly were assigned to ginger or placebo groups [22 in ginger group and 19 in control group], received 2 g/day of ginger powder supplement or lactose as placebo for 12 weeks. The serum concentrations of fasting blood sugar, Hemoglobin A1c, apolipoprotein B, apolipoprotein A-I and malondialdehyde were analyzed before and after the intervention. Ginger supplementation significantly reduced the levels of fasting blood sugar, hemoglobin A1c, apolipoprotein B, apolipoprotein B/apolipoprotein A-I and malondialdehyde in ginger group in comparison to baseline, as well as control group, while it increased the level of apolipoprotein A-I [p<0.05]. It seems that oral administration of ginger powder supplement can improves fasting blood sugar, hemoglobin A1c, apolipoprotein B, apolipoprotein A-I, apolipoprotein B/apolipoprotein A-I and malondialdehyde in type 2 diabetic patients. So it may have a role in alleviating the risk of some chronic complications of diabetes

Altered suppressor function of regulatoryT cells in type 1 diabetes

Background: Type 1 diabetes [T1D] is a T cell mediated autoimmune disease targetingthe insulin-producing beta cells within pancreatic islets. Autoimmune diseases maydevelop as a consequence of altered balance between regulatory [Tregs] andautoreactive T cells

Objectives: To evaluate Treg cells frequency and suppressivefunction in the peripheral blood of newly diagnosed T1D patients in comparison withhealthy controls

Methods: Fifteen new cases of T1D patients and 15 age- and sexmatchedhealthy controls were recruited to this study. Their peripheral bloodmononuclear cells [PBMCs] were isolated and CD4[+]CD25[+]FoxP3[+]CD127[-/low] Treg cellswere studied by flowcytometry technique. Thereafter, Tregs were isolated by Magnetic-Activated Cell Separation [MACS] technology and by using CFSE [carboxyfluoresceinsuccinimidyl ester] dilution assay, their suppressive activity was evaluated in thecoculture of CD4[+]CD25[-] T responder cells with Treg cells

Results: The percentage ofCD4[+]CD25[+]FoxP3[+]CD127[-/low] Tregs did not differ between T1D patients and healthycontrols but the MFI [mean fluorescence intensity] of transcription factor FoxP3[forkhead box protein P3] was significantly decreased in T1D patients [20.03 +/- 1.4 vs.31.33 +/- 2.95, p=0.0017]. Moreover, the suppressive function of CD4[+]CD25[+]CD127[-/low]Treg cells was significantly diminished in T1D patients in comparison with controlgroup [35.16 +/- 4.93% vs. 60.45 +/- 5.26%, respectively, p=0.0015]

Conclusion: Presentstudy indicates an impaired immune regulation among T1D patients, characterized bydefects in suppressive function and expression of FoxP3 in Treg cells without anysignificant decrease in their frequency in peripheral blood

effect of sumac rhuscoriaria L. powder on serum glycemic status, ApoB, ApoA-I and total antioxidant capacity in type 2 diabetic patients

Sumac Rhuscoriaria L. is used as an herbal remedy in traditional medicine. The aim of this study was to determine the effects of sumac [R. coriaria] on serum glycemic status, apolipoprotein [apo] B, apoA-I and total antioxidant capacity [TAC] in type 2 diabetic patients. This double blind randomized controlled clinical trial was conducted on 41type 2 diabetic volunteers randomly assigned into 3g/day sumac powder [n=22] or placebo [n=19] groups over 3 months. Blood samples were collected before and after the intervention. Serum glucose and HbA1c were measured using enzymatic and turbidimetric inhibition immunoassay methods, respectively. ApoB, apoA-I and TAC were determined using turbidimetric immunoassay and spectrophotometric methods, respectively. There were significant decreases in serum glucose and HbA1c and als oapoB levels at the end of study compared with initial values [P< 0.0001, P= 0.002 and P< 0.0001, respectively]. Also, there was a significant difference in HbA1c and TAC levels between placebo and sumac groups at the end of study [P< 0.05]. In sumac group, there were significant increase in apoA-I and TAC [P< 0.0001] compared with initial values. The mean of differences of serum glucose, HbA1c, apoB, apoA-I, apoB/apoA-I ratio and TAC between groups were significant [P< 0.05]. In conclusion, these results showed the favorite effect of sumac consumption on serum glycemic status, apoB, apoA-I and TAC levels in in type 2 diabetic patients

Effects of pure eicosapentaenoic and docosahexaenoic acids on oxidative stress, inflammation and body fat mass in patients with type 2 diabetes

N 3 Fatty acids reduce the risk of cardiovascular disease. Previous studies have shown that they may reduce inflammation, oxidative stress, and fat mass in patients with type 2 diabetes, but the results are inconclusive, due, in part, to type of omega 3 fatty acids used. The aim of this study was to determine the effects of pure eicosapentaenoic [EPA] and docosahexaenoic acids [DHA], the two major omega 3 fatty acids, on inflammation, oxidative stress, and fat mass in patients with type 2 diabetes. Sixty patients with DM II were randomly allocated to receive daily either tilde1 gr EPA or tilde1 gr DHA, or a canola oil as placebo for 12 weeks in a randomized triple blind, placebo controlled trial. Serum MDA, CRP, body weight, BMI, and fat mass were measured at baseline and after intervention. Forty five patients with a mean [ +/- SD] age of 54.9 +/- 8.2 years with BMI of 27.6 +/- 4.1 kg/m[2] and fasting blood glucose 96.0 +/- 16.2 mg/dl completed the intervention. Neither EPA nor DHA had significant effects on serum FBS, C reactive protein, body weight, BMI, and fat mass after intervention [P > 0.05]. In addition, while MDA increased 18% in the placebo group [P = 0.009], it did not change in the EPA or DHA group [P > 0.05]. Twelve weeks of supplementation with 1gr/d EPA or DHA prevent increasing oxidative stress without changing marker of inflammation. This study is the first report demonstrating that neither EPA nor DHA have effects on body fat mass in type 2 diabetic patients

Increased expression of trail and its receptors on peripheral T-cells in type 1 diabetic patients

Type-I diabetes is an autoimmune inflammatory disease in which pancreatic beta-cells are selectively destroyed by infiltrating cells. TNF-related apoptosis-inducing ligand [TRAIL] is a type-II membrane protein of the TNF superfamily which is expressed in different tissues, including pancreas and lymphocytes. In humans, TRAIL interacts with four membrane receptors. TRAIL-R1 and TRAIL-R2 have cytoplasmic death domains, and can activate both caspases and NF?B pathways. The other two receptors, TRAIL-R3 and TRAIL-R4, are decoy receptors not capable of activating caspase cascade but may activate NF-?B and block apoptosis. As human beta cells are sensitive to TRAIL induced apoptosis, signaling via these molecules is considered to be a probable way of beta cell destruction. These molecules also are important in suppression of autorective T cells and immunoregulation. To explore the importance of TRAIL and its receptors at pathogenesis of type-I diabetes, we compared expression of these molecules on T-cells of diabetic patients and healthy controls. In this study, expression of TRAIL and its receptors at protein and mRNA levels were studied in freshly isolated peripheral T cells of 55 type I diabetic patients and 50 healthy individuals by flowcytometry, western blot and RT-PCR. We found that expression of TRAIL and its receptors in peripheral T-cells at both protein and mRNA levels are significantly increased in patients [except for TRAIL-R2 mRNA which was slightly higher in controls] but increase in TRAIL, TRAILR3 [2.7% vs. >0.5%] and TRAIL-R4 [2.6% vs. >0.5%] is more considerable. sTRAIL in sera of patients was significantly lower than in controls [p=0.01]. Our results explain resistance of autoreactive T-cells to immunoregulatory mechanisms. Besides, increased expression of TRAIL in autoreactive T-cells may play an important role in betacell destruction. Lower level of sTRAIL in diabetic patients may be a reason for hyperactivation of autoreactive T-cells

Production and characterization of a monoclonal antibody against an antigen on the surface of non-small cell carcinoma of the lung

Lung carcinoma is a multiple type cancer comprising of small cell and non-small cell carcinomas [NSCLC]. For therapeutic and diagnostic purposes, serum monoclonal antibodies have been produced against lung cancer. To characterize a murine monoclonal antibody [ME3D11] reactive with human NSCLC. A murine monoclonal antibody [ME3D11] reactive with human NSCLC was selected after immunization of BALB/c mice with a human large cell carcinoma with neuroendocrine differentiation, and was tested by immunofloursence staining and Western blot analysis. Our study showed that the antigen recognized by ME3D11 antibody was a cell surface antigen of 170kDa. This antigen is expressed on the cell surface of all NSCLC and a few carcinoma cell lines. In contrast, this antigen is neither expressed on the cell surface of human sarcoma, nor on the hematopoietic and normal cell lines. This antibody had no effect on spontaneous proliferation of Mehr-80 cell line in vitro. High degree of binding of this monoclonal antibody to NSCLC and some other carcinoma cells warrants further studies on its potential use in diagnosis and therapy of cancer by conjugation to drugs, toxins or radionuclides