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Abstract

Background

The development of complementary treatment strategies that focuses on achieving a balance between adaptive and apoptotic unfolded protein response (UPR), enhancing endoplasmic reticulum (ER) homeostasis, and thus preserving β cell mass and function is particularly warranted.

Aim

This study was designed to investigate the effectiveness of the combined treatment by Quercetin (QUE) and Liraglutide (LIRA) in modulating hyperglycemia, insulin-insensitivity, UPR/ER stress markers, apoptosis, oxidative stress and inflammation using a high-fat diet/streptozotocin −induced type 2 diabetic rat model.

Methods

Sixty male albino rats were allocated into five equal groups: normal control, diabetic control, LIRA treated diabetic; QUE treated diabetic and combined treatment diabetic groups. Fasting glucose, insulin, CHOP, macrophage inflammatory protein −1 α (MIP-1α) and Bax, Bcl2 levels were estimated by ELISA; mRNA expression levels of the spliced X-box binding protein 1 (XBP1) were estimated using quantitative real-time RT-PCR, while MDA, advanced oxidation protein products, reduced glutathione levels and protein disulfide isomerase (PDI) activity were evaluated spectrophotometrically. Pancreatic tissues were also subjected to histopathological examination.

Results

The combined treatment with both LIRA and QUE causes significant improvements in all the studied parameters; including XBP1 splicing, CHOP, MIP-1α, Bax/Bcl2 ratio, PDI activity, as well as oxidative stress markers as compared to either treatment alone. It also attenuated pancreatic histopathological damage.

In conclusion

Our study nominates this combination to be used in T2DM to achieve adequate glycaemic control and to preserve optimal β cell function.

Vanillin as a new modulator candidate for renal injury induced by cisplatin in experimental rats

Posted by M M.Elseweidy, S E.Elswefy, M Shawky, et al. on 2017-09-18 20:02:59

Abstract

Cisplatin is commonly prescribed for the treatment of various solid tumors but its use is limited due to certain side effects and renal injury is a true example. Oxidative stress and inflammation may contribute to the cisplatin induced nephrotoxicity. Accordingly, we evaluated the effect of oral vanillin intake (100 mg/kg body weight) daily for 4 weeks to combat this hazard. The present results have demonstrated significant attenuation of oxidative stress and renal injury where reduced glutathione (GSH) showed significant increase along with malondialdehyde (MDA) decrease. Fibrotic markers like fibroblast growth factor-23 (FGF-23), transforming growth factor-β1 (TGF-β1), inflammatory mediators such as nuclear factor-κB (NF-κB) and tumor necrosis factor-α (TNF-α) showed also significant decrease in vanillin treated rats as compared with the control group.

Renal function showed also significant improvement where urea and creatinine demonstrated significant decrease and the histopathological study presented a good support to the biochemical markers results. Our conclusion that vanillin is a potent antioxidant, anti-inflammatory and anti-fibrotic agent. Additionally, it is a good modulator candidate for the renal injury induced by cisplatin intake.

Abstract

Insulin resistance is prevalent worldwide and is associated with many metabolic diseases, in particular, type 2 diabetes mellitus (T2DM), obesity, nonalcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS) and metabolic syndrome (MetS). Angiopoietin-like protein 8 (ANGPTL8), a newly-identified secreted protein composing of 198 amino acids, is enriched in the liver of human. Considering its promising potential for β-cell proliferation and therapeutic prospect for diabetes, ANGPTL8 has aroused extensive interests. However, a recent collaborative study confirmed that ANGPTL8 didn’t stimulate dramatic β-cell regeneration. At present, a controversial scientific discussion on whether and how ANGPTL8 regulate insulin resistance has been ongoing. Interestingly, several in vitro and in vivo studies have suggested the complex roles of ANGPTL8 in insulin resistance. Data resulting from cross-sectional and longitudinal researches in human individuals involving the influence of ANGPTL8 on the development of insulin resistance were controversial. We therefore summarize currently clinical literature to exploit whether this exciting hormone could be applied for clinical application as a potential clinical biomarker to predict insulin resistance and related disorders.

Abstract

Calcineurin, a serine/threonine phosphatase is a calcium dependent protein which on activation triggers transcriptional up regulation of inflammatory genes associated with inflammation in the arteries and progressive formation of plaques in CAD. The present investigation is aimed to study the possible association of Calcineurin encoding gene PPP3R1 (CnB 5I/5D) polymorphism in correlation with serum levels of calcineurin in coronary artery disease (CAD). A total of 300 angiographically documented CAD patients and 300 age, gender ethnicity matched healthy controls were recruited for the study. Serum Calcineurin levels were estimated by enzyme-linked immunosorbent assay (ELISA) and genotypes were determined based on PCR-RFLP. The CnB 5I/5D variation was found to be significantly associated with CAD (p < 0.03), correlated to elevated serum calcineurin levels encoded by (< 0.01) 5I/5D allele authenticated by Insilco analysis. Multiple logistic regression analysis also confirmed these findings [adjusted OR for DD genotype was 3.19 (95% CI 1.40–7.24) and p = 0.001]. The results suggest that 5-base pair deletion results in increased serum calcineurin levels and may trigger up regulation of calcineurin which mediates vascular inflammation and atherosclerosis in CAD.

ABSTRACT

Introduction: Total pancreatectomy (TP) markedly improves quality of life in children with chronic pancreatitis (CP), but results in brittle, insulinopenic diabetes. TP with IAT (TPIAT) may preserve insulin secretion. Minimal data are available regarding TPIAT in pediatric patients (Pts).

Methods: Between 2009-2016, TPIAT was performed in 13 Pts (7 boys) with median age 10.3 yrs (range 7-17 yrs). Six (46%) had a PRSS1 (protease, serine, 1) mutation, 2 (15.4%) had a CFTR (Cystic fibrosis transmembrane conductance regulator) mutation, 2 (15.4%) had combined CFTR/SPINK1 (serine protease inhibitor, Kazal-type, 1) mutations. All were euglycemic prior to TPIAT (normal fasting glucose and HbA1c; normal response to mixed meal tolerance test in a subset). Islet cells, isolated after TP, were infused in the portal vein. Pts were kept on an insulin infusion for (average) 6.8 days, then switched to MDI, with tight glycemic control.

Results: Six months after TPIAT, 5 Pts (38%) did not require insulin (HbA1c 5.5-6.1%), 3 Pts (23%) were on basal insulin only (0.03-0.35 U/Kg/day), with HbA1c of 5.5-6.7%, and 5 Pts (39%) required basal/bolus insulin therapy (0.5-1 U/Kg/day, median 0.6) with a HbA1c of 6.8-10.2%, median 7.6. Insulin requirements did not correlate with BMI-SDS (r=0.18) or number of islets/kg infused (r=-0.21). Pts with PRSS1 mutation had borderline lower (p=0.05, t-test) insulin requirements (0.1 U/kg/day) than Pts with CFTR mutation (0.46 U/kg/day). Ten Pts (77%) discontinued pain medication with complete pain resolution within 3 months. Complications including pyloric stenosis, intraabdominal adhesions, and gastroparesis occurred in 3 Pts; Spontaneous/exercise-induced hypoglycemia in 2 Pts.

Conclusions: TPIAT is an effective treatment for CP in children and adolescents. Within 6 months, it provided pain resolution in 77% and allowed good glycemic control with no insulin or low dose basal insulin in 61% of patients in this series.

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