Cryoprotective role of vacuum infused inulin on the quality of artichoke: Interactive effects of freezing, thawing and storage period.

Freezing of artichoke is a promising alternative to storing it in brine and canning. The perishable vegetable was vacuum infused with inulin to improve freezing tolerance. Artichokes with and without inulin were frozen by static, air blast and individual quick freezing (IQF) methods and thawed by microwave, 25 °C and 4 °C temperature levels at each month of 6-months storage. Process conditions were evaluated by multivariate analysis of variance (MANOVA) and were found significant on the quality parameters. Inulin infusion better conserved the aw, color, texture, ascorbic acid and overall integrity of artichokes during frozen storage. Inulin incorporation and IQF showed mutual positive effect on drip loss. Polyphenol oxidase (PPO) activity values fitted to 2nd order kinetic and the highest residuals were determined in static freezing. PPO showed alleviating effect on total phenolic content. Vacuum impregnation caused a color difference prior to freezing, but was found effective for maintaining color during storage. As a result, the use of quick freezing techniques together with the addition of cryoprotectant was effective in the preservation of artichoke quality attributes during frozen storage.

Functionality Enhancement of Pea Protein Powder via High-Intensity Ultrasound: Screening in-vitro Digestion, o/w Emulsion Properties and Testing in Gluten-Free Bread.

Structural modification of protein prior to food application is an emergent approach to improve functionalization. The effectiveness of high-power ultrasound at varying amplitudes (0-100%) on the properties of pea protein powder was investigated in this study. The resulting modification was also tested with model gluten-free bread formulation and by screening the emulsion properties within vegetable oil. The 50% and beyond amplitude levels had significant impact on protein solubility, viscosity, Fourier Transform Infrared (FTIR) spectra, emulsion activity and stability. Foaming capacity and stability were enhanced with 75 and 100% amplitudes while the 25% amplitude exhibited the highest absolute zeta-potential. There was a concomitant increase in ultrasound amplitude and oil-binding capacity (2.83-6.43 g/g) where the water-holding capacity gradually decreased (5.78-3.61 g/g) with the increase in ultrasound power. The increase in ultrasound power led to decrease in L* values but progressively increased the total color difference (ΔE). Sonication (50% amplitude) also promoted the in-vitro digestibility of proteins by 22% as compared to the untreated sample. Scanning electron microscopy (SEM) fairly depictured the structural modification and FTIR spectra clearly demonstrated conformational changes in protein powders. The fortification with restructured pea protein powder significantly affected the volume and adhesiveness of glutenfree bread.

Exendin-4 protects endothelial cells from lipoapoptosis by PKA, PI3K, eNOS, p38 MAPK, and JNK pathways.

Experimental studies have indicated that endothelial cells play an important role in maintaining vascular homeostasis. We previously reported that human coronary artery endothelial cells (HCAECs) express the glucagon-like peptide 1 (GLP1) receptor and that the stable GLP1 mimetic exendin-4 is able to activate the receptor, leading to increased cell proliferation. Here, we have studied the effect of exendin-4 and native GLP1 (7-36) on lipoapoptosis and its underlying mechanisms in HCAECs. Apoptosis was assessed by DNA fragmentation and caspase-3 activation, after incubating cells with palmitate. Nitric oxide (NO) and reactive oxidative species (ROS) were analyzed. GLP1 receptor activation, PKA-, PI3K/Akt-, eNOS-, p38 MAPK-, and JNK-dependent pathways, and genetic silencing of transfection of eNOS were also studied. Palmitate-induced apoptosis stimulated cells to release NO and ROS, concomitant with upregulation of eNOS, which required activation of p38 MAPK and JNK. Exendin-4 restored the imbalance between NO and ROS production in which ROS production decreased and NO production was further augmented. Incubation with exendin-4 and GLP1 (7-36) protected HCAECs against lipoapoptosis, an effect that was blocked by PKA, PI3K/Akt, eNOS, p38 MAPK, and JNK inhibitors. Genetic silencing of eNOS also abolished the anti-apoptotic effect afforded by exendin-4. Our results support the notion that GLP1 receptor agonists restore eNOS-induced ROS production due to lipotoxicity and that such agonists protect against lipoapoptosis through PKA-PI3K/Akt-eNOS-p38 MAPK-JNK-dependent pathways via a GLP1 receptor-dependent mechanism.

Exendin-4 restores glucolipotoxicity-induced gene expression in human coronary artery endothelial cells.

Exendin-4, a stable GLP-1 receptor agonist, has been shown to stimulate insulin secretion. It has also been shown to exert beneficial effects on endothelial function that are independent of its glycemic effects. The molecular mechanisms underlying the protective actions of exendin-4 against diabetic glucolipotoxicity in endothelial cells largely remain elusive. We have investigated the long-term in vitro effect of palmitate or high glucose (simulating the diabetic milieu) and the role of exendin-4 on gene expression in human coronary artery endothelial cells. Gene expression profiling in combination with Western blotting revealed that exendin-4 regulates expression of a number of genes involved in angiogenesis, inflammation and thrombogenesis under glucolipotoxic conditions. Our results indicate that exendin-4 may improve endothelial cell function in diabetes through regulating expression of the genes, whose expression was disrupted by glucolipotoxicity. As endothelial dysfunction appears to be an early indicator of vascular damage, and predicts both progression of atherosclerosis and incidence of cardiovascular events, exendin-4 and possibly other incretin-based strategies may confer additional cardiovascular benefit beyond improved glycemic control.

Effects of some anti-diabetic and cardioprotective agents on proliferation and apoptosis of human coronary artery endothelial cells.

BACKGROUND: The leading cause of death for patients suffering from diabetes is macrovascular disease. Endothelial dysfunction is often observed in type 2 diabetic patients and it is considered to be an important early event in the pathogenesis of atherogenesis and cardiovascular disease. Many drugs are clinically applied to treat diabetic patients. However, little is known whether these agents directly interfere with endothelial cell proliferation and apoptosis. This study therefore aimed to investigate how anti-diabetic and cardioprotective agents affect human coronary artery endothelial cells (HCAECs). METHODS: The effect of anti-diabetic and cardioprotective agents on HCAEC viability, proliferation and apoptosis was studied. Viability was assessed using Trypan blue exclusion; proliferation in 5 mM and 11 mM of glucose was analyzed using [3H]thymidine incorporation. Lipoapoptosis of the cells was investigated by determining caspase-3 activity and the subsequent DNA fragmentation after incubation with the free fatty acid palmitate, mimicking diabetic lipotoxicity. RESULTS: Our data show that insulin, metformin, BLX-1002, and rosuvastatin improved HCAEC viability and they could also significantly increase cell proliferation in low glucose. The proliferative effect of insulin and BLX-1002 was also evident at 11 mM of glucose. In addition, insulin, metformin, BLX-1002, pioglitazone, and candesartan significantly decreased the caspase-3 activity and the subsequent DNA fragmentation evoked by palmitate, suggesting a protective effect of the drugs against lipoapoptosis. CONCLUSION: Our results suggest that the anti-diabetic and cardioprotective agents mentioned above have direct and beneficial effects on endothelial cell viability, regeneration and apoptosis. This may add yet another valuable property to their therapeutic effect, increasing their clinical utility in type 2 diabetic patients in whom endothelial dysfunction is a prominent feature that adversely affect their survival.

Endothelial dysfunction induced by triglycerides is not restored by exenatide in rat conduit arteries ex vivo.

Exenatide (synthetic exendin-4) is a stable analogue of glucagon-like peptide 1 (GLP-1) and has recently been approved for clinical use against type 2 diabetes. Exenatide is believed to exert its effects via the GLP-1 receptor with almost the same potency as GLP-1 in terms of lowering blood glucose. Short term exenatide treatment normalizes the altered vascular tone in type 2 diabetic rats, probably due to the reduction in glycemia. The aim of this study was to investigate whether exenatide directly protects against triglyceride-induced endothelial dysfunction in rat femoral arterial rings ex vivo. Short term pre-incubation with Intralipid (0.5 and 2%) was found to dose-dependently induce endothelial dysfunction, in that it elicited a significant reduction in ACh-induced vasorelaxation by 29% and 35%, respectively. Paradoxically, this occurred with a concomitant increase in endothelial nitric oxide synthase (eNOS) activity. No such reduction in vasorelaxation by Intralipid was seen in response to the NO donor sodium nitroprusside (SNP), revealing an endothelium-dependent vascular dysfunction by Intralipid. However, exenatide did not protect against Intralipid-induced endothelial dysfunction. More surprisingly, the maximum vasorelaxation induced by exenatide (without Intralipid was only 3+/-2%, compared to the 23+/-4%, 38+/-4%, 79+/-3% and 97+/-4% relaxations induced by GLP-1, GLP-1 (9-36), ACh and SNP, respectively. This unexpected finding prompted us to ascertain that the exenatide preparation was biologically active, and both exenatide (10(-11) mol/l) and GLP-1 (10(-9) mol/l) significantly increased insulin secretion in pancreatic beta-cells from ob/ob mice in vitro. In conclusion, exenatide could neither confer any acute protective effects against triglyceride-induced endothelial dysfunction nor exert any significant vasorelaxant actions in this model of rat conduit arteries ex vivo.