scholarly journals Select Polyphenol-Rich Berry Consumption to Defer or Deter Diabetes and Diabetes-Related Complications

Nutrients ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2538
Author(s):  
Ahsan Hameed ◽  
Mauro Galli ◽  
Edyta Adamska-Patruno ◽  
Adam Krętowski ◽  
Michal Ciborowski
Keyword(s):  
Oxidative Stress ◽  
Short Chain Fatty Acids ◽  
Clinical Findings ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Human Diet ◽  
Markers Of Oxidative Stress ◽  
Healthy Obese ◽  
Berry Extracts

Berries are considered “promising functional fruits” due to their distinct and ubiquitous therapeutic contents of anthocyanins, proanthocyanidins, phenolic acids, flavonoids, flavanols, alkaloids, polysaccharides, hydroxycinnamic, ellagic acid derivatives, and organic acids. These polyphenols are part of berries and the human diet, and evidence suggests that their intake is associated with a reduced risk or the reversal of metabolic pathophysiologies related to diabetes, obesity, oxidative stress, inflammation, and hypertension. This work reviewed and summarized both clinical and non-clinical findings that the consumption of berries, berry extracts, purified compounds, juices, jams, jellies, and other berry byproducts aided in the prevention and or otherwise management of type 2 diabetes mellitus (T2DM) and related complications. The integration of berries and berries-derived byproducts into high-carbohydrate (HCD) and high-fat (HFD) diets, also reversed/reduced the HCD/HFD-induced alterations in glucose metabolism-related pathways, and markers of oxidative stress, inflammation, and lipid oxidation in healthy/obese/diabetic subjects. The berry polyphenols also modulate the intestinal microflora ecology by opposing the diabetic and obesity rendered symbolic reduction of Bacteroidetes/Firmicutes ratio, intestinal mucosal barrier dysfunction-restoring bacteria, short-chain fatty acids, and organic acid producing microflora. All studies proposed a number of potential mechanisms of action of respective berry bioactive compounds, although further mechanistic and molecular studies are warranted. The metabolic profiling of each berry is also included to provide up-to-date information regarding the potential anti-oxidative/antidiabetic constituents of each berry.

scholarly journals Effect of liposome-encapsulated hemoglobin resuscitation on proteostasis in small intestinal epithelium after hemorrhagic shock

2016 ◽  
Vol 311 (1) ◽  
pp. G180-G191 ◽  
Author(s):  
Geeta Rao ◽  
Vivek R. Yadav ◽  
Shanjana Awasthi ◽  
Pamela R. Roberts ◽  
Vibhudutta Awasthi
Keyword(s):  
Oxidative Stress ◽  
Hemorrhagic Shock ◽  
Multiorgan Failure ◽  
Sprague Dawley ◽  
Barrier Dysfunction ◽  
Protective Mechanisms ◽  
Unfolded Protein ◽  
Sprague Dawley Rats ◽  
Markers Of Oxidative Stress ◽  
Protein Response

Gut barrier dysfunction is the major trigger for multiorgan failure associated with hemorrhagic shock (HS). Although the molecular mediators responsible for this dysfunction are unclear, oxidative stress-induced disruption of proteostasis contributes to the gut pathology in HS. The objective of this study was to investigate whether resuscitation with nanoparticulate liposome-encapsulated hemoglobin (LEH) is able to restore the gut proteostatic mechanisms. Sprague-Dawley rats were recruited in four groups: control, HS, HS+LEH, and HS+saline. HS was induced by withdrawing 45% blood, and isovolemic LEH or saline was administered after 15 min of shock. The rats were euthanized at 6 h to collect plasma and ileum for measurement of the markers of oxidative stress, unfolded protein response (UPR), proteasome function, and autophagy. HS significantly increased the protein and lipid oxidation, trypsin-like proteasome activity, and plasma levels of IFNγ. These effects were prevented by LEH resuscitation. However, saline was not able to reduce protein oxidation and plasma IFNγ in hemorrhaged rats. Saline resuscitation also suppressed the markers of UPR and autophagy below the basal levels; the HS or LEH groups showed no effect on the UPR and autophagy. Histological analysis showed that LEH resuscitation significantly increased the villus height and thickness of the submucosal and muscularis layers compared with the HS and saline groups. Overall, the results showed that LEH resuscitation was effective in normalizing the indicators of proteostasis stress in ileal tissue. On the other hand, saline-resuscitated animals showed a decoupling of oxidative stress and cellular protective mechanisms.

scholarly journals Effects of α-Tocopherol and Mixed Tocopherol Supplementation on Markers of Oxidative Stress and Inflammation in Type 2 Diabetes

2007 ◽  
Vol 53 (3) ◽  
pp. 511-519 ◽  
Author(s):  
Jason HY Wu ◽  
Natalie C Ward ◽  
Adeline P Indrawan ◽  
Coral-Ann Almeida ◽  
Jonathan M Hodgson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Type 2 Diabetes ◽  
Vitamin E ◽  
Antioxidant Enzyme ◽  
Enzyme Activities ◽  
Ex Vivo ◽  
Controlled Trial ◽  
Antioxidant Enzyme Activities ◽  
Markers Of Oxidative Stress

Abstract Background: Vitamin E isomers may protect against atherosclerosis. The aim of this study was to compare the effects of supplementation with either α-tocopherol (αT) or mixed tocopherols rich in γ-tocopherol (γT) on markers of oxidative stress and inflammation in patients with type 2 diabetes. Methods: In a double-blind, placebo-controlled trial, 55 patients with type 2 diabetes were randomly assigned to receive (500 mg/day) (a) αT, (b) mixed tocopherols, or (c) placebo for 6 weeks. Cellular tocopherols, plasma and urine F2-isoprostanes, erythrocyte antioxidant enzyme activities, plasma inflammatory markers, and ex vivo assessment of eicosanoid synthesis were analyzed pre- and postsupplementation. Results: Neutrophil αT and γT increased (both P <0.001) with mixed tocopherol supplementation, whereas αT (P <0.001) increased and γT decreased (P <0.005) after αT supplementation. Both αT and mixed tocopherol supplementation resulted in reduced plasma F2-isoprostanes (P <0.001 and P = 0.001, respectively) but did not affect 24-h urinary F2-isoprostanes or erythrocyte antioxidant enzyme activities. Neither αT nor mixed tocopherol supplementation affected plasma C-reactive protein, interleukin 6, tumor necrosis factor-α, or monocyte chemoattractant protein-1. Stimulated neutrophil leukotriene B4 production decreased significantly in the mixed tocopherol group (P = 0.02) but not in the αT group (P = 0.15). Conclusions: The ability of tocopherols to reduce systemic oxidative stress suggests potential benefits of vitamin E supplementation in patients with type 2 diabetes. In populations with well-controlled type 2 diabetes, supplementation with either αT or mixed tocopherols rich in γT is unlikely to confer further benefits in reducing inflammation.

scholarly journals N-Acetyl Serotonin Alleviates Oxidative Damage by Activating Nuclear Factor Erythroid 2-Related Factor 2 Signaling in Porcine Enterocytes

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 303
Author(s):  
Haiwei Liang ◽  
Ning Liu ◽  
Renjie Wang ◽  
Yunchang Zhang ◽  
Jingqing Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gastrointestinal Diseases ◽  
Mucosal Barrier ◽  
Related Factor ◽  
Protective Effects ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Downstream Target ◽  
Underlying Mechanisms ◽  
And Function

Apoptosis of intestinal epithelial cells following oxidative stress is a major cause of mucosal barrier dysfunction and is associated with the pathogenesis of various gastrointestinal diseases. Although L-tryptophan (Trp) is known to improve intestinal integrity and function, a beneficial effect of N-acetyl serotonin (NAS), a metabolite of Trp, on the apoptosis of enterocytes and the underlying mechanisms remain largely unknown. In the present study, we showed that porcine enterocytes treated with 4-hydroxy-2-nonenal (4-HNE), a metabolite of lipid peroxidation, led to upregulation of apoptotic proteins, including Bax and cleaved caspase-3, and reduction of tight junction proteins. These effects of 4-HNE were significantly abrogated by NAS. In addition, NAS reduced ROS accumulation while increasing the intracellular concentration of glutathione (GSH), and the abundance of the Nrf2 protein in the nucleus and its downstream target proteins. Importantly, these protective effects of NAS were abrogated by Atra, an inhibitor of Nrf2, indicating a dependence on Nrf2 signaling. Taken together, we demonstrated that NAS attenuated oxidative stress-induced cellular injury in porcine enterocytes by regulating Nrf2 signaling. These findings provide new insights into a functional role of NAS in maintaining intestinal homeostasis.

scholarly journals Markers of Oxidative Stress during Diabetes Mellitus

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Brahm Kumar Tiwari ◽  
Kanti Bhooshan Pandey ◽  
A. B. Abidi ◽  
Syed Ibrahim Rizvi
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Large Body ◽  
Vascular Diseases ◽  
Peripheral Vascular ◽  
Markers Of Oxidative Stress ◽  
Prevalence Of Diabetes Mellitus ◽  
Biomarkers Of Oxidative Stress

The prevalence of diabetes mellitus is rising all over the world. Uncontrolled state of hyperglycemia due to defects in insulin secretion/action leads to a variety of complications including peripheral vascular diseases, nephropathy, neuropathy, retinopathy, morbidity, and/or mortality. Large body of evidence suggests major role of reactive oxygen species/oxidative stress in development and progression of diabetic complications. In the present paper, we have discussed the recent researches on the biomarkers of oxidative stress during type 2 diabetes mellitus.

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