•French tropical fruits are natural sources of vitamin C, carotenoids, polyphenols.•Passion fruit constitutes an abundant source of polyphenols.•Flavonoids, phenolic acids and piceatannol are ...detected in French tropical fruits.•Polyphenols from French tropical fruits exert free radical-scavenging activities.•Polyphenols from French tropical fruits protect cells against oxidative stress.
Much attention is paid to the beneficial action of fruits against obesity-related oxidative stress. This study evaluated nutritional and antioxidant properties of banana, litchi, mango, papaya, passion fruit and pineapple from Réunion French Island. Results showed that total amounts of carbohydrates, vitamin C and carotenoids were 7.7–67.3g glucose equivalent, 4.7–84.9mg ascorbic acid equivalent and 26.6–3829.2μg β-carotene equivalent/100g fresh weight, respectively. Polyphenols were detected as the most abundant antioxidants (33.0–286.6mg gallic acid equivalent/100g fresh weight) with the highest content from passion fruit. UPLC-MS analysis led to identify epigallocatechin and quercetin derivatives from banana and litchi, ferulic, sinapic, syringic and gallic acids from pineapple and mango, and piceatannol from passion fruit. Polyphenol-rich extracts protected red blood cells and preadipose cells against oxidative stress. Altogether, these findings highlight nutritional benefits of French tropical fruits and their possible interest to improve antioxidant capacities of the body during obesity.
Gut microbiota LPS contributes to obesity-related chronic inflammation and oxidative stress, promoting insulin resistance. Periodontal disease also represents a risk factor for type 2 diabetes and is ...associated with obesity. This study compared the effect of LPS from P. gingivalis periodontopathogen and E. coli enterobacteria on inflammatory adipokine secretion and redox status of 3T3-L1 adipocytes. We found that both LPS activated TLR2- and TLR4-mediated signaling pathways involving MyD88 adaptor and NFκB transcription factor, leading to an increased secretion of leptin, resistin, IL-6 and MCP-1. These effects were partly blocked by inhibitors targeting p38 MAPK, JNK and ERK. Moreover, P. gingivalis LPS reduced adiponectin secretion. Both LPS also enhanced ROS production and the expression of NOX2, NOX4 and iNOS genes. P. gingivalis LPS altered catalase gene expression. Collectively, these results showed that LPS of periodontal bacteria induced pro-inflammatory adipokine secretory profile and oxidative stress in adipocytes which may participate to obesity-related insulin resistance.
•Periodontal LPS induces the secretion of pro-inflammatory adipokines.•Periodontal LPS decreases adiponectin secretion.•Periodontal LPS effect is mediated through TLR2 and TLR4-dependent pathways.•Periodontal LPS action involves p38 MAPK, JNK and ERK.•Periodontal LPS promotes oxidative stress by altering redox enzyme production.
Scope
Hyperglycemia alters cerebral endothelial cell and blood‐brain barrier functions, aggravating cerebrovascular complications such as stroke during diabetes. Redox and inflammatory changes play a ...causal role. This study evaluates polyphenol protective effects in cerebral endothelial cells and a mouse stroke model during hyperglycemia.
Methods and results
Murine bEnd.3 cerebral endothelial cells and a mouse stroke model are exposed to a characterized, polyphenol‐rich extract of Antirhea borbonica or its predominant constituent caffeic acid, during hyperglycemia. Polyphenol effects on redox, inflammatory and vasoactive markers, infarct volume, and hemorrhagic transformation are determined. In vitro, polyphenols improve reactive oxygen species levels, Cu/Zn superoxide dismutase activity, and both NAPDH oxidase 4 and nuclear factor erythroid 2‐related factor 2 (Nrf2) gene expression deregulated by high glucose. Polyphenols reduce Nrf2 nuclear translocation and counteract nuclear factor‐ĸappa B activation, interleukin‐6 secretion, and the altered production of vasoactive markers mediated by high glucose. In vivo, polyphenols reduce cerebral infarct volume and hemorrhagic transformation aggravated by hyperglycemia. Polyphenols attenuate redox changes, increase vascular endothelial‐Cadherin production, and decrease neuro‐inflammation in the infarcted hemisphere.
Conclusion
Polyphenols protect against hyperglycemia‐mediated alterations in cerebral endothelial cells and a mouse stroke model. It is relevant to assess polyphenol benefits to improve cerebrovascular damages during diabetes.
Hyperglycemia induces oxidative stress and inflammation, promoting cerebral endothelial dysfunction and vascular disorders such as stroke. This study evaluates the protective effects of Antirhea borbonica polyphenols and caffeic acid in cerebral endothelial cells and a mouse stroke model exposed to hyperglycemic condition. Data show that polyphenols improve redox, pro‐inflammatory, and vasoactive markers, and decrease cerebrovascular damages aggravated by hyperglycemia.
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In obesity, gut microbiota LPS may translocate into the blood stream and then contribute to adipose tissue inflammation and oxidative stress, leading to insulin resistance. A causal ...link between periodontal infection, obesity and type 2 diabetes has also been suggested. We evaluated the ability of polyphenols from Antirhea borbonica medicinal plant to improve the inflammatory and redox status of 3T3-L1 adipocytes exposed to LPS of Porphyromonas gingivalis periodontopathogen or Escherichia coli enterobacteria. Our results show that LPS enhanced the production of Toll-like receptor-dependent MyD88 and NFκB signaling factors as well as IL-6, MCP-1, PAI-1 and resistin. Plant polyphenols reduced LPS pro-inflammatory action. Concomitantly, polyphenols increased the production of adiponectin and PPARγ, known as key anti-inflammatory and insulin-sensitizing mediators. Moreover, both LPS increased intracellular ROS levels and the expression of genes encoding ROS-producing enzymes including NOX2, NOX4 and iNOS. Plant polyphenols reversed these effects and up-regulated MnSOD and catalase antioxidant enzyme gene expression. Noticeably, preconditioning of cells with caffeic acid, chlorogenic acid or kaempferol identified among A. borbonica major polyphenols, led to similar protective properties. Altogether, these findings demonstrate the anti-inflammatory and antioxidant effects of A. borbonica polyphenols on adipocytes, in response to P. gingivalis or E. coli LPS. It will be of major interest to assess A. borbonica polyphenol benefits against obesity-related metabolic disorders such as insulin resistance in vivo.
Hyperglycemia alters the function of cerebral endothelial cells from the blood-brain barrier, increasing the risk of cerebrovascular complications during diabetes. This study evaluated the protective ...effect of polyphenols on inflammatory and permeability markers on bEnd3 cerebral endothelial cells exposed to high glucose concentration. Results show that hyperglycemic condition increased nuclear factor kappa B (NFκB) activity, deregulated the expression of interleukin-1 beta (
), interleukin-6 (
), tumor necrosis factor-alpha (
), cyclooxygenase-2 (
), inducible nitric oxide synthase (
), interleukin-10 (
) and endothelial-leukocyte adhesion molecule (
) genes, raised MCP-1 secretion and elevated monocyte adhesion and transendothelial migration. High glucose decreased occludin, claudin-5, zona occludens-1 (ZO-1) and zona occludens-2 (ZO-2) tight junctions production and altered the endothelial permeability. Characterized polyphenolic extracts from the French medicinal plants
,
,
and
, and their major polyphenols quercetin, caffeic, chlorogenic and gallic acids limited the pro-inflammatory and permeability alterations caused by high glucose. Peroxisome proliferator-activated receptor gamma (PPARγ) agonist also attenuated these damages while PPARγ antagonist aggravated them, suggesting PPARγ protective action. Interestingly, polyphenols improved
gene expression lowered by high glucose. Moreover, polyphenols were detected at the intracellular level or membrane-bound to cells, with evidence for breast cancer resistance protein (BCRP) efflux transporter role. Altogether, these findings emphasize the ability of polyphenols to protect cerebral endothelial cells in hyperglycemic condition and their relevance for pharmacological strategies aiming to limit cerebrovascular disorders in diabetes.
Stroke in context of type 2 diabetes (T2D) is associated with a poorer outcome than in non-diabetic conditions. We aimed at creating a new reproducible mouse model of stroke in impaired glucose ...tolerance conditions induced by high-fat diet.
Adult C57BL6 mice were fed for 2 months with either normal diet (ND) or high-fat diet (HFD). We used a model of Middle Cerebral Artery Occlusion (MCAO) for 90 min. Oral Glucose Tolerance Test (OGTT) and Insulin Tolerance Test (ITT) were used to assess pre-diabetic status. Brain infarct volume, hemorrhagic transformation (HT) as well as systemic and cerebral inflammatory markers were evaluated.
HFD was associated with an increased body weight and glycemia following OGTT. The HFD group presented a significant increase in brain infarct volume (38.7 (IQR 30-46.7%) vs. 28.45 (IQR 21-30%);
= 0.016) and HT (HFD: 2 (IQR 1-5) vs. ND: 0 (IQR 0-1);
= 0.012) and higher levels of IL-6 and MCP-1 in infarcted hemisphere compared to the ND group.
Two months of HFD in adult mice were sufficient to alter the lipid profile and the control of hyperglycemia. These metabolic perturbations were significantly associated with increased infarct volume and hemorrhagic complications.
Type 2 diabetes is associated with major vascular dysfunctions, leading to clinical complications such as stroke. It is also known that hyperglycemia dysregulates blood-brain barrier homeostasis by ...altering cerebral endothelial cell function. Oxidative stress may play a critical role. The aim of this study was to evaluate the effect of hyperglycemia and insulin on the production of redox, inflammatory and vasoactive markers by cerebral endothelial cells. Murine bEnd.3 cerebral endothelial cells were exposed to hyperglycemia in the presence or not of insulin. Results show that hyperglycemia altered the expression of genes encoding the ROS-producing enzyme Nox4, antioxidant enzymes Cu/ZnSOD, catalase and HO-1 as well as Cu/ZnSOD, MnSOD and catalase enzymatic activities, leading to a time-dependent modulation of ROS levels. Cell preconditioning with inhibitors targeting PI3K, JNK, ERK, p38 MAPK or NFĸB signaling molecules partly blocked hyperglycemia-induced oxidative stress. Conversely, AMPK inhibitor exacerbated ROS production, suggesting a protective role of AMPK on the antioxidant defense system. Hyperglycemia also modulated both gene expression and nuclear translocation of the redox-sensitive transcription factor Nrf2. Moreover, hyperglycemia caused a pro-inflammatory response by activating NFĸB-AP-1 pathway and IL-6 secretion. Hyperglycemia reduced eNOS gene expression and NO levels, while increasing ET-1 gene expression. Importantly, insulin counteracted all the deleterious effects of hyperglycemia. Collectively, these results demonstrate that hyperglycemia dysregulated redox, inflammatory and vasoactive markers in cerebral endothelial cells. Insulin exerted a protective action against hyperglycemia effects. Thus, it will be of high interest to evaluate the benefits of antioxidant and anti-inflammatory strategies against hyperglycemia-mediated vascular complications in type 2 diabetes.
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•Hyperglycemia promotes oxidative stress in cerebral endothelial cells.•Hyperglycemia alters redox enzyme genes expression, SOD and catalase activities.•Hyperglycemia action involves PI3K, JNK, ERK, p38 MAPK, NFĸB and AMPK mediators.•Hyperglycemia modulates Nrf2 nuclear translocation, IL-6 secretion and NO levels.•Insulin exerts antioxidant and anti-inflammatory roles against hyperglycemia action.
Adipokines are essential mediators produced by adipose tissue and exert multiple biological functions. In particular, adiponectin, leptin, resistin, IL-6, MCP-1 and PAI-1 play specific roles in the ...crosstalk between adipose tissue and other organs involved in metabolic, immune and vascular health. During obesity, adipokine imbalance occurs and leads to a low-grade pro-inflammatory status, promoting insulin resistance-related diabetes and its vascular complications. A causal link between obesity and gut microbiota dysbiosis has been demonstrated. The deregulation of gut bacteria communities characterizing this dysbiosis influences the synthesis of bacterial substances including lipopolysaccharides and specific metabolites, generated via the degradation of dietary components, such as short-chain fatty acids, trimethylamine metabolized into trimethylamine-oxide in the liver and indole derivatives. Emerging evidence suggests that these bacterial metabolites modulate signaling pathways involved in adipokine production and action. This review summarizes the current knowledge about the molecular links between gut bacteria-derived metabolites and adipokine imbalance in obesity, and emphasizes their roles in key pathological mechanisms related to oxidative stress, inflammation, insulin resistance and vascular disorder. Given this interaction between adipokines and bacterial metabolites, the review highlights their relevance (i) as complementary clinical biomarkers to better explore the metabolic, inflammatory and vascular complications during obesity and gut microbiota dysbiosis, and (ii) as targets for new antioxidant, anti-inflammatory and prebiotic triple action strategies.
Context: Cannabinoid CB1 receptor blockade decreases weight and hyperinsulinemia in obese animals and humans in a way greatly independent from food intake.
Objective: The objective of this study was ...to investigate the regulation and function of the endocannabinoid system in adipocytes and pancreatic β-cells.
Design, Setting, and Patients: Mouse 3T3-F442A adipocytes and rat insulinoma RIN-m5F β-cells, pancreas and fat from mice with diet-induced obesity, visceral and sc fat from patients with body mass index equal to or greater than 30 kg/m2, and serum from normoglycemic and type 2 diabetes patients were studied.
Main Outcome Measure: Endocannabinoid enzyme and adipocyte protein expression, and endocannabinoid and insulin levels were measured.
Results: Endocannabinoids are present in adipocytes with levels peaking before differentiation, and in RIN-m5F β-cells, where they are under the negative control of insulin. Chronic treatment of adipocytes with insulin is accompanied by permanently elevated endocannabinoid signaling, whereas culturing of RIN-m5F β-cells in high glucose transforms insulin down-regulation of endocannabinoid levels into up-regulation. Epididymal fat and pancreas from mice with diet-induced obesity contain higher endocannabinoid levels than lean mice. Patients with obesity or hyperglycemia caused by type 2 diabetes exhibit higher concentrations of endocannabinoids in visceral fat or serum, respectively, than the corresponding controls. CB1 receptor stimulation increases lipid droplets and decreases adiponectin expression in adipocytes, and it increases intracellular calcium and insulin release in RIN-m5F β-cells kept in high glucose.
Conclusions: Peripheral endocannabinoid overactivity might explain why CB1 blockers cause weight-loss independent reduction of lipogenesis, of hypoadiponectinemia, and of hyperinsulinemia in obese animals and humans.
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