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Morgane Bayle

Bio: Morgane Bayle is an academic researcher from University of Montpellier. The author has contributed to research in topics: Ghrelin & Secretagogue. The author has an hindex of 3, co-authored 4 publications receiving 30 citations.

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TL;DR: Animal and in vitro studies selected in this review highlight the direct action of polyphenols on pancreatic β-cells, stimulating insulin secretion through the activation of specific cellular targets and protecting these cells from damages mediated by oxidative stress and inflammation, both typically elevated in diabetes.
Abstract: Diabetes mellitus is a complex metabolic disorder and is considered a fast-growing global health problem. Type 2 diabetes (T2D) represents the majority of total diabetes prevalence and β-cell dysfunction has been described as a crucial point for this disease development and progression. To date, all of the common anti-hyperglycaemic drugs used for diabetes management cause undesirable side effects or problems with long-term efficacy or safety and the development of alternative approaches for the prevention as well as for the treatment of T2D might be a valuable solution to meet this rising demand. In this regards, numerous epidemiological studies indicate that exposure to certain polyphenol compounds is associated with the prevention of chronic diseases, including diabetes. Here, we review growing evidence suggesting that polyphenols can modulate the activity of various molecular targets, which are known to control β-cell function, involved in the development and the progression of this diabetes. The protective effects of polyphenols on β-cell function is reported with a particular focus on the mechanism of action behind polyphenol putative bioactivity. Animal and in vitro studies selected in this review, reporting about both flavonoid and non-flavonoid compounds, highlight the direct action of polyphenols on pancreatic β-cells, stimulating insulin secretion through the activation of specific cellular targets and protecting these cells from damages mediated by oxidative stress and inflammation, both typically elevated in diabetes. Some of the reviewed studies describe polyphenol effects comparable to those exerted by many drugs commonly used in diabetes treatment, and, in some occasions, synergistic polyphenol-drug interactions. Finally, future studies need to be addressed to the effects of specific polyphenol human and microbial metabolites, which are still poorly studied, in order to better define the preventive and therapeutic approach to contrast β-cell failure and diabetes progression.

19 citations

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TL;DR: This highly specific and sensitive liquid chromatography-electrospray ionization-tandem mass spectrometry method for the determination of urolithin C in rat plasma was used to analyze samples collected during preclinical pharmacokinetic studies in rats.

13 citations

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TL;DR: It is reported that urolithin C enhanced glucose‐induced extracellular signal‐regulated kinases 1/2 (ERK1/2) activation as shown by higher phosphorylation levels in INS‐1 β‐cells, indicating that the pharmacological action of urolithsin C on insulin secretion relies, in part, on its capacity to enhance glucose‐ induced ERK1 /2 activation.
Abstract: Polyphenols exert pharmacological actions through protein-mediated mechanisms and by modulating intracellular signalling pathways. We recently showed that a gut-microbial metabolite of ellagic acid named urolithin C is a glucose-dependent activator of insulin secretion acting by facilitating L-type Ca2+ channel opening and Ca2+ influx into pancreatic β-cells. However, it is still unknown whether urolithin C regulates key intracellular signalling proteins in β-cells. Here, we report that urolithin C enhanced glucose-induced extracellular signal-regulated kinases 1/2 (ERK1/2) activation as shown by higher phosphorylation levels in INS-1 β-cells. Interestingly, inhibition of ERK1/2 with two structurally distinct inhibitors led to a reduction in urolithin C effect on insulin secretion. Finally, we provide data to suggest that urolithin C-mediated ERK1/2 phosphorylation involved insulin signalling in INS-1 cells. Together, these data indicate that the pharmacological action of urolithin C on insulin secretion relies, in part, on its capacity to enhance glucose-induced ERK1/2 activation. Therefore, our study extends our understanding of the pharmacological action of urolithin C in β-cells. More generally, our findings revealed that urolithin C modulated the activation of key multifunctional intracellular signalling kinases which participate in the regulation of numerous biological processes.

4 citations

Journal ArticleDOI
TL;DR: In this paper, Liver-Expressed Antimicrobial Peptide 2 (LEAP2) was recognized as an endogenous G-protein coupled receptor (GPCR) ligand that blocks ghrelin-induced actions.
Abstract: Background The hormone ghrelin is the endogenous agonist of the G-protein coupled receptor (GPCR) termed growth-hormone secretagogue receptor (GHSR). Ghrelin inhibits glucose-stimulated insulin secretion by activating pancreatic GHSR. Recently, Liver-Expressed Antimicrobial Peptide 2 (LEAP2) was recognized as an endogenous GHSR ligand that blocks ghrelin-induced actions. Nonetheless, the effect of LEAP2 on glucose-stimulated insulin secretion from pancreatic islets is unknown. Objectives We aimed at exploring the activity of LEAP2 on glucose-stimulated insulin secretion. Methods Islets of Langerhans isolated from rat pancreas were exposed to glucose in the presence or in the absence of LEAP2 and ghrelin and then insulin secretion was assayed. Results LEAP2 did not modulate glucose-stimulated insulin secretion. However, LEAP2 blocked the insulinostatic action of ghrelin. Conclusion Our data show that LEAP2 behaves as an antagonist of pancreatic GHSR.

3 citations

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TL;DR: In this paper , a triazole-derived modulator of growth hormone secretagogue receptor (GHSR) is proposed to mitigate several pathological features associated with eating and metabolic disorders.

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TL;DR: Results from recent research have increased the interest in ellagic acid, both as a potential protective agent of the liver and skin and as a possible anticancer agent, due to the specific mechanisms affecting cell proliferation, apoptosis, DNA damage, and angiogenesis.
Abstract: Ellagic acid is a common metabolite present in many medicinal plants and vegetables. It is present either in free form or as part of more complex molecules (ellagitannins), which can be metabolized to liberate ellagic acid and several of its metabolites, including urolithins. While ellagic acidʼs antioxidant properties are doubtless responsible for many of its pharmacological activities, other mechanisms have also been implicated in its various effects, including its ability to reduce the lipidemic profile and lipid metabolism, alter pro-inflammatory mediators (tumor necrosis factor-α, interleukin-1β, interleukin-6), and decrease the activity of nuclear factor-κB while increasing nuclear factor erythroid 2-related factor 2 expression. These events play an important role in ellagic acidʼs anti-atherogenic, anti-inflammatory, and neuroprotective effects. Several of these activities, together with the effect of ellagic acid on insulin, glycogen, phosphatases, aldose reductase, sorbitol accumulation, advanced glycation end-product formation, and resistin secretion, may explain its effects on metabolic syndrome and diabetes. In addition, results from recent research have increased the interest in ellagic acid, both as a potential protective agent of the liver and skin and as a potential anticancer agent, due to the specific mechanisms affecting cell proliferation, apoptosis, DNA damage, and angiogenesis and its aforementioned anti-inflammatory properties. Taken together, these effects make ellagic acid a highly interesting compound that may contribute to different aspects of health; however, more studies are needed, especially on the compoundʼs pharmacokinetic profile. In this review, we selected papers published from 2005 to the present.

195 citations

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TL;DR: The utilization of microencapsulated polyphenols, instead of free compounds, can effectively alleviate the deficiencies of phenolic compounds, and this review provided valuable insight that may be useful for identifying trends in the commercialization ofmicroencapsulation -technological products or for identifying new research areas.
Abstract: Background Studies on and the application of polyphenolic compounds, have recently attracted great interest in the functional foods due to their potential health benefits to humans. However, the major disadvantage associated with phenolic compounds is their constrained bioavailability, mainly caused by its low aqueous solubility, poor stability and limited membrane permeability. Scope and approach The aim of this study is to give an overview of the microencapsulation technology to enhance bioavailability of phenolic compounds. Furthermore, the anti-diabetic effect of microencapsulated phenolic compounds and capability of them to produce new functional foods will be discussed. Key findings and conclusions The utilization of microencapsulated polyphenols, instead of free compounds, can effectively alleviate the deficiencies. This review provided valuable insight that may be useful for identifying trends in the commercialization of microencapsulation -technological products or for identifying new research areas. The results published to date confirm that the encapsulation promotes the protection of active compounds, enabling industrial applications of active packaging.

97 citations

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TL;DR: It is demonstrated that UA alleviates myocardial ischemia/reperfusion injury probably through PI3K/Akt pathway.

81 citations

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TL;DR: A broad-spectrum study covering all aspects of occurrence, detection and removal is required to meet the fundamental levels of knowledge on the effects of NSAIDs in all exposed environmental aspects and focuses on classifying the sources and entry points of residual NSAIDs.

53 citations

Journal ArticleDOI
TL;DR: The molecular mechanisms for 3 actions of (poly)phenols on oxidative processes where there is evidence in vivo from human intervention or animal studies are reviewed.
Abstract: The hypothesis that dietary (poly)phenols promote well-being by improving chronic disease-risk biomarkers, such as endothelial dysfunction, chronic inflammation and plasma uric acid, is the subject of intense current research, involving human interventions studies, animal models and in vitro mechanistic work. The original claim that benefits were due to the direct antioxidant properties of (poly)phenols has been mostly superseded by detailed mechanistic studies on specific molecular targets. Nevertheless, many proposed mechanisms in vivo and in vitro are due to modulation of oxidative processes, often involving binding to specific proteins and effects on cell signalling. We review the molecular mechanisms for 3 actions of (poly)phenols on oxidative processes where there is evidence in vivo from human intervention or animal studies. (1) Effects of (poly) phenols on pathways of chronic inflammation leading to prevention of some of the damaging effects associated with the metabolic syndrome. (2) Interaction of (poly)phenols with endothelial cells and smooth muscle cells, leading to effects on blood pressure and endothelial dysfunction, and consequent reduction in cardiovascular disease risk. (3) The inhibition of xanthine oxidoreductase leading to modulation of intracellular superoxide and plasma uric acid, a risk factor for developing type 2 diabetes.

52 citations