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3. Glycomacropeptide as an Efficient Agent to Fight Pathophysiological Mechanisms of Metabolic Syndrome

Author

Sauvé, Mathilde Foisy, primary, Feldman, Francis, additional, Sané, Alain Théophile, additional, Koudoufio, Mireille, additional, Patey, Natalie, additional, Spahis, Schohraya, additional, Butcher, James, additional, Duan, Haonan, additional, Figeys, Daniel, additional, Marcil, Valérie, additional, Stintzi, Alain, additional, and Levy, Emile, additional

Published
2024
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4. Unraveling Chylomicron Retention Disease Enhances Insight into SAR1B GTPase Functions and Mechanisms of Actions, While Shedding Light of Intracellular Chylomicron Trafficking.

Author

Levy, Emile, Fallet-Bianco, Catherine, Auclair, Nickolas, Patey, Natalie, Marcil, Valérie, Sané, Alain Théophile, and Spahis, Schohraya

Subjects
FAT-soluble vitamins, HUMAN abnormalities, PATHOLOGY, CONGENITAL disorders, GUANOSINE triphosphatase, COAT proteins (Viruses)
Abstract

Over the past three decades, significant efforts have been focused on unraveling congenital intestinal disorders that disrupt the absorption of dietary lipids and fat-soluble vitamins. The primary goal has been to gain deeper insights into intra-enterocyte sites, molecular steps, and crucial proteins/regulatory pathways involved, while simultaneously identifying novel therapeutic targets and diagnostic tools. This research not only delves into specific and rare malabsorptive conditions, such as chylomicron retention disease (CRD), but also contributes to our understanding of normal physiology through the utilization of cutting-edge cellular and animal models alongside advanced research methodologies. This review elucidates how modern techniques have facilitated the decoding of CRD gene defects, the identification of dysfunctional cellular processes, disease regulatory mechanisms, and the essential role of coat protein complex II-coated vesicles and cargo receptors in chylomicron trafficking and endoplasmic reticulum (ER) exit sites. Moreover, experimental approaches have shed light on the multifaceted functions of SAR1B GTPase, wherein loss-of-function mutations not only predispose individuals to CRD but also exacerbate oxidative stress, inflammation, and ER stress, potentially contributing to clinical complications associated with CRD. In addition to dissecting the primary disease pathology, genetically modified animal models have emerged as invaluable assets in exploring various ancillary aspects, including responses to environmental challenges such as dietary alterations, gender-specific disparities in disease onset and progression, and embryonic lethality or developmental abnormalities. In summary, this comprehensive review provides an in-depth and contemporary analysis of CRD, offering a meticulous examination of the CRD current landscape by synthesizing the latest research findings and advancements in the field. [ABSTRACT FROM AUTHOR]

Published
2024
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10. Cranberry Proanthocyanidins as a Therapeutic Strategy to Curb Metabolic Syndrome and Fatty Liver-Associated Disorders

Author

Feldman, Francis, primary, Koudoufio, Mireille, additional, El-Jalbout, Ramy, additional, Sauvé, Mathilde Foisy, additional, Ahmarani, Lena, additional, Sané, Alain Théophile, additional, Ould-Chikh, Nour-El-Houda, additional, N’Timbane, Thierry, additional, Patey, Natalie, additional, Desjardins, Yves, additional, Stintzi, Alain, additional, Spahis, Schohraya, additional, and Levy, Emile, additional

Published
2022
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13. Specialized Pro-Resolving Mediators Derived from N-3 Polyunsaturated Fatty Acids: Role in Metabolic Syndrome and Related Complications

Author

Dubé, Laurent, primary, Spahis, Schohraya, additional, Lachaîne, Karelle, additional, Lemieux, Andreanne, additional, Monhem, Hanine, additional, Poulin, Sarah-Maude, additional, Randoll, Carolane, additional, Travaillaud, Eva, additional, Ould-Chikh, Nour-El-Houda, additional, Marcil, Valérie, additional, Delvin, Edgard, additional, and Levy, Emile, additional

Published
2022
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14. Cranberry Proanthocyanidins as a Therapeutic Strategy to Curb Metabolic Syndrome and Fatty Liver-Associated Disorders.

Author

Feldman, Francis, Koudoufio, Mireille, El-Jalbout, Ramy, Sauvé, Mathilde Foisy, Ahmarani, Lena, Sané, Alain Théophile, Ould-Chikh, Nour-El-Houda, N'Timbane, Thierry, Patey, Natalie, Desjardins, Yves, Stintzi, Alain, Spahis, Schohraya, and Levy, Emile

Subjects
METABOLIC syndrome, PROANTHOCYANIDINS, INSULIN resistance, TYPE 2 diabetes, FATTY liver, FISH oils
Abstract

While the prevalence of metabolic syndrome (MetS) is steadily increasing worldwide, no optimal pharmacotherapy is readily available to address its multifaceted risk factors and halt its complications. This growing challenge mandates the development of other future curative directions. The purpose of the present study is to investigate the efficacy of cranberry proanthocyanidins (PACs) in improving MetS pathological conditions and liver complications; C57BL/6J mice were fed either a standard chow or a high fat/high sucrose (HFHS) diet with and without PACs (200 mg/kg), delivered by daily gavage for 12 weeks. Our results show that PACs lowered HFHS-induced obesity, insulin resistance, and hyperlipidemia. In conjunction, PACs lessened circulatory markers of oxidative stress (OxS) and inflammation. Similarly, the anti-oxidative and anti-inflammatory capacities of PACs were noted in the liver in association with improved hepatic steatosis. Inhibition of lipogenesis and stimulation of beta-oxidation could account for PACs-mediated decline of fatty liver as evidenced not only by the expression of rate-limiting enzymes but also by the status of AMPKα (the key sensor of cellular energy) and the powerful transcription factors (PPARα, PGC1α, SREBP1c, ChREBP). Likewise, treatment with PACs resulted in the downregulation of critical enzymes of liver gluconeogenesis, a process contributing to increased rates of glucose production in type 2 diabetes. Our findings demonstrate that PACs prevented obesity and improved insulin resistance likely via suppression of OxS and inflammation while diminishing hyperlipidemia and fatty liver disease, as clear evidence for their strength of fighting the cluster of MetS abnormalities. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Role of the apical and basolateral domains of the enterocyte in the regulation of cholesterol transport by a high glucose concentration

Author

Grenier, Emilie, Mailhot, Genevieve, Dion, Danielle, Ravid, Zaava, Spahis, Schohraya, Bendayan, Moise, and Levy, Emile

Subjects
Cell research, Cholesterol metabolism -- Research, Glucose metabolism -- Research, Biological sciences
Abstract

We have recently shown that a high glucose (HG) concentration raised intestinal cholesterol (CHOL) transport and metabolism in intestinal epithelial cells. The objective of the present work is to determine whether the stimulus for increased CHOL absorption by glucose originates from the apical site (corresponding to the intestinal lumen) or from the basolateral site (related to blood circulation). We tackled this issue by using differentiated Caco-2/15 cells. Only basolateral medium, supplemented with 25 mmol/L glucose, stimulated [[sup.14]C]-CHOL uptake via the up-regulation of the critical CHOL transporter NPC1L1 protein, as confirmed by its specific ezetimibe inhibitor that abolished the rise in glucose-mediated CHOL capture. No significant changes were noted in SR-BI and CD36. Elevated CHOL uptake was associated with an increase in the transcription factors SREBP-2, LXR-β, and ChREBP, along with a fall in RXR-α. Interestingly, although the HG concentration in the apical medium caused modest changes in CHOL processing, its impact was synergetic with that of the basolateral medium. Our results suggest that HG concentration influences positively intestinal CHOL uptake when present in the basolateral medium. In addition, excessive consumption of diets containing high levels of carbohydrates may strengthen intestinal CHOL uptake in metabolic syndrome, thereby contributing to elevated levels of circulating CHOL and, consequently, the risk of developing type 2 diabetes and cardiovascular disease. Key words: cholesterol absorption, cholesterol transporters, cholesterol synthesis, transcription factors, glucose. Nous avons recemment montre qu'une concentration elevee de glucose (HG) accroit le transport et le metabolisme du cholesterol dans les cellules epitheliales intestinales. L'objectif du present travail est de determiner si le stimulus derriere l'augmentation de l'absorption de cholesterol, induit par le glucose, provient du site apical (correspondant a la lumiere intestinale) ou du site basolateral (relie a la circulation sanguine). Nous avons aborde ce probleme a l'aide de cellules Caco-2/15 differenciees cultivees sur des filtres Transwell. Seul le milieu basolateral, supplemente avec 25 mmol/L de glucose stimule la captation de [[sup.14]C]-cholesterol en regulant a la hausse NPC1L1, le transporteur cle de cholesterol. La confirmation a ete obtenue grace a l'utilisation de l'ezetimibe, son inhibiteur specifique, qui abolit l'augmentation de captation du cholesterol provoquee par le glucose. Aucun changement significatif des autres transporteurs de cholesterol SR- BI et CD36 n'a ete note. La captation accrue de cholesterol est associee a la fois a une stimulation des facteurs de transcription SREBP-2, LXR-β et ChREBP, et a une diminution de RXR-α. De facon interessante, meme si la concentration elevee de glucose dans le milieu apical produit juste de modestes changements dans le metabolisme du cholesterol, son impact est synergique avec celui du milieu basolateral. Nos resultats suggerent donc que le glucose influence positivement la captation de cholesterol par l'intestin lorsqu'il est present en grande concentration dans le milieu basolateral. Il est donc possible que la consommation excessive de dietes comprenant de grandes quantites de glucides peut favoriser la captation du cholesterol dans les conditions du syndrome metabolique, contribuant ainsi au niveau eleve de cholesterol dans la circulation et, consequemment, au risque de developper un diabete de type 2 et une maladie cardiovasculaire. [Traduit par la Redaction] Mots-cles: absorption de cholesterol, transporteurs de cholesterol, synthese de cholesterol, facteurs de transcription, glucose., Introduction Multiple studies have emphasized the contribution of elevated blood cholesterol (CHOL) levels to atherosclerotic coronary heart disease (CHD). Growing evidence has now pointed to the role of the absorption [...]

Published
2013
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16. Glycomacropeptide for Management of Insulin Resistance and Liver Metabolic Perturbations

Author

Sauvé, Mathilde Foisy, primary, Feldman, Francis, additional, Koudoufio, Mireille, additional, Ould-Chikh, Nour-El-Houda, additional, Ahmarani, Lena, additional, Sane, Alain, additional, N’Timbane, Thierry, additional, El-Jalbout, Ramy, additional, Patey, Nathalie, additional, Spahis, Schohraya, additional, Stintzi, Alain, additional, Delvin, Edgard, additional, and Levy, Emile, additional

Published
2021
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29. Physiopathologies cardiométaboliques associées à l'obésité : mécanismes sous-jacents et thérapie nutritionnelle

Author

Spahis, Schohraya and Levy, Emile

Subjects
Gluconéogenèse, Steatosis, Stéatose, Functional foods, Mitochondria dysfunction, Syndrome métabolique, Protéomique, NAFLD, Cardiometabolic disorders, Obésité, Obesity, Cardiométabolisme, Traitement, Omega-3 Fatty acids, Résistance à l’insuline, Nutrition, Inflammation, Lipogenesis, Stress oxydatif, Dysfonction mitochondriale, Gluconeogenesis, Proteomic profile, Insulin resistance, Endotoxémie, Aliments fonctionnels, Acides gras Omega-3, Metabolic syndrome, Endotoxemia, Treatment, Oxidative stress, Lipogenèse
Abstract

Le tractus digestif et le foie interagissent continuellement, non seulement à travers les connexions anatomiques, mais également par des liens physiologiques/fonctionnels. Le déséquilibre de l’axe intestin-foie apparait de plus en plus comme un facteur primordial dans les désordres cardiométaboliques, à savoir l’obésité, le syndrome métabolique, le diabète de type 2 et la stéatose hépatique non alcoolique (NAFLD), pour lesquels la prévalence demeure alarmante, les mécanismes moléculaires encore méconnus, et les traitements peu efficaces. L’hypothèse centrale du présent projet de recherche est que la combinaison d’anomalies génétiques et nutritionnelles affecte la sensibilité de l’insuline intestinale, ce qui conduit à une surproduction des chylomicrons, à une dyslipidémie, une insulinorésistance systémique et des répercussions sur le foie. Dans cet agencement, le foie développe une NAFLD progressive, impliquant plusieurs sentiers métaboliques intrinsèques et des mécanismes comprenant le stress oxydatif, l’inflammation et l’insulinorésistance. En revanche, des nutriments, comme les acides gras polyinsaturés (AGPI) n-3, peuvent présenter des effets bénéfiques en ciblant plusieurs circuits pathogéniques. L’objectif central de cette thèse consiste à : (i) Démontrer que des gènes codant pour les protéines intestinales clés associées au transport des lipides, comme c’est le cas du Sar1b GTPase, peuvent interagir avec l’environnement nutritionnel pour produire l’obésité et des dérangements cardiométaboliques, incluant la NAFLD ; (ii) Explorer les mécanismes hépatiques sous-jacents à la NAFLD; et (iii) Identifier les effets et les cibles thérapeutiques des AGPI n-3 sur la NAFLD. Ces objectifs seront soutenus par une prospection de la littérature scientifique disponible dans les champs du syndrome métabolique et de la NAFLD afin d’en disséquer les forces et les faiblesses au bénéfice de la communauté scientifique. À ces fins, nous avons utilisé des modèles animaux et cellulaires manipulés génétiquement, des animaux exposés de façon chronique à des diètes riches en lipides, des spécimens de tissus hépatiques obtenus durant la chirurgie bariatrique d’obèses morbides, et une cohorte d’adolescents obèses souffrant de NAFLD et qui seront traités avec les AGPI n-3. L’ensemble de nos expériences ont soutenu nos hypothèses et ont mis en évidence les concepts et mécanismes suivants : (i) L’abondance d’un gène crucial (notamment Sar1b GTPase) au niveau de l’intestin, en synergie avec une alimentation obésogène, perturbe l’homéostasie locale et mène à des dérangements cardiométaboliques, défiant même l’axe intestin-foie ; (ii) Les causes développementales de la NAFLD comprennent les dérangements du métabolisme des acides gras, du statut redox et inflammatoire, de la sensibilité à l’insuline, des sentiers métaboliques (lipogenèse, β-oxydation, gluconéogenèse) et de l’expression des facteurs de transcription; et (iii) Les AGPI n-3 représentent un robuste arsenal thérapeutique des dérangements cardiométaboliques, notamment la NAFLD, en agissant sur plusieurs cibles pathogéniques. Globalement, nos résultats montrent le rôle indéniable de l’intestin comme organe insulino-sensible interagissant de près avec les aliments et capable de déclencher des troubles métaboliques. Plusieurs mécanismes gouvernant les désordres métaboliques ont été dévoilés par nos travaux. En outre, nos études cliniques ont pointé la force thérapeutique des AGPI n-3 qui interviennent dans de nombreux processus de régulation métaboliques et notamment dans le stress oxydatif et l’inflammation., The digestive tract and liver interact continuously, not only through anatomical connections, but also through physiological / functional links. The imbalance of the intestine-liver axis is increasingly emerging as a key factor in cardiometabolic disorders (CMD), namely obesity, metabolic syndrome, type 2 diabetes, and non alcoholic fatty liver disease (NAFLD), for which prevalence remains alarmingly high, molecular mechanisms are poorly understood, and treatments are largely inefficient. The central hypothesis of this research project is that the combination of genetic and nutritional abnormalities affect intestinal insulin sensitivity, leading to overproduction of chylomicrons, dyslipidemia, systemic insulin resistance and dysregulated intestine-liver axis. In this situation, the liver develops progressive NAFLD, implicating several intrinsic metabolic pathways and mechanisms, including oxidative stress, inflammation and insulin resistance. In contrast, functional foods, such as omega-3 polyunsaturated fatty acids (n-3 PUFA), may have beneficial effects by targeting several pathogenic pathways. The central objective of this thesis is to: (i) Demonstrate that genes coding for key intestinal proteins associated with lipid transport, as is the case with Sar1b GTPase, can interact with the nutritional environment to produce obesity and CMD, including hepatic steatosis; (ii) explore the mechanisms underlying NAFLD; and (iii) identify the effects and therapeutic targets of n-3 PUFA. These objectives will be supported by a critical review on metabolic syndrome and NAFLD in order to dissect their strengths and weaknesses for the benefit of the scientific community. For these purposes, we used genetically engineered animal and cell models, chronic exposure of animals to high-fat diets, liver tissue specimens obtained during bariatric surgery of morbidly obese patients, and treatment of obese NAFLD adolescents with n-3 PUFA. All of our experiments supported our hypotheses and highlighted the following concepts and mechanisms: (i) The abundance of a crucial gene (notably Sar1b GTPase) in the intestine, in synergy with an obesogenic diet, disrupts local homeostasis and leads to CMD, challenging even the intestine-liver axis; (ii) Developmental causes of NAFLD include disturbances of fatty acid metabolism, redox and inflammatory status, insulin sensitivity, metabolic pathways (lipogenesis, β-oxidation, gluconeogenesis), and expression of transcription factors; and (iii) n-3 PUFA represent a robust therapeutic arsenal of CMD, including NAFLD, by acting on several pathogenic targets. Overall, our results show the undeniable role of the intestine, as an insulin-sensitive organ, interacting closely with obesogenic food, and capable of triggering CMD, including perturbations of the intestine-liver axis. Several mechanisms governing metabolic disorders have been unveiled by our work. In addition, our clinical studies have pointed to the therapeutic potential of n-3 PUFA involved in many regulatory processes, including oxidative stress and inflammation.

Published
2019

32. Prevalence of Malnutrition in Pediatric Hospitals in Developed and In-Transition Countries: The Impact of Hospital Practices

Author

McCarthy, Andrea, primary, Delvin, Edgard, additional, Marcil, Valerie, additional, Belanger, Veronique, additional, Marchand, Valerie, additional, Boctor, Dana, additional, Rashid, Mohsin, additional, Noble, Angela, additional, Davidson, Bridget, additional, Groleau, Veronique, additional, Spahis, Schohraya, additional, Roy, Claude, additional, and Levy, Emile, additional

Published
2019
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34. Apple peel polyphenols reduce mitochondrial dysfunction in mice with DSS-induced ulcerative colitis

Author

Yeganeh, Pantea Rahmani, primary, Leahy, Jade, additional, Spahis, Schohraya, additional, Patey, Natalie, additional, Desjardins, Yves, additional, Roy, Denis, additional, Delvin, Edgard, additional, Garofalo, Carole, additional, Leduc-Gaudet, Jean-Philippe, additional, St-Pierre, David, additional, Beaulieu, Jean-François, additional, Marette, André, additional, Gouspillou, Gilles, additional, and Levy, Emile, additional

Published
2018
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38. Su1969 N-3 Fatty Acid Supplementation Improves Hepatic- and Cardiometabolic-Related Biomarkers in Pediatric Patients With Non-Alcoholic Fatty Liver Disease: A Randomized Controlled Intervention

Author

Spahis, Schohraya, primary, Alvarez, Fernando, additional, Delvin, Edgard, additional, Dubois, Josee, additional, Peretti, Noel, additional, Ahmad, Najma, additional, Moreau, Alain, additional, Garofalo, Carole, additional, Tang, An, additional, Seidman, Ernest G., additional, and Levy, Emile, additional

Published
2016
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39. Su1196 Functional Role of Sar1 GTPase in the Regulation of Intestinal Lipid Transport and Cholesterol Homeostasis: Using Genetically Engineered Intestinal Cells to Understand Chylomicron Retention Disease

Author

Sané, Alain Théophile, primary, Spahis, Schohraya, additional, Marcil, Valerie, additional, Preston, Katarina, additional, Brisebois-Picard, Marie-Lou, additional, Garofalo, Carole, additional, Delvin, Edgard, additional, Beaulieu, Jean-Francois, additional, Seidman, Ernest G., additional, and Levy, Emile, additional

Published
2016
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50. Mo2004 Development of Obesity, Insulin Resistance and Metabolic Derangements in Mice Overexpressing Sar1b Whose Mutation Causes Chylomicron Retention Disease

Author

Spahis, Schohraya, primary, Garofalo, Carole, additional, Emonnot, Lea, additional, Marcil, Valerie, additional, Montoudis, Alain, additional, Delvin, Edgard, additional, Sanchez, Rocio, additional, Sinnett, Daniel, additional, Seidman, Ernest G., additional, Sane, Alain T., additional, and Levy, Emile, additional

Published
2013
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