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A polyphenol-rich cranberry extract protects from diet-induced obesity, insulin resistance and intestinal inflammation in association with increased Akkermansia spp. population in the gut microbiota of mice
  1. Fernando F Anhê1,2,
  2. Denis Roy2,
  3. Geneviève Pilon1,2,
  4. Stéphanie Dudonné2,
  5. Sébastien Matamoros2,
  6. Thibault V Varin2,
  7. Carole Garofalo3,
  8. Quentin Moine3,
  9. Yves Desjardins2,
  10. Emile Levy3,4,
  11. André Marette1,2
  1. 1Department of Medicine, Faculty of Medicine, Cardiology Axis of the Quebec Heart and Lung Institute, Quebec, Quebec, Canada
  2. 2Institute of Nutrition and Functional Foods, Laval University, Quebec, Quebec, Canada
  3. 3Research Centre, Sainte-Justine Hospital, Montreal, Quebec, Canada
  4. 4Department of Nutrition, Faculty of Medicine, University of Montreal, Montreal, Quebec, Canada
  1. Correspondence to Dr André Marette, Cardiology Axis of the Quebec Heart and Lung Institute, Laval University, Quebec, Canada, Hôpital Laval, Pavillon Marguerite d'Youville, Bureau Y4340, Ste-Foy, Québec, Canada G1V 4G5; andre.marette{at}criucpq.ulaval.ca

Abstract

Objective The increasing prevalence of obesity and type 2 diabetes (T2D) demonstrates the failure of conventional treatments to curb these diseases. The gut microbiota has been put forward as a key player in the pathophysiology of diet-induced T2D. Importantly, cranberry (Vaccinium macrocarpon Aiton) is associated with a number of beneficial health effects. We aimed to investigate the metabolic impact of a cranberry extract (CE) on high fat/high sucrose (HFHS)-fed mice and to determine whether its consequent antidiabetic effects are related to modulations in the gut microbiota.

Design C57BL/6J mice were fed either a chow or a HFHS diet. HFHS-fed mice were gavaged daily either with vehicle (water) or CE (200 mg/kg) for 8 weeks. The composition of the gut microbiota was assessed by analysing 16S rRNA gene sequences with 454 pyrosequencing.

Results CE treatment was found to reduce HFHS-induced weight gain and visceral obesity. CE treatment also decreased liver weight and triglyceride accumulation in association with blunted hepatic oxidative stress and inflammation. CE administration improved insulin sensitivity, as revealed by improved insulin tolerance, lower homeostasis model assessment of insulin resistance and decreased glucose-induced hyperinsulinaemia during an oral glucose tolerance test. CE treatment was found to lower intestinal triglyceride content and to alleviate intestinal inflammation and oxidative stress. Interestingly, CE treatment markedly increased the proportion of the mucin-degrading bacterium Akkermansia in our metagenomic samples.

Conclusions CE exerts beneficial metabolic effects through improving HFHS diet-induced features of the metabolic syndrome, which is associated with a proportional increase in Akkermansia spp. population.

  • Obesity
  • Diabetes Mellitus
  • Prebiotic
  • Intestinal Permeability
  • Intestinal Bacteria

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