Effects of a novel polyphenol-rich plant extract on body composition, inflammation, insulin sensitivity, and glucose homeostasis in obese mice.


Journal

International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108

Informations de publication

Date de publication:
09 2021
Historique:
received: 14 02 2021
accepted: 18 05 2021
revised: 05 05 2021
pubmed: 4 6 2021
medline: 27 1 2022
entrez: 3 6 2021
Statut: ppublish

Résumé

The worldwide prevalence of obesity, metabolic syndrome and type 2 diabetes (T2D) is reaching epidemic proportions that urge the development of new management strategies. Totum-63 is a novel, plant-based polyphenol-rich active principle that has been shown to reduce body weight, fasting glycemia, glucose intolerance, and fatty liver index in obese subjects with prediabetes. Here, we investigated the effects and underlying mechanism(s) of Totum-63 on metabolic homeostasis in insulin-resistant obese mice. Male C57Bl6/J mice were fed a high-fat diet for 12 weeks followed by supplementation with Totum-63 for 4 weeks. The effects on whole-body energy and metabolic homeostasis, as well as on tissue-specific inflammation and insulin sensitivity were assessed using a variety of immunometabolic phenotyping tools. Totum-63 decreased body weight and fat mass in obese mice, without affecting lean mass, food intake and locomotor activity, and increased fecal energy excretion and whole-body fatty acid oxidation. Totum-63 reduced fasting plasma glucose, insulin and leptin levels, and improved whole-body insulin sensitivity and peripheral glucose uptake. The expression of insulin receptor β and the insulin-induced phosphorylation of Akt/PKB were increased in liver, skeletal muscle, white adipose tissue (WAT) and brown adipose tissue (BAT). Hepatic steatosis was also decreased by Totum-63 and associated with a lower expression of genes involved in fatty acid uptake, de novo lipogenesis, inflammation, and fibrosis. Furthermore, a significant reduction in pro-inflammatory macrophages was also observed in epidydimal WAT. Finally, a potent decrease in BAT mass associated with enhanced tissue expression of thermogenic genes was found, suggesting BAT activation by Totum-63. Our results show that Totum-63 reduces inflammation and improves insulin sensitivity and glucose homeostasis in obese mice through pleiotropic effects on various metabolic organs. Altogether, plant-derived Totum-63 might constitute a promising novel nutritional supplement for alleviating metabolic dysfunctions in obese people with or without T2D.

Sections du résumé

BACKGROUND/OBJECTIVES
The worldwide prevalence of obesity, metabolic syndrome and type 2 diabetes (T2D) is reaching epidemic proportions that urge the development of new management strategies. Totum-63 is a novel, plant-based polyphenol-rich active principle that has been shown to reduce body weight, fasting glycemia, glucose intolerance, and fatty liver index in obese subjects with prediabetes. Here, we investigated the effects and underlying mechanism(s) of Totum-63 on metabolic homeostasis in insulin-resistant obese mice.
METHODS
Male C57Bl6/J mice were fed a high-fat diet for 12 weeks followed by supplementation with Totum-63 for 4 weeks. The effects on whole-body energy and metabolic homeostasis, as well as on tissue-specific inflammation and insulin sensitivity were assessed using a variety of immunometabolic phenotyping tools.
RESULTS
Totum-63 decreased body weight and fat mass in obese mice, without affecting lean mass, food intake and locomotor activity, and increased fecal energy excretion and whole-body fatty acid oxidation. Totum-63 reduced fasting plasma glucose, insulin and leptin levels, and improved whole-body insulin sensitivity and peripheral glucose uptake. The expression of insulin receptor β and the insulin-induced phosphorylation of Akt/PKB were increased in liver, skeletal muscle, white adipose tissue (WAT) and brown adipose tissue (BAT). Hepatic steatosis was also decreased by Totum-63 and associated with a lower expression of genes involved in fatty acid uptake, de novo lipogenesis, inflammation, and fibrosis. Furthermore, a significant reduction in pro-inflammatory macrophages was also observed in epidydimal WAT. Finally, a potent decrease in BAT mass associated with enhanced tissue expression of thermogenic genes was found, suggesting BAT activation by Totum-63.
CONCLUSIONS
Our results show that Totum-63 reduces inflammation and improves insulin sensitivity and glucose homeostasis in obese mice through pleiotropic effects on various metabolic organs. Altogether, plant-derived Totum-63 might constitute a promising novel nutritional supplement for alleviating metabolic dysfunctions in obese people with or without T2D.

Identifiants

pubmed: 34079069
doi: 10.1038/s41366-021-00870-x
pii: 10.1038/s41366-021-00870-x
doi:

Substances chimiques

Plant Extracts 0
Polyphenols 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

2016-2027

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

Hendrik J P van der Zande (HJP)

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.

Joost M Lambooij (JM)

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.

Vivien Chavanelle (V)

Valbiotis R&D Riom Center, Riom, France.

Anna Zawistowska-Deniziak (A)

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.

Yolanda Otero (Y)

Valbiotis R&D Riom Center, Riom, France.

Frank Otto (F)

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands.

Louise Lantier (L)

Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA.
Vanderbilt Mouse Metabolic Phenotyping Center, Nashville, TN, USA.

Owen P McGuinness (OP)

Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA.
Vanderbilt Mouse Metabolic Phenotyping Center, Nashville, TN, USA.

Florian Le Joubioux (F)

Valbiotis R&D Perigny Center, Périgny, France.

Martin Giera (M)

Center for Proteomics and Metabolomics, Leiden University Medical Center, Leiden, The Netherlands.

Thierry Maugard (T)

LIENSs UMR CNRS 7266, La Rochelle Université, La Rochelle, France.

Sébastien L Peltier (SL)

Valbiotis R&D Perigny Center, Périgny, France.

Pascal Sirvent (P)

Valbiotis R&D Riom Center, Riom, France.

Bruno Guigas (B)

Department of Parasitology, Leiden University Medical Center, Leiden, The Netherlands. b.g.a.guigas@lumc.nl.

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