(Wh)olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N)utrition (WHEN) to Curb Obesity and Related Disorders

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Abstract

The discovery of the endocannabinoidome (eCBome) is evolving gradually with yet to be elucidated functional lipid mediators and receptors. The diet modulates these bioactive lipids and the gut microbiome, both working in an entwined alliance. Mounting evidence suggests that, in different ways and with a certain specialisation, lipid signalling mediators such as N-acylethanolamines (NAEs), 2-monoacylglycerols (2-MAGs), and N-acyl-amino acids (NAAs), along with endocannabinoids (eCBs), can modulate physiological mechanisms underpinning appetite, food intake, macronutrient metabolism, pain sensation, blood pressure, mood, cognition, and immunity. This knowledge has been primarily utilised in pharmacology and medicine to develop many drugs targeting the fine and specific molecular pathways orchestrating eCB and eCBome activity. Conversely, the contribution of dietary NAEs, 2-MAGs and eCBs to the biological functions of these molecules has been little studied. In this review, we discuss the importance of (Wh) olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N) utrition (WHEN), in the management of obesity and related disorders.

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Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity.

Amandine Everard, Clara Belzer, Lucie Geurts … (2013)

Obesity and type 2 diabetes are characterized by altered gut microbiota, inflammation, and gut barrier disruption. Microbial composition and the mechanisms of interaction with the host that affect gut barrier function during obesity and type 2 diabetes have not been elucidated. We recently isolated Akkermansia muciniphila, which is a mucin-degrading bacterium that resides in the mucus layer. The presence of this bacterium inversely correlates with body weight in rodents and humans. However, the precise physiological roles played by this bacterium during obesity and metabolic disorders are unknown. This study demonstrated that the abundance of A. muciniphila decreased in obese and type 2 diabetic mice. We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion. Finally, we demonstrated that all these effects required viable A. muciniphila because treatment with heat-killed cells did not improve the metabolic profile or the mucus layer thickness. In summary, this study provides substantial insight into the intricate mechanisms of bacterial (i.e., A. muciniphila) regulation of the cross-talk between the host and gut microbiota. These results also provide a rationale for the development of a treatment that uses this human mucus colonizer for the prevention or treatment of obesity and its associated metabolic disorders.

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Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease.

Kerry Donnelly, Coleman I. Smith, Sarah Schwarzenberg … (2005)

Nonalcoholic fatty liver disease (NAFLD) is characterized by the accumulation of excess liver triacylglycerol (TAG), inflammation, and liver damage. The goal of the present study was to directly quantify the biological sources of hepatic and plasma lipoprotein TAG in NAFLD. Patients (5 male and 4 female; 44 +/- 10 years of age) scheduled for a medically indicated liver biopsy were infused with and orally fed stable isotopes for 4 days to label and track serum nonesterified fatty acids (NEFAs), dietary fatty acids, and those derived from the de novo lipogenesis (DNL) pathway, present in liver tissue and lipoprotein TAG. Hepatic and lipoprotein TAG fatty acids were analyzed by gas chromatography/mass spectrometry. NAFLD patients were obese, with fasting hypertriglyceridemia and hyperinsulinemia. Of the TAG accounted for in liver, 59.0% +/- 9.9% of TAG arose from NEFAs; 26.1% +/- 6.7%, from DNL; and 14.9% +/- 7.0%, from the diet. The pattern of labeling in VLDL was similar to that in liver, and throughout the 4 days of labeling, the liver demonstrated reciprocal use of adipose and dietary fatty acids. DNL was elevated in the fasting state and demonstrated no diurnal variation. These quantitative metabolic data document that both elevated peripheral fatty acids and DNL contribute to the accumulation of hepatic and lipoprotein fat in NAFLD.

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Glucagon-like peptide 1 (GLP-1)

T.D. Müller, B. Finan, S.R. Bloom … (2019)

Background The glucagon-like peptide-1 (GLP-1) is a multifaceted hormone with broad pharmacological potential. Among the numerous metabolic effects of GLP-1 are the glucose-dependent stimulation of insulin secretion, decrease of gastric emptying, inhibition of food intake, increase of natriuresis and diuresis, and modulation of rodent β-cell proliferation. GLP-1 also has cardio- and neuroprotective effects, decreases inflammation and apoptosis, and has implications for learning and memory, reward behavior, and palatability. Biochemically modified for enhanced potency and sustained action, GLP-1 receptor agonists are successfully in clinical use for the treatment of type-2 diabetes, and several GLP-1-based pharmacotherapies are in clinical evaluation for the treatment of obesity. Scope of review In this review, we provide a detailed overview on the multifaceted nature of GLP-1 and its pharmacology and discuss its therapeutic implications on various diseases. Major conclusions Since its discovery, GLP-1 has emerged as a pleiotropic hormone with a myriad of metabolic functions that go well beyond its classical identification as an incretin hormone. The numerous beneficial effects of GLP-1 render this hormone an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, and neurodegenerative disorders

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Author and article information

Contributors

Jyoti Sihag:

ORCID: https://orcid.org/0000-0002-3218-4292

Jyoti.Sihag.1@ulaval.ca

Vincenzo Di Marzo:

ORCID: https://orcid.org/0000-0002-1490-3070

vincenzo.dimarzo.1@ulaval.ca

Journal

Journal ID (nlm-ta): Lipids Health Dis

Journal ID (iso-abbrev): Lipids Health Dis

Title: Lipids in Health and Disease

Publisher: BioMed Central (London )

ISSN (Electronic): 1476-511X

Publication date (Electronic): 14 January 2022

Publication date PMC-release: 14 January 2022

Publication date Collection: 2022

Volume: 21

Electronic Location Identifier: 9

Affiliations

[1 ]GRID grid.23856.3a, ISNI 0000 0004 1936 8390, Faculty of Medicine, , University of Laval, ; Quebec, Canada

[2 ]GRID grid.23856.3a, ISNI 0000 0004 1936 8390, Faculty of Agriculture and Food Sciences, , University of Laval, ; Quebec, Canada

[3 ]GRID grid.23856.3a, ISNI 0000 0004 1936 8390, Canada Excellence Research Chair on the Microbiome-Endocannabinoidome Axis in Metabolic Health (CERC-MEND), , University of Laval, ; Quebec, Canada

[4 ]University Institute of Cardiology and Pneumology, Quebec, Canada

[5 ]GRID grid.23856.3a, ISNI 0000 0004 1936 8390, Institute of Nutrition and Functional Foods (INAF) and Centre Nutrition, Santé et Société (NUTRISS), , University of Laval, ; Quebec, Canada

[6 ]GRID grid.7151.2, ISNI 0000 0001 0170 2635, Department of Foods and Nutrition, , Chaudhary Charan Singh Haryana Agricultural University, ; Hisar, India

[7 ]Institute of Biomolecular Chemistry of the National Research Council (ICB-CNR), Naples, Italy

[8 ]Endocannabinoid Research Group, Naples, Italy

[9 ]GRID grid.23856.3a, ISNI 0000 0004 1936 8390, Joint International Research Unit between the Italian National Research Council (CNR) and University of Laval, for Chemical and Biomolecular Research on the Microbiome and its impact on Metabolic Health and Nutrition (UMI-MicroMeNu), ; Quebec, Canada

Author information

Jyoti Sihag https://orcid.org/0000-0002-3218-4292

Vincenzo Di Marzo https://orcid.org/0000-0002-1490-3070

Article

Publisher ID: 1609

DOI: 10.1186/s12944-021-01609-3

PMC ID: 8759188

PubMed ID: 35027074

SO-VID: bc72fcb8-211c-483c-b9b1-7070eb276fd0

License:

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

History

Date received : 14 October 2021

Date accepted : 5 December 2021

Funding

Funded by: FundRef http://dx.doi.org/10.13039/501100002784, Canada Excellence Research Chairs, Government of Canada;

Custom metadata

ScienceOpen disciplines: Biochemistry

Keywords: endocannabinoids,endocannabinoidome,microbiome,nutrition,obesity

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ScienceOpen disciplines: Biochemistry

Keywords: endocannabinoids, endocannabinoidome, microbiome, nutrition, obesity

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(Wh)olistic (E)ndocannabinoidome-Microbiome-Axis Modulation through (N)utrition (WHEN) to Curb Obesity and Related Disorders

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Tick microbiome

Most cited references 247

Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity.

Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease.

Glucagon-like peptide 1 (GLP-1)

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Cited by 12

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