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The 17th international symposium in obesity; targeting the gut to treat obesity and its metabolic comorbidities

International Journal of Obesity Supplements volume 6, pages S1–S2 (2016)Cite this article

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Obesity (body mass index equal of above 30 kg m−2) prevalence has risen considerably over the last decades. Globally, more than 1 out of 10 adults is now obese (http://www.who.int/mediacentre/factsheets/fs311/en/). This situation is pre-occupying as obesity, in particular in its severe forms (morbid and visceral), is associated with costly diseases, which include type 2 diabetes and atherosclerosis.1, 2 Obesity translates an imbalance between energy intake and energy expenditure and results from complex gene-environment interactions. Indeed, our modern environment, which has become obesogenic by promoting a sedentary lifestyle and overeating, proves to be particularly ‘obesity-inducing’ in individuals genetically predisposed to positive energy balance.

The full understanding of the physiopathology of obesity requires an extensive knowledge of the mechanisms behind energy balance or homeostasis regulation, which depends on controls exerted on both energy intake and expenditure. Energy homeostasis is achieved through highly coordinated communications between neurobiological circuits and peripheral homeostatic pathways that control food intake and energy expenditure.3, 4, 5 This involves interconnected brain structures such as the prefrontal cortex, the insula, which contributes together with the striatum, ventral tegmental area, hypothalamus and brainstem to establish the pleasurable/hedonic value of food and ultimately govern the decision to eat or engage in physical activity. The hypothalamus and the brainstem also govern autonomic energy expenditure responses such as brown fat thermogenesis, whose role in energy balance may not be trivial.6 The neurons involved in energy balance regulation express various receptor types upon which act different peptides or classic neurotransmitters that have been grouped into ‘anabolic’ (promoting fat deposition) and ‘catabolic’ (preventing fat deposition) chemical mediators.3, 7 These mediators include pro-opiomelanocortin (POMC), neuropeptide Y (NPY), agouti-related peptide (AgRP), steroidogenic factor 1 (SF1), melanin-concentrating hormones (MCH), corticotropin-releasing factor (CRF), gamma-aminobutyric acid (GABA), glutamate, among others.

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Acknowledgements

This article is published as part of a supplement sponsored by the Université Laval’s Research Chair in Obesity, in an effort to inform the public on the causes, consequences, treatments and prevention of obesity.

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  1. Denis Richard: D Richard is the recipient of the Université Laval’s Research Chair in Obesity and Director of the Centre de recherche de l'Institut universitaire de cardiologie et de pneumologie de Québec (CRIUCPQ)

Authors and Affiliations

  1. Université Laval’s Research Chair in Obesity, Centre de Recherche de l'Institut Universitaire de Cardiologie et de Pneumologie de Québec (CRIUCPQ), Université Laval, Quebec, Canada

    Denis Richard

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Correspondence to Denis Richard.

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Richard, D. The 17th international symposium in obesity; targeting the gut to treat obesity and its metabolic comorbidities. Int J Obes Supp 6 (Suppl 1), S1–S2 (2016). https://doi.org/10.1038/ijosup.2016.1

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