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

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.

The hypothalamus and the brainstem along with other structures such as the circumventricular organs⁸ are implicated in interfacing important peripheral homeostatic signals (for example, signals informing the brain about the energy balance and nutritional status).^{3, 5} The variations in the adipose-derived hormone leptin or in the gastrointestinal hormones ghrelin, glucagon-like peptide 1 (GLP-1) and peptide tyrosine-tyrosine (PYY) constitute significant homeostatic signals. It is through its effects on gastrointestinal hormones such as GLP-1 and PYY, which are secreted via the intestinal L cells, and through other gastrointestinal influences, such as those exerted by changes in the gut microbiota and in the bile salts production, that the bariatric surgery procedures alter energy balance.⁹

The recent renewed interest for the gut as a potential target to develop therapies to combat obesity and its complications prompted us to plan a symposium that we entitled: ‘Targeting the gut to treat obesity and its metabolic comorbidities’. The symposium was held by the Université Laval’s Research Chair in Obesity, at the Auberge Saint-Antoine in Québec City, in November 2014. It was the 17th of the international symposium series of Université Laval’s Research Chair in Obesity. The meeting involved a total of eight speakers among the most renowned researchers in the field covered by the symposium, which was chaired by Dr Denis Richard (Scientific Director of the Université Laval’s Research Chair in Obesity). Dr Richard was very competently assisted by Drs Keith Sharkey and André Carpentier, who chaired the morning (Basic Mechanisms) and afternoon sessions (‘Bariatric Surgery’), respectively.

Since its creation in 1997, the Université Laval’s Research Chair in Obesity has organized so far, annually, 16 international symposia entirely devoted to obesity research. The first symposium of the series, entitled ‘The uncoupling proteins and obesity’, was held in 1998.¹⁰ The second symposium, organized in 1999, was oriented towards ‘Recent advances in adipose tissue biology and their implications for obesity’.¹¹ In 2000, the third symposium, entitled ‘The ponderostat: from behavior to neural substrates’,¹² focused on the mechanisms whereby energy balance is regulated.¹² The fourth symposium, organized in November 2002, and entitled ‘Complications of obesity: the inflammatory link’, summarized the latest most important findings in the mechanisms underlying the link between obesity and its complications such as diabetes and cardiovascular diseases.¹³ In 2003, the fifth symposium brought a comprehensive view on ‘The role of gene regulation in obesity and its complications’ and, specifically, on the regulation of PPARs, PGC-1, FOXO1 and SIR2.¹⁴ In 2004, the sixth symposium focused on the understanding of ‘The Endocannabinoid system and its role in energy homeostasis and abdominal obesity management’.¹⁵ The seventh symposium in 2005 explored the complexity of ‘The neurobiology of obesity’.¹⁶ Our eighth symposium organized in 2006 was dedicated to ‘AMP-activated protein kinase in obesity’.¹⁷ In 2007, for the 10th anniversary of the Merck Frosst/CIHR Research Chair in Obesity, a double program was held during 2 consecutive days. The first symposium focused on the ‘Gastrointestinal tract, obesity and diabetes’.¹⁸ The second one explored the concept of ‘Childhood obesity: Biological/environmental determinants and preventative strategies’.¹⁸ In 2008, the Chair organized for the 11th annual symposium series, a program called ‘Obesity in a modern world: when pleasure meets homeostasis’, and dedicated to the ‘reward system’.¹⁹ In 2009, an advisory committee to the Chair recommended, ten years after the symposium on ‘Recent advances in adipose tissue biology’, to revisit this theme by organizing for the 12th annual symposium series, a program dedicated to the ‘Brown adipose tissue’.²⁰ In October 2010, the 13th symposium focused on how ‘Bariatric/metabolic surgery influences the energy balance regulation’.²¹ In November 2011, the 14th symposium focused on ‘High-fat feeding’.²² In November 2012, the 15th symposium focused on ‘G-protein-coupled receptors in energy homeostasis’.²³ In November 2013, the 16th symposium addressed again the metabolic role of the brown adipocytes in a meeting entitled: ‘White, beige, brown: what determines the colour of adipose tissue’.²⁴

The mission of the Université Laval’s Research Chair in Obesity is to promote and support academic research and educational activities on the causes, complications, treatment and prevention of obesity. It is within our mission to disseminate knowledge regarding obesity. In that regard, the purpose of our annual symposium is to address an important topic in obesity research.

In conclusion, our gratitude goes to all the invited scientists, who for their comprehensive and stimulating presentations and their enthusiastic participation to the symposium. We would finally like to acknowledge the contribution of the Centre de recherche de l’Institut universitaire de cardiologie et de pneumologie de Québec affiliated to the Université Laval for their support to the symposium.