News Archive 2022

Dr Harriët Schellekens’ PROTECT project awarded BINC funding

4 May 2022
Dr Harriët Schellekens

Congratulations to Dr Harriët Schellekens who has been awarded BINC Foundation funding to explore the role of the gut microbiota in mediating the effects of early-life nutrition on neurodevelopment of appetite, food reward and food preference in adulthood.

Dr. Harriët Schellekens, a funded investigator with APC Microbiome Ireland SFI Research Centre and lecturer in the Department of Anatomy & Neuroscience was awarded funding from the Geneva-based BIOSTIME Institute Nutrition & Care (BINC) Foundation for her project “PROTECT: PRiming fOr healThy Eating via the diet-miCrobioTa-gut-brain axis”, The project team includes collaborators Dr Siobhain O’Mahony, Department of Anatomy and Neuroscience UCC,  Professor Suzanne Dickson, Department of Physiology, University of Gothenburg, and PhD student Cristina Cuesta Marti, who will work under the co-supervision of Dr Schellekens and her colleague Dr Ger Clarke.

Dr Schellekens explains how “early life exposure to high-fat and high-sugar diets can negatively impact metabolic health later in life. Early life diet is crucial in the development of appetite signalling in the brain and impacts energy metabolism and the brain pathways that determine how we process rewarding foods, especially those high in calories. This can have consequences later in life on the types of food we like to eat, driving the preference for fatty and sugary foods, which increases the risk for obesity and type 2 diabetes.

Early life exposure to unhealthy diets has also been shown to alter how the bacterial community in our gastrointestinal tract develops and changes in gut microbiota have been linked to alterations in food intake and host eating behaviour. However, it is currently not known if the gut microbiome in early life is critical for the establishment of healthy eating behaviour in adulthood.”

This PROTECT project will specifically focus on the ‘hunger-hormone’, ghrelin, which uniquely stands out as the only gastrointestinal signal that stimulates food intake, regulates appetite and reward signalling in the brain, and modulates fat preference and food choice. Ghrelin levels are modulated by the gut microbiota and ghrelin plays a role in the development of brain feeding pathways in early life.

Dr Schellekens and her team will investigate the extent to which the gut microbiota in early life are involved in the establishment of healthy eating behaviour in adulthood, and if the effects are mediated via ghrelin signalling , and whether microbiota-targeted interventions can protect against diet-induced negative effects on appetite, food preference and reward processing.

The PROTECT team will initially investigate the role of the intestinal microbiota following early life exposure to high-fat/high-sugar (HFHS) diet on food intake behaviour, food preference and central reward signalling in adulthood. The second part of the project will seek to validate the effectiveness of microbiota-targeted approaches, in preventing the detrimental neurobehavioral outcomes, lowering metabolic risk later in life. One strategy that will be explored, will be supplementation with a metabolically active Bifidobacterium longum strain (APC1472), which was recently identified in a study by Dr Schellekens and colleagues, Professor Catherine Stanton, Professor John Cryan and Professor Ted Dinan (Schellekens et al. EBioMedicine, 2021) to have anti-obesity effects in mice and in humans. This strain since has shown to modulate ghrelin signalling in the brain of mice (unpublished data).

PROTECT will be the first study investigating the impact of early life nutrition and microbiota priming on sustained dietary preference in adulthood. Findings from this study will be directly relevant for the research to BINC-Geneva and the development of comprehensive microbiota-targeted health solutions in the field of infant and maternal nutrition and care, providing the best possible start in life.

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News item and photographs B. Riedewald

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