Tina Bake, Kim T.Hellgren, Suzanne L. Dickson
Presented at the European Obesity Summit, June 2016
Ghrelin is a gut peptide released from the empty stomach that increases food intake. It has also been linked to food-related behaviours such as food motivation, food reward and food anticipatory activity. Ghrelin levels in the blood are linked to meal pattern, increasing prior to feeding. To mimic human meal eating behaviour in animals we used a scheduled feeding (SF) paradigm in which rodents have ad libitum access to chow and in addition 2h access to highly palatable high fat diet (HFD). Previous studies with this paradigm have shown that both rats and mice will rapidly adapt their feeding behaviour and as a result binge-eat on HFD.
Here we sought to investigate the role of ghrelin during binge-like meal eating induced by SF. We utilised a combination of two different animal models: pharmacologically manipulated rats via acute administration of ghrelin or genetically modified mice lacking the growth hormone secretagogue receptor 1A (GHS-R1A). For acute injections of either ghrelin or vehicle into the lateral ventricle (ICV) or intra-VTA, rats were surgically implanted with guide cannulas and then habituated to SF for at least 2 weeks prior to injections. GHS-R1A-KO mice and their wildtype (WT) littermates were scheduled-fed for 4 weeks.
Remarkably and unexpectedly, we found that acutely injecting ghrelin ICV or intra-VTA resulted in a shift in food preference from high fat diet towards chow during the SF period without altering total daily energy consumption. However an increase of body weight was observed after ICV ghrelin. A fasting challenge also led to an increase in chow intake during the SF session but HFD intake did not reduce at the same time. GHS-R1A-KO mice were able to adapt and maintain large meals of HFD in a similar fashion as WT mice suggesting that the ghrelin signalling system may not have a critical role in acquisition or maintenance in this kind of feeding behaviour.
In conclusion, ghrelin appears to act as a modulating factor for binge-like eating behaviour by shifting the food preference towards a healthier choice (from HFD to chow), effects that were clearly divergent from fasting.
Supported by EC (Nudge-it, 607310).