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Gut Hormones Can Mimic Food Effects On Brain



Hunger and satiety are mediated by a range of peripheral signals to the brain.

A new study by Akila de Silva and colleagues from Imperial College London, UK, published in Cell Metabolism, shows that infusion of two gut hormones can reduce food intake and mimic the central effects of a meal in humans.

Specifically, the researchers used functional magnetic resonance imaging (fMRI) to examine the effect of infusing the gut hormones PYY(3-36) and GLP-1(7-36 amide) on brain activation with presentation of food-salient images in six brain regions known to be involved in ingestive behaviour (amygdala, caudate, insula, nucleus accumbens, orbitofrontal cortex, and putamen) of 16 young normal-weight volunteers.

In addition, the researchers looked at the effect of these gut hormones on hunger and eating behaviour before and after a standardized breakfast and an ad libitum buffet lunch.

Combined infusion of these hormones not only led to similar activation/suppression of brain regions as seen after the standardized meal, but also reduced subsequent energy intake.

Not only does this study provide further insight into how the gut talks to the brain but also provides evidence for the involvement of these hormones in ingestive behaviour.

Whether or not such insights can be harnessed to provide better treatments for obesity remains to be seen.

AMS
San Francisco, CA

p.s. Hat tip to Bill Colmers for alerting me to this article

De Silva A, Salem V, Long CJ, Makwana A, Newbould RD, Rabiner EA, Ghatei MA, Bloom SR, Matthews PM, Beaver JD, & Dhillo WS (2011). The Gut Hormones PYY(3-36) and GLP-1(7-36 amide) Reduce Food Intake and Modulate Brain Activity in Appetite Centers in Humans. Cell metabolism, 14 (5), 700-6 PMID: 22000927

4 Comments

  1. It’s my understanding that there isn’t a significant difference between the amount of food that larger vs. smaller people consume. If you know of studies to the contrary, I’d like to take a look at them.

    Assuming that’s true – that fat people don’t, in general, eat a lot more than thin people – then isn’t this type of research barking up the wrong tree? Maybe the right approach is not to try to get fat people to eat less, but to try to figure out why our bodies like to store so much energy.

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  2. DeeLeigh, the scientific community is generally moving towards a consensus that it is an increase in food intake rather than a decrease in energy expenditure that has been the main driver in the intake / expenditure energy balance equation (here is an example piece of comprehensive research that is evidence against a decline in energy expenditure – http://www.ncbi.nlm.nih.gov/pubmed/18504442).

    Furthermore, a significant number of earlier scientific studies which pointed the figure at a reduced energy expenditure in obese people were studies using self-reported food intake but later studies showed that overweight and obese people under report their intake by 20 – 30%

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  3. I pressed submit a bit early! I was going to continue to say that research using doubly labelled water actually showed that in absolute terms overweight / obese people have higher energy expenditures than their lean counterparts due to the increases in resting metabolism associated with their greater bodymass and increased energy cost of physical activity associated with moving a greater bodymass. Furthermore, the bodymass corrected resting metabolism in overweight / obese people is not significantly different from that of lean people until you start to get to morbidly obese people when the rate of increase does not continue at the same rate (probably because after a certain weight, the proportion of increased bodymass that is metabolically active).

    There are of course a number of other factors that are hypothesised to be contributing to the increase in obesity e.g. decreases in sleep duration, changes in ambient temperature, environmental pollutants, viral infections etc.

    However, targeting energy intake is likely to have the most significant impact on reducing rates of obesity and is and has been the prime focus of the majority of pharmacological interventions. Saying this, there are a number of therapies at the early stage which do not target food intake reduction that have had promising results in pre-clinical and early stage human trials e.g. Ablaris Therapeutic’s Adipotide and Zafgen’s ZGN-433. It would be remiss to fail to note as well that in issue with increasing energy expenditure using drugs has generally been associated with increases in sympathetic nervous system output which lead to increases in blood pressure and/or heart rate that may be counter-productive in diminishing any cardiovascular benefits associated with weight loss.

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  4. Rafi, when i physically measure (by weight or volume, depending on foodstuff) EVERY bite and drink that goes into my body, then enter this information into Fitday, and i find that i average between 1200-1800 calories per day, then HOW on god’s earth can you explain that it’s all about my underestimation of intake that i can’t lose weight? the CICO hypothesis is garbage, and it’s discouraging that researchers keep coming back to it.

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