Welcome to r/science! This is a heavily moderated subreddit in order to keep the discussion on science. However, we recognize that many people want to discuss how they feel the research relates to their own personal lives, so to give people a space to do that, personal anecdotes are allowed as responses to this comment. Any anecdotal comments elsewhere in the discussion will be removed and our normal comment rules apply to all other comments.

I am a bot, and this action was performed automatically. Please contact the moderators of this subreddit if you have any questions or concerns.

Abstract: >Animals must adapt their dietary choices to meet their nutritional needs. How these needs are detected and translated into nutrient-specific appetites that drive food-choice behaviours is poorly understood. Here we show that enteroendocrine cells of the adult female Drosophila midgut sense nutrients and in response release neuropeptide F (NPF), which is an ortholog of mammalian neuropeptide Y-family gut-brain hormones. Gut-derived NPF acts on glucagon-like adipokinetic hormone (AKH) signalling to induce sugar satiety and increase consumption of protein-rich food, and on adipose tissue to promote storage of ingested nutrients. Suppression of NPF-mediated gut signalling leads to overconsumption of dietary sugar while simultaneously decreasing intake of protein-rich yeast. Furthermore, gut-derived NPF has a female-specific function in promoting consumption of protein-containing food in mated females. Together, our findings suggest that gut NPF-to-AKH signalling modulates specific appetites and regulates food choice to ensure homeostatic consumption of nutrients, providing insight into the hormonal mechanisms that underlie nutrient-specific hungers.

I wonder how efficient that method of "diet" would be.

It surpresses sugar cravings, but promotes storage of fats. Depends on the balance of these effects, but I'm guessing it'll end up cancelling eachother out.

I guess it depends if it helps break an addiction and leads to better long term eating. A month or two of gaining fat to change long term diet into a healthier one once off this hormone would be a worthwhile exchange for many people.

Advertisements are stronger. We should ban them first and I would expect quite a change.

Exactly. Disgusts me that we allow companies to plaster all their products in vibrant colours, mascots, questionable wording. The kids are especially vulnerable to this sort of advertising. And ironically kids food are some of the most unhealthy, especially in terms of how calorie-dense they are.

Doesn’t that sound exactly like the sort of thing somebody wishing to enter ketosis would be seeking?

This is basically how the new diabetic medication mounjaro works. It's a glp-1/gip and it's extremely effective at weight loss.

[removed]

Isn’t “promoting storage of fats” the same as saying “reduces glycogen available for muscles and brain”? So would this lead to lower energy levels? Seems like we’re attenuating one of the only benefits of fast absorbing carbs.

Quite interesting.

I’ve also often wondered if any hormones are mediated by bacteria and other parts of the microbiome.

That and trying to find food without sugar. There are about 20 different names for sugar and they all use it to conceal what's in the food. Wife had to do a sugar free diet one time holy crap what a pita it's in everything.

So what makes this work differently than a GLP-1 agonist? everything hear sounds like this is another potential weight-loss drug by a well known mechanism

I'd make an existential wager on the accumulation of evidence for similar mechanisms influencing metabolic pathways in human appetite.

[removed]

Those melanogasters were always binge eaters, good they found a solution.

Drosophila melanogaster is a name i hope to forget one day

Yep, it's in a pita.

[removed]

Other way around, they want the fat cells to be releasing energy not storing it, I think?

> These NPF-induced changes in food intake were likewise not associated with altered triacylglyceride (TAG) or circulating sugar levels (Extended Data Fig. 1l,m), supporting a direct role for gut-derived NPF in governing feeding behaviour, rather than effects of NPF on metabolism that then lead secondarily to altered behaviour. Together, these results indicate that NPF from these EECs is both necessary and sufficient to inhibit food intake and prevent food overconsumption.

GLP-1 agonists alter insulin patterns and average blood sugar, in addition to appetite suppression and modifying feeding behavior.

Seems like this drug, analogue to NPY in humans, mainly affects feeding behaviors.