Over the last few years (since 2010) I’ve tried variations of high protein and high fat diets along with zero carb (“keto”) diets and OMAD (One Meal A Day).
They all work. In my case this is at least partly because I pay more attention to what I’m eating and tend to bolus more accurately.
I’ve also at least mentioned these “fad” diets to my endo. He didn’t much care. He didn’t care about my annoying (to me and my wife) habit of scarfing down peanuts late at night; high protein and high fat.
What I did find is that the peanut thing does not help me; it sends me high overnight and I have to wake up (I always do) and rage bolus (I often do) to bring my BG down. OMAD was the best; maybe I got a high afterward but it was manageable and it only happened once a day.
Keto worked fine but it caused me to get annoyed at supermarket checkout stands which had those magazines with “keto” cooking which involved way more carbs than I would ever consumed, keto or not. I did learn quite a bit about how many carbs there are in stuff like coffee (a lot; it’s a bean) and vegetables; it is necessary to cut back on the veggies a lot.
But yes; eating less reduces hunger.
For me exercising more (a lot more) also reduces hunger.
Both of these things (more exercise, less food) reduce my insulin resistance but the biggest effect by far is the massive reduction from significant increases in exercise level. I don’t have enough experience but I suspect the “massive” part of that is temporary; if I did, in fact, keep up that exercise level my metabolism would, I think, level off and my insulin resistance, while lower, wouldn’t be that low.
So if a GLP-1 [receptor] agonist reduces appetite and, as a result, food intake then I would certainly expect it to lower insulin resistance in those of us with higher than minimal food intake (e.g. me but not necessarily @Terry ).
I guess that is, in fact, testable; what happens when people with low but sufficient calorie diets, where the calorific intake is close to the minimum to sustain life when they take GLP-1s? Show me the research… Alternatively what happens to the insulin resistance of people who take GLP-1s but continue to consume their previous, stable, amount of calories?
Note that I am not dissing GLP-1s; I know full well that my T2, never overweight, eldest brother-in-law has been doing nicely with the one he is taking. Whatever it is doing it is helping him deal with the problems of reduced mobility (seriously damaged back) and, perhaps, lack of exercise.
That’s my current conclusion for GLP-1s; they really are a useful tool for many people but they are not a solution in themselves, rather a means to a solution which might otherwise be unattainable.