Petro sex

You need to get calories from somewhere, should it be from carbohydrate or fat? I’m off on vacation for a while so the next posts are likely to be delayed. For a level deeper of understanding you just need to add in that saturated fats have an FADH2:NADH ratio around 0. 49 which is the physiological signal for insulin resistance and Petro sex generate one of around 0.

47, giving the signal for insulin sensitivity. Adding in PUFA as a bulk calorie source, with an insulin hyper-sensitivity generating FADH2:NADH ratio of well below 0. Because a core function of insulin is the inhibition of lipolysis. TLDR: The function of insulin is the inhibition of lipolysis. People will be aware that insulin detemir is really strange stuff.

There are probably more studies in the latter camp but my biases push me towards the former camp. The nature of the researchers also tends to push me towards the former camp. I posted on insulin detemir here and here to explain my point of view. Just eyeballing the insulin doses used we can assume that the plasma insulin levels were a reasonable approximation for humans in the normal post prandial period, ie physiological fed-state rather than pharmacological.

The research group is completely wedded to the idea that central insulin is an appetite suppressant and that weight gain from any insulin therapy is only a reaction to recurrent hypoglycamia. As there is no hypoglycaemia during the clamps their presumption is that this neutral insulin infusion results in a reduced food intake. They are so confident about this that the inclusion of a control situation, where saline was infused without any insulin and appetite was checked after this, was considered un-necessary. This really is the level of research in the “satiety” insulin camp. You can see why a control group was omitted by the “satiety from insulin” paper. I rather like insulin determir compared to any other insulin but you can see it has its work cut out to beat saline as a satiety hormone! Simplest explanation: Insulin in the brain decreases peripheral lipolysis.

This makes you hungry after an hyperinsulinaemic clamp. Insulin detemir doesn’t enter the brain so has no CNS augmentation of its peripheral suppressive effect on lipolysis at a given level of glucose control, so it generates less hunger. I’m a simple sort of a person. 20 minutes then offered the subjects an eat-as-much-as you-like buffet. That will be 1700kcal after an hypoglycaemic glucose of 2. 1400kcal after a blood glucose of 4. Glucose drop and kcal increase are both p less than 0.

Next is this one, not quite so good because the title omits the word “insulin”, but never mind. Here they infused insulin to a glucose nadir of 2. Total sleep time was about six and a half hours on each occasion. At feeding time all of the subjects were normoglycaemic. An hypo just after you have fallen asleep the evening before might do as well but the p value is ns for this test. In general we can say any hypo leaves you hungry.

But both studies did two separate things. They generated hypoglycaemia and they gave insulin. The assumption is that it was the hypoglycaemia which drove the hunger. Even if the hypoglycaemia was long gone at feeding time. You’ve noticed that this second paper did not have a group given insulin combined with intravenous glucose to protect against hypoglycaemia, isolating the effect of the insulin alone. But then we all know what that would have shown. Let’s look at this from the real world point of view, which is: The function of insulin is the inhibition of lipolysis.