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The function of insulin is the inhibition of lipolysis. Does resisting insulin facilitate lipolysis? This the next paper: How can I already tell they are going to find that insulin suppresses appetite?
End aside, sniggering excepted. The only parts I am interested in are the clamps and the appetite scores no food intakes in this one. So we have a low insulin clamp and a high insulin clamp looking a lot like this: These are the hunger ratings during the clamps: I think we can say that hunger kicked in at around minutes under the low dose insulin clamp and at around minutes in the high dose insulin clamp.
We'll never know because So anyway, there we have it. Time to shut up shop and go back to kayaking in my free time. But just one moment. I think it might be worth looking at this study in the units of insulin concentration that we are most used to working with.
In old money that is 6. This is pretty well "normal" for physiological post prandial insulin after eating a meal of junk. If anyone thinks this sort of insulin level has anything to do with appetite control in the physiology of humans, then they may be mistaken.
But this level of insulin exposure does delay the onset of hunger, by over two hours in this study Now, here is a sideways way of looking at CNS insulin. If the physiological role of insulin in the VMH is to augment fat storage, what might be the effect of CNS insulin resistance?
I dare you to say that the effect might be partial failure to suppress lipolysis, less suppression of FFAs and so reduced appetite augmentation.
Resisting insulin allows you to resist its hunger generating effects. How's that for a bizarre idea? Feel free to point out faults in the logic. I've long been interested in the concept that exposure to insulin itself induces insulin resistance.
There are a whole slew of papers to suggest this, some better than others. Overall I find the concept quite convincing. If we want to actually see insulin resistance kick in rapidly, and measure it, we have to go to cell culture.
Here we can overdose by decent amounts, using nanomoles rather than picomoles, and watch the reduction in signalling triggered by these high insulin concentrations.
Insulin receptor IR phosphorylation drops within 45 minutes from the initial peak at 10 minutes after exposure. It's in this paper if anyone is interested in the details Insulin Resistance Induced by Hyperinsulinemia Coincides with a Persistent Alteration at the Insulin Receptor Tyrosine Kinase Domain but this is a typical graph: If we convert the nanomolar concnetration from cell culture to the picomoles of in-vivo clamps then the two higher concentrations used in this graph would be 17,pmol and ,pmol, similar to those from the high dose clamp used in the human study.
Especially when you consider that 17,pmol and ,pmol have indistinguishable effects on IR phosphorylation and acute generation of resistance to that phosphorylation effect in cell culture. That limitation on insulin signalling would obtund the normal inhibition of lipolysis but not eliminate it entirely and so defer the normal onset of hunger routinely induced by the physiological action of insulin.
Obviously no one does a study without a pilot trial to make sure they will get the results they want. A saline infusion produces no significant increase in hunger over minutesthough the trend in hunger is upwards because supper was a long time ago by the end of that particular study!
I'll take a pause here because I think this current concept is quite controversial enough to be stated as simply as possible. Obviously there are more studies which we can look at to explore the usefulness of this idea.of over 7, results for "high quality paper plates" Amazon's Choice for "high quality paper plates" Premium Quality Heavyweight Plastic Plates China Like.
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