Hyperlipid

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Faces of the District. Weber Elementary's Marnie Saeugling Comments That means you eat more subsequently. By just enough to make up for the deficit.

Because you skimped on a meal. So there is no weight loss for three weeks My hypothesis is that after three weeks on 40iu of intranasal insulin four times a day the VMH develops CNS insulin resistance.

At this point the effect of intranasal insulin is lost. Also lost is the physiological CNS effect of augmented calorie storage derived from endogenous pancreatic insulin entering the brain. People will then eat more at each meal because it takes longer for their peripheral cells to get full, so there will be more food in the gut at the time of satiation kicking in.

But, with less CNS augmentation of insulin's peripheral action, lipolysis is free to proceed at a higher rate per unit insulin in the blood stream. So hunger is deferred by the augmented availability of stored FFAs. Oxidising these stored FFAs is, by definition, fat loss. Men lose fat mass once they lose the CNS mediated fat storage effect of insulin. That makes sense to me and explains why men who are already insulin resistant derive no benefit from intranasal insulin.

Peter BTW, I'd expect the 40iu dose to work better long term than the iu dose provided the systemic leakage of insulin after iu outweighs the localised effect of developing insulin resistance within the CNS only. At four times the dose the CNS insulin resistance should occur sooner, to facilitate fat loss, but the systemic spill-over will always augment fat storage.

It would be interesting to know what might have happened. Or maybe they did a pilot study and decided not to go there. Posted by Peter at Wednesday, September 12, No comments: Insulin makes you hungry 8 Blokes.

Sunday, September 09, Insulin makes you hungry 7 superoxide is satiety. What causes satiety, if it's not insulin? This has to be understood if there is to be any chance of understanding the effects of intranasal insulin from the metabolic point of view.

Let's begin with individual cells, these are the entities which need to control metabolic substrate availability. You eat some food. In the early stages of food absorption both glucose and FFAs enter cells under the facilitation of insulin.

They do this easily, the cells are "hungry". As an individual cell becomes replete it has to signal that it doesn't want any more metabolic substrate. This is achieved via the CoQ couple acting as the master sensor for metabolic energy status. Given a high delta psi ie minimal consumption of the proton motive force because ATP is already plentiful this CoQ reduction eventually facilitates RET through complex I to give superoxide generation in order to stop insulin signalling.

Which then limits cellular caloric ingress. This can be thought of as the "cellular satiety" signal. It is ROS generated. Let's say that again: Satiety in peripheral cells is an ROS signal. It is generated in the mitochondria. This is pure Protons. Now let's scale that up. As more and more peripheral cells decide that they no longer need to respond to insulin then there is less and less of a "sump" available for absorbed calories to drop in to.

The availability of calories which no longer have anywhere to go is the whole-body driver of the need to signal satiety. These people have the correct sort of idea: Fuel utilization by hypothalamic neurons: Posted by Peter at Sunday, September 09, 2 comments: Insulin makes you hungry 7 superoxide is satiety. Thursday, August 23, Insulin makes you hungry 6 except when you snort it. The action of insulin is the inhibition of lipolysis.

This is our next paper: Intranasal insulin does interesting things. I just wanted to run through the initial results following a single dose of 40iu of intranasal insulin and a subsequent successful! These are the levels of insulin in cerebrospinal fluid CSF of volunteers as measured by sampling through a spinal catheter placed at the L4-L5 level ouch! Posted by Peter at Thursday, August 23, 7 comments: Insulin makes you hungry 6 except when you snort it.

Tuesday, August 21, Another brief housekeeping post. I published the "awaiting moderation" comments. Lots of them are insightful and need a response. Time for this is not looking good at the moment! Please feel free to re comment if you wish. Posted by Peter at Tuesday, August 21, 2 comments: Insulin makes you hungry 5 except when you resist.

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: Friday, August 03, Holiday reading. I'm off on vacation for a while so the next posts are likely to be delayed. If anyone would like a light summary of the ideas I'm thinking about, this is a nice review: Yin and Yang of hypothalamic insulin and leptin signaling in regulating white adipose tissue metabolism For a level deeper of understanding you just need to add in that saturated fats have an FADH2: NADH ratio around 0.

NADH ratio of well below 0. Because a core function of insulin is the inhibition of lipolysis. Posted by Peter at Friday, August 03, 2 comments: Wednesday, August 01, Insulin makes you hungry 4 unless you keep it out of your brain.

Especially via the brain. Where insulin detemir doesn't go. People will be aware that insulin detemir is really strange stuff. There are perfectly respectable papers showing that it cannot enter the brain and blocks the entry of normal insulin in to the brain too or that it is fantastic at entering the brain, much better than more normal insulins. 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. Now there is this paper: 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. As insulin detemir gives less food intake after a normoglycaemic clamp than neutral insulin does, then their conclusion is that insulin detemir is having a more potent central appetite suppressing effect than the neutral insulin.

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. Posted by Peter at Wednesday, August 01, 10 comments: Insulin makes you hungry 4 unless you keep it out of your brain.

Monday, July 30, Insulin makes you hungry 3 a matter of semantics and free fatty acids. There is absolutely nothing technically incorrect with the description of the results contained within the title of this paper: Effects of insulin-induced hypoglycaemia on energy intake and food choice at a subsequent test meal They gave a small dose of insulin low enough to not need rescue glucose within the study period as a single bolus, waited for 20 minutes then offered the subjects an eat-as-much-as you-like buffet.

This is what the glucose levels did. Posted by Peter at Monday, July 30, 5 comments: Insulin makes you hungry 3 a matter of semantics and free fatty acids. Tuesday, July 24, Insulin makes you hungry 2 even in the presence of hyperglycaemia.

This is the paper cited by Woo: Posted by Peter at Tuesday, July 24, No comments: Insulin makes you hungry 1. If you want to think about the central effects of insulin you could do a great deal worse than working through this paper: Brain insulin controls adipose tissue lipolysis and lipogenesis It is jammed full of exquisite quotes: Thus, at the doses administered, brain insulin infusion inhibited lipolysis to a similar extent as that achieved with peripheral hyperinsulinemia" Here it is in pictures.

What does a CNS infusion of insulin do to lipolysis, at what are purported to be physiological dose rates? Obviously, it does exactly what peripheral insulin does, but using minuscule amounts; it suppresses lipolysis: Posted by Peter at Tuesday, July 24, 3 comments: Sunday, July 22, Butter gives you fatty liver!

This paper is an absolute gem: It contains no trace of understanding in its entirety, but the numbers in the results are fascinating. How do we sum it up? If you pay people to over eat kcal per day for three weeks they gain weight and they gain liver fat. Posted by Peter at Sunday, July 22, 14 comments: Butter gives you fatty liver!

Tuesday, July 17, Oops. OMG, just seen how many comments are awaiting moderation now I'm back to occasional posting. I'll see what I can do, if desperate I'll just delete the spam and hit post for them all. Apologies for the inattention over the past few weeks Posted by Peter at Tuesday, July 17, No comments: Woo had a bit of a rant about acipimox.

Here's my simplified idea. I've been interested in acipimox, in a round about sort of a way, for a very long time. To me, the core fascination is that it is not only an effective suppressor of lipolysis, but it is pretty well weight-neutral and it most certainly does not result in weight gain. Which, you have to admit, is interesting.

How can this be? I feel something of a clue can be found in the studies using a similar drug, nicotinic acid. Both drugs effectively suppress plasma free fatty acids via the same receptor but the neatest study happens use nicotinic acid.

People may recall that I posted about the role of FFAs in the secretion of insulin as demonstrated by an isolated rodent pancreatic preparation, some time ago. The core concept here is that insulin secretion is dependent on the chain length and saturation of the FFAs used for perfusing the pancreas along with the glucose.

This phenomenon appears to be well appreciated by the authors of this next paper same research group: Circulating fatty acids are essential for efficient glucose-stimulated insulin secretion after prolonged fasting in humans So what happens to in-tact humans when you fast them for 24 hours to raise FFAs and then bolus them with intravenous glucose?

Or fast them, artificially drop their FFAs with nicotinic acid, and then bolus them with glucose? This is what happens: Posted by Peter at Tuesday, July 17, 8 comments: Monday, May 28, Speculation on the effect of subcutaneous adipocytes implanted in to the mesentery of mice. Taking a piece of subcutaneous fat from a sacrificed mouse and implanting in to the mesentery of a recipient mouse causes weight loss in the recipient , starting once the surgery has healed.

We know that healing takes something just over six weeks: Posted by Peter at Monday, May 28, 6 comments: Speculation on the effect of subcutaneous adipocytes implanted in to the mesentery of mice. Sunday, May 20, Guddling in the dark for a respiratory quotient 2. Multiple papers have values that don't make sense, which is an issue making me doubt my sanity and is damaging to my personal extensive set of confirmation biases.

They also produce basic contradictions of the physiology of the oxidation of glucose vs the oxidation of fatty acids. But now I think I can go back and explain much of the peculiarity in this image from Kahn's group, the one which triggered this previous post. Two sets of mice, on the same chow, having sustained differences in RQ, in a way I couldn't understand: Posted by Peter at Sunday, May 20, 12 comments: Guddling in the dark for a respiratory quotient 2.

I picked up this paper via Face-ache so cannot recall to whom I should credit for the find. The post is also highly speculative.

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