tag:blogger.com,1999:blog-1629175743855013102.post5469989443860652914..comments2024-02-25T02:24:14.972-08:00Comments on Whole Health Source: Fat Tissue Insulin Sensitivity and ObesityStephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger84125tag:blogger.com,1999:blog-1629175743855013102.post-43616265070713745122011-10-26T21:41:13.723-07:002011-10-26T21:41:13.723-07:00Hi Steohan,
I have a question on Insulin Resistan...Hi Steohan,<br /><br />I have a question on Insulin Resistance...<br /><br />Does IR have any effect on calories in vs out? i.e. how does it effect weight loss/weight gain? does the person with IR have more of the incoming calories stored as fat (rather than muscle or "other areas where it is needed") than the non-IR person?<br /><br />Thanks!Thomas Thttps://www.blogger.com/profile/10865769658020737018noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-39881662471258219982011-10-15T07:20:22.726-07:002011-10-15T07:20:22.726-07:00http://vimeo.com/27563465
warning: might cause co...http://vimeo.com/27563465<br /><br />warning: might cause cognitive dissonance?STGhttps://www.blogger.com/profile/09380122485704802342noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-79539659701370577452011-10-06T09:15:38.208-07:002011-10-06T09:15:38.208-07:00interesting article, by the way if you have leaky ...interesting article, by the way if you have leaky fat cells that is bad, this is a indication that the fat cells cell membranes are deficient in cholesterol. this keeps the cells guts intact.<br /><br />also fat cells can release fat in high insulin simply because the other cells cannot use glucose very well and depend on fat more than anything and hence adrenalin forces fat release in enviroment of high insulin, hence the gitteriness and hard to sleep at night problem when insulin levels are still to high.<br /><br />also fat cells can become glucose intolerant due to malnutrtion lack of enough calcium, fats, vita d, cholesterol to handle the transport of a highly oxidative substance as gluocose through their cytoplasm to the mitrochondria, <br /><br />this happens in all cells not just fat cells in fact fat cells are also responsible for cholesterol storage, cholesterol repair, and storage of fat soluable vitamins when these tend to be reduced. hoarding as it were prventing other cells from having calcium vita d etc for themselves to handle glucose. if you are releaseing calcitron (I can't spell worth anyting) your fat cells will proliferate to handle the storage needs of a glucose intolerant person, also your fat cells are responsible for turning glucose into fat and if your cells cannot use gluocse they have to use fat. in other words you get fat due to malfunction of your metabolism. <br /><br />malnutrtion will ensure this, if your a dieter (hypocaloire diets) or a low fat eater, or heavy process eater your malnorished. personally I did not realize glucose was like gasoline in your system it reacts readily to oxygen. and whoever said our inners were combustion engines especially if you don't change to oil or put oil in there in sufficient quantity in the first place or use poor quality oils.<br /><br />in fat saturated fats are the most least oxidative substance for fuel. it lasts longer and oh yea forgot your fats are not just used for energy, but for cellular membranes which turnover fats daily as the fat become rancid. 50 percent of cells are composed of fats. cholesterol too which has to be turned over regularly for repair.<br /><br />source is article the "obesity is the metabolic syndrome a nutrtional deficency" with links to other articles about cholesterol and sat fat and glucose and fructose. check it out.<br /><br />rosarobrobhttps://www.blogger.com/profile/08543110396112149963noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-85704428465324161292011-09-21T01:06:14.667-07:002011-09-21T01:06:14.667-07:00I think the food reward hypothesis is an interesti...I think the food reward hypothesis is an interesting and credible insight into <a href="http://www.bhrcenter.com/weight-gain-in-women.html" rel="nofollow">weight gain</a>, and it certainly deserves further study.Unknownhttps://www.blogger.com/profile/09280579387453233846noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-80690864280824018942011-09-20T20:28:42.160-07:002011-09-20T20:28:42.160-07:00I am having my first serious challenge to the blan...I am having my first serious challenge to the bland food diet - I really want Cheetos!Laurahttps://www.blogger.com/profile/08714172233493373383noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75955729456917324802011-09-20T14:39:36.255-07:002011-09-20T14:39:36.255-07:00Interesting about the gut flora.
Additionally, d...Interesting about the gut flora. <br /><br />Additionally, didn't Cincotta and Meier find insulin sensitivity controlled by the brain?<br /><br />and yet, the topic is always discussed from the angle of peripheral tissue.Terryhttps://www.blogger.com/profile/11021251810761751772noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-52647930567561127292011-09-19T08:44:00.543-07:002011-09-19T08:44:00.543-07:00Obese patients with a constellation of symptoms kn...Obese patients with a constellation of symptoms known as prediabetes improved insulin sensitivity with a fecal transplant from healthy thin donors, researchers here reported.<br /><br />Click here for the full story: http://www.medpagetoday.com/MeetingCoverage/EASD/22352Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-4217025826645772972011-09-19T04:05:56.308-07:002011-09-19T04:05:56.308-07:00I second rosenfeltc. More fermented buckwheat, les...I second rosenfeltc. More fermented buckwheat, less Taubes. <br /><br /><br /><br /><a href="http://www.genericwebpharmacy.com" rel="nofollow">generic pharmacy</a>Unknownhttps://www.blogger.com/profile/02238642535794619680noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-2307072571298919242011-09-18T08:59:51.350-07:002011-09-18T08:59:51.350-07:00@dimsum,
There's often little point arguing a...@dimsum,<br /><br />There's often little point arguing about which analogy more closely reflects reality, because the trouble with analogies is they're never exact.<br /><br />However, the evidence is that insulin resistance is related to the size of the adipocyte. Your analogy decouples the analogue of insulin resistance from the analogue of adipocyte size, so it doesn't seem likely to explain very much.<br /><br />You could modify your analogy so that the efficiency of the pump is somehow affected by the size of the balloon, but then explore what happens. The only way of reducing the efficiency of the pump is to increase the volume of the balloon and that means the fuel supply must first have increased. The fuel supply doesn't increase instantaneously, so it is unphysical to imagine that you can go from a state in which the balloon is being inflated (the fuel supply increased a bit) to a state in which the balloon is deflating (the pump efficiency decreased ) without going through an intermediate state in which the balloon is neither inflating nor deflating (the reduction in pump efficiency exactly balanced the increased fuel supply). Once you reach that state, that's where you stay, but importantly, the balloon is a bit bigger than it was.<br /><br />This is the consequence of any dynamic equilibrium or “settling point” explanation. The specifics of how insulin sensitivity varies with adipocyte size do not matter, all that matters is that the former depends on the latter; in that case, more insulin will ALWAYS correspond to a larger adipocyte for the reasons I just gave.Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75758431104804995832011-09-18T07:58:49.130-07:002011-09-18T07:58:49.130-07:00@Todd and Strontium
I think the leaky balloon anal...@Todd and Strontium<br />I think the leaky balloon analogy is a bit off – insulin is not the balloon pump. Instead, it is more like the fuel the balloon pump uses to do its job. The more fuel the body supplies to the pump, the more pressure it provides. Now suppose the balloon pump for some reason becomes less efficient at using the fuel. Then the pump needs to be provided with more fuel in order to maintain the same level of pressure. Increased fuel (insulin) only results in a bigger balloon if the increase is sufficiently large enough to overcome the decreased efficiency of the pump. <br /><br />While it’s theoretically possible for hyperinsulinemia in the obese be high enough to overcome the effects of insulin resistance, there doesn’t seem to be any evidence that this is what is happening, and quite a bit of evidence against it. <br /><br />It’s possible there are other pathways by which hyperinsulinemia might be a factor in the development of obesity, like leptin resistance or reactive hypoglycemia. But the specific theory Taubes has advocated doesn’t seem to be plausible.dim sum massacrehttps://www.blogger.com/profile/15564410185844037045noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-6279327631604454222011-09-18T03:26:58.301-07:002011-09-18T03:26:58.301-07:00@Evelyn,
Thanks for pointing that out! I should p...@Evelyn,<br /><br />Thanks for pointing that out! I should proofread my posts a bit better ...<br /><br />I should have said VLDL, but the point remains, I think.Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-6346540599917405892011-09-17T21:15:15.897-07:002011-09-17T21:15:15.897-07:00...
4. Geoff “ultimately, the hypothalamus decide......<br /><br />4. Geoff “ultimately, the hypothalamus decides whether to release fat or not based on what it thinks is going on in the body. Again, I would say that the "weak" form of the insulin hypothesis put forward has much more problems explaining the release from fat tissue, because somehow the body needs to get access to this fat in spite of the elevated insulin inhibiting lipolysis.”<br /><br />Todd: The hypothalamus’ “decision” about whether to release fat is governed by how much leptin crosses the blood-brain barrier. Hyperinsulinemia impairs detection of leptin, so the body holds onto fat. This is a direct consequence of the weak insulin hypothesis, which holds that both carbohydrates AND insulin resistance are required for obesity. While hyperinsulinemia thus “inhibits” lipolysis and fat oxidation, it certainly doesn’t shut it down. This inhibition becomes progressively inefficient in advanced obesity, while still being sufficient to maintain obesity. – as Strontium’s “balloon” analogy nicely illustrates. However, if you administer ocretotide or another insulin agonist, obesity disappears!<br /><br />The weak insulin hypothesis is consistent with all the above facts, so I see no reason to abandon it at this point.Toddhttps://www.blogger.com/profile/03405544644098341454noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-76864952938474743622011-09-17T21:14:31.032-07:002011-09-17T21:14:31.032-07:00Geoff,
I’d like to address a few points you’ve ma...Geoff,<br /><br />I’d like to address a few points you’ve made:<br /><br />1. Geoff: “Imagine the body is a car. In this car, insulin would be like the wheels, leptin is the engine, and the hypothalamus is the driver.”<br /><br />Todd: I fail to see how this analogy explains obesity. Obesity is not caused by excess insulin or leptin, but rather by insensitivity (“resistance”) to insulin and leptin (in combination with an insulin stimulus like carbohydrates). There is no exact car analogy, but it would be like a car with a plugged or leaky fuel valve that responded slowly and inefficiently to the accelerator, so it would “grow” a larger gas tank and waste gas trying to get up to speed or something. This inefficiency “explains” why the driver pushes the gas pedal excessively. There is no need for psychological postulates about the driver.<br /><br />2. Geoff: “…people who are hyperinsulinemic, as far as I know, usually or always have high fasting glucose. The question is what causes this high fasting glucose, and I don't think that dietary carbohydrates are a good explanation for this.”<br /><br />Todd: I agree that dietary carbohydrates don’t cause hyperinsulinemia or hyperglycemia. The cause of elevated blood glucose is no mystery: Insulin resistance reduces the number and efficiency GLUT4, allowing glucose levels to rise. The pancreas upregulates insulin secretion to counteract this to some extent, but process is still inefficient. Once IR is in place, however, carbohydrate ingestion maintains obesity by not allowing basal insulin to fall.<br /><br />3. Geoff: “You still have not explained how the body of an obese, IR individual goes into overdrive in response to overeating if it is insulin driving fat storage in response to dietary carbohydrates rather than the brain in response to elevated leptin levels in the blood. This is the major problem with settling point theories of obesity. They explain what prevents the level from going down, but they don't explain what prevents it from going up.”<br /><br />Todd: It’s not either/or. It is the combination of IR and carbohydrates that drive obesity. The weak insulin hypothesis holds only that high carbohydrate consumption is a necessary condition; insulin- (and leptin-) resistance are also required to drive obesity. <br /><br />You claim that leptin resistance, not insulin resistance is the driver (or at least a necessary condition) for obesity. However, experiments by Lustig suggest that hyperinsulinemia causes leptin resistance:<br /><br />http://bit.ly/r0BpDV<br /><br />By administering an insulin agonist (octreotide-LAR) to obese adults, he reversed their hyperinsulinemia and secondarily their leptin resistance, leading to dramatic weight loss. This is a pretty strong demonstration of the essential causal role that hyperinsulinemia (which results from IR) plays in obesity. <br /><br />...to be continuedToddhttps://www.blogger.com/profile/03405544644098341454noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-60572945582061373902011-09-17T21:12:24.869-07:002011-09-17T21:12:24.869-07:00Geoff,
I’d like to address a few points you’ve ma...Geoff,<br /><br />I’d like to address a few points you’ve made:<br /><br />1. Geoff: “Imagine the body is a car. In this car, insulin would be like the wheels, leptin is the engine, and the hypothalamus is the driver.”<br /><br />Todd: I fail to see how this analogy explains obesity. Obesity is not caused by excess insulin or leptin, but rather by insensitivity (“resistance”) to insulin and leptin (in combination with an insulin stimulus like carbohydrates). There is no exact car analogy, but it would be like a car with a plugged or leaky fuel valve that responded slowly and inefficiently to the accelerator, so it would “grow” a larger gas tank and waste gas trying to get up to speed or something. This inefficiency “explains” why the driver pushes the gas pedal excessively. There is no need for psychological postulates about the driver.<br /><br />2. Geoff: “…people who are hyperinsulinemic, as far as I know, usually or always have high fasting glucose. The question is what causes this high fasting glucose, and I don't think that dietary carbohydrates are a good explanation for this.”<br /><br />Todd: I agree that dietary carbohydrates don’t cause hyperinsulinemia or hyperglycemia. The cause of elevated blood glucose is no mystery: Insulin resistance reduces the number and efficiency GLUT4, allowing glucose levels to rise. The pancreas upregulates insulin secretion to counteract this to some extent, but process is still inefficient. Once IR is in place, however, carbohydrate ingestion maintains obesity by not allowing basal insulin to fall.<br /><br />3. Geoff: “You still have not explained how the body of an obese, IR individual goes into overdrive in response to overeating if it is insulin driving fat storage in response to dietary carbohydrates rather than the brain in response to elevated leptin levels in the blood. This is the major problem with settling point theories of obesity. They explain what prevents the level from going down, but they don't explain what prevents it from going up.”<br /><br />Todd: It’s not either/or. It is the combination of IR and carbohydrates that drive obesity. The weak insulin hypothesis holds only that high carbohydrate consumption is a necessary condition; insulin- (and leptin-) resistance are also required to drive obesity. <br /><br />You claim that leptin resistance, not insulin resistance is the driver (or at least a necessary condition) for obesity. However, experiments by Lustig suggest that hyperinsulinemia causes leptin resistance:<br /><br />http://bit.ly/r0BpDV<br /><br />By administering an insulin agonist (octreotide-LAR) to obese adults, he reversed their hyperinsulinemia and secondarily their leptin resistance, leading to dramatic weight loss. This is a pretty strong demonstration of the essential causal role that hyperinsulinemia (which results from IR) plays in obesity. <br /><br />4. Geoff “ultimately, the hypothalamus decides whether to release fat or not based on what it thinks is going on in the body. Again, I would say that the "weak" form of the insulin hypothesis put forward has much more problems explaining the release from fat tissue, because somehow the body needs to get access to this fat in spite of the elevated insulin inhibiting lipolysis.”<br /><br />Todd: The hypothalamus’ “decision” about whether to release fat is governed by how much leptin crosses the blood-brain barrier. Hyperinsulinemia impairs detection of leptin, so the body holds onto fat. This is a direct consequence of the weak insulin hypothesis, which holds that both carbohydrates AND insulin resistance are required for obesity. While hyperinsulinemia thus “inhibits” lipolysis and fat oxidation, it certainly doesn’t shut it down. This inhibition becomes progressively inefficient in advanced obesity, while still being sufficient to maintain obesity. – as Strontium’s “balloon” analogy nicely illustrates. However, if you administer ocretotide or another insulin agonist, obesity disappears!<br /><br />The weak insulin hypothesis is consistent with all the above facts, so I see no reason to abandon it at this point.Toddhttps://www.blogger.com/profile/03405544644098341454noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-44587557077593993092011-09-17T18:34:35.978-07:002011-09-17T18:34:35.978-07:00@Strontium Pup: "If there's little trigl...@Strontium Pup: <i>"If there's little triglyceride synthesis, there will be far fewer chylomicrons and thus there will be far less substrate for the action of LPL. "</i><br /><br />Chylomicrons are solely the lipoprotein particles from dietary fat. The liver makes triglyceride lipoproteins from chylo remnants, but the chylos themselves are distinct.CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-60881953757699087892011-09-17T14:52:46.725-07:002011-09-17T14:52:46.725-07:00A better way of expressing my point about Chris Ma...A better way of expressing my point about Chris Masterjohn's post is this.<br /><br />From his ref. 13: They [the LIRKO mice] also display focal dysplasia and hyperplastic nodules in their livers and a 50% reduction in albumin levels, as well as a similar reduction in serum triglycerides and free fatty acids (9, 10), which could be explained, at least in part, by the inability of insulin to promote triglyceride synthesis in liver ...<br /><br />If there's little triglyceride synthesis, there will be far fewer chylomicrons and thus there will be far less substrate for the action of LPL. This will considerably blunt the efficacy of insulin to promote fat accumulation, so the high insulin levels would not necessarily be expected to result in obesity.Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-50978168845346749142011-09-16T15:45:23.653-07:002011-09-16T15:45:23.653-07:00Some Wikipedia definitions:
http://en.wikipedia.o...Some Wikipedia definitions:<br /><br />http://en.wikipedia.org/wiki/Sensory-specific_satiety<br />http://en.wikipedia.org/wiki/Palatability.https://www.blogger.com/profile/09917531397118353422noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-32607327201519872632011-09-16T14:28:52.634-07:002011-09-16T14:28:52.634-07:00@Geoff,
Dude, our minds are never going to meet o...@Geoff,<br /><br />Dude, our minds are never going to meet on this one, but it's been fun.Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-30220370707058898342011-09-16T14:00:47.052-07:002011-09-16T14:00:47.052-07:00@Strontium Pup
"For example, how does your m...@Strontium Pup<br /><br />"For example, how does your model explain the release of fuel from the fat cells, mechanistically?"<br /><br />There are probably a number of ways this happens, but ultimately, the hypothalamus decides whether to release fat or not based on what it thinks is going on in the body. Again, I would say that the "weak" form of the insulin hypothesis put forward has much more problems explaining the release from fat tissue, because somehow the body needs to get access to this fat in spite of the elevated insulin inhibiting lipolysis.<br /><br />It excludes the insulin hypothesis because it posits that insulin is a slave in a master-slave relationship. Insulin is the hammer, not the guy swinging it.Geoffhttps://www.blogger.com/profile/08509184330732763342noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-76539899531382435182011-09-16T12:33:17.614-07:002011-09-16T12:33:17.614-07:00@Geoff,
I like your tenacity.
I agree with you t...@Geoff,<br /><br />I like your tenacity.<br /><br />I agree with you that excess dietary carbohydrate is an unlikely explanation of fasting hyperglycaemia, but I don't see the relevance of that to Todd's “weak” hypothesis.<br /><br />As to postprandial thermogenesis in the obese, in a previous post, you suggested that the mechanism is something like: excess calories → fat storage → increased leptin → thermogenesis. What I don't understand is how this excludes the insulin hypothesis. How about: excess calories (some of which are carbohydrate) → BG excursion → insulin secretion → fat storage → increased leptin → thermogenesis? I don't say this is what happens, I say it is not inconsistent with your ideas. Also bear in mind that leptin is secreted by the peripheral tissues in response to nutrient sensing: excess calories → increased leptin → thermogenesis.<br /><br />I think the settling point models have additional explanatory power. For example, how does your model explain the release of fuel from the fat cells, mechanistically? The insulin hypothesis would say: thermogenesis (which includes glucose oxidation) → lower BG → lower insulin → FFA release → lower leptin → less thermogenesis → a new settling point, eventually.<br /><br />I'm not here to defend the insulin hypothesis because I believe in it; I'm saying that many of the arguments that have been deployed here (like the insulin resistance argument) to demolish it, do not. To that extent, they get in the way of an objective assessment and I don't think that's helpful.Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-42610780090709929472011-09-16T07:03:42.177-07:002011-09-16T07:03:42.177-07:00@Strontium Pup
I explain everything related to in...@Strontium Pup<br /><br />I explain everything related to insulin in that post by the following: leptin resistance causes obesity and insulin resistance. Stephan made a great analogy in the comments on another post somewhere. Imagine the body is a car. In this car, insulin would be like the wheels, leptin is the engine, and the hypothalamus is the driver. So while the car cannot drive without the wheels, which is like a type 1 diabetic trying to store fat, it is not the wheels that drive the car. In fact it isn't even the engine, although the engine does power the wheels. It is the person pushing the gas pedal that drives the car. <br /><br />To the question of hypoglycemia, again, I really don't know enough about it to comment, but people who are hyperinsulinemic, as far as I know, usually or always have high fasting glucose. The question is what causes this high fasting glucose, and I don't think that dietary carbohydrates are a good explanation for this. There are too many counter examples. I think that the neolithic agents of disease are a better explanation, and I am including hyperrewarding properties in there as the fourth NAD, though I suspect that it is possible that at the end of the day, it may turn out that the hyperrewarding foods are the NADs, particularly linoleic acid and wheat.<br /><br />You still have not explained how the body of an obese, IR individual goes into overdrive in response to overeating if it is insulin driving fat storage in response to dietary carbohydrates rather than the brain in response to elevated leptin levels in the blood. This is the major problem with settling point theories of obesity. They explain what prevents the level from going down, but they don't explain what prevents it from going up.Geoffhttps://www.blogger.com/profile/08509184330732763342noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-80267316612023597122011-09-16T05:49:46.262-07:002011-09-16T05:49:46.262-07:00congrats! keep up the good work/this is a great pr...congrats! keep up the good work/this is a great presentation. <br /><br /><a href="http://diabetes2diabetic.com/pre-diabetes-diet/" rel="nofollow">Pre Diabetes Diet</a>Vanihttps://www.blogger.com/profile/01629544079087502422noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-61929309609454488312011-09-16T01:19:27.762-07:002011-09-16T01:19:27.762-07:00@Geoff,
Thanks from me too for the link to Chris ...@Geoff,<br /><br />Thanks from me too for the link to Chris Masterjohn’s leptin post. Food for thought indeed.<br /><br />There's no doubt leptin plays a significant role in all this.<br /><br />When I first read Chris's commentary on the LIRKO mice, I thought, “RIP insulin hypothesis.” But then I thought, hang on, is he right when he says, “So if high insulin levels are what act on our adipose tissue to make us fat, these mice should be really, really, really fat?”<br /><br />Even if you adopt the position that the insulin hypothesis describes everything as far as overall fat mass is concerned, you still don’t conclude that higher insulin (in the LIRKO mice) implies higher fat mass, because insulin is only going to promote fat storage if there’s fat to be stored. In other words, you would expect the rate of fat storage to depend on insulin, yes, but also on the levels of circulating TGs and FFAs, and in the LIRKO mice, TGs and FFAs are about half what they are in the controls.<br /><br />At a naïve level, you might then think that the insulin-promoted influx of FFAs into the fat tissue is going to be about half what you would expect so see in the controls. How would that explain away a seven-fold increase in fasting insulin? The answer could be that the reduction in plasma TGs and FFAs results in a huge increase in the FFAs leaving the cells because of an enormous change in the relative concentrations of FFAs on either side of the cell membrane.<br /><br />Go back to my balloon “analogy” and imagine that the pump is running along nicely and keeping the pressure inside the balloon about 20% higher than atmospheric. Let’s say that maps onto a normal individual with normal insulin levels.<br /><br />Now, what happens if you suddenly reduce the external air pressure by 50%? Answer: the pump is now only half as efficient and the pressure difference across the skin of the balloon goes from 20% of an atmosphere to 70% of an atmosphere: 3½ times as much. By how much do I need to increase the work rate of the pump to keep things as they were? By a factor of seven.<br /><br />So, it is by no means clear that the increased insulin levels in the LIRKO mice should be obesogenic if the insulin hypothesis is correct, because you have to take into account the other changes (including plasma FFA and TG concentrations) as compared with the controls.<br /><br />Maybe I should ask Chris for his views on this?Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-55135126549275714482011-09-15T22:54:20.537-07:002011-09-15T22:54:20.537-07:00@rosenfeltc & John,
I third Rosenfeltc.
i...@rosenfeltc & John,<br /><br />I third Rosenfeltc.<br /><br />i'm also more interested in health & prevention of civilized (degenerative) diseases rather than obesity.<br /><br />regards,Dr. Curmudgeon Geehttps://www.blogger.com/profile/14484363083738134100noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-41201543087998711032011-09-15T21:40:25.733-07:002011-09-15T21:40:25.733-07:00Quick question--seeing as how insulin has been vin...Quick question--seeing as how insulin has been vindicated, more or less, who is the conductor on the train to hell? More clearly--who should I be blaming when i get fatigued after eating a high carb meal (coming from whole foods)?<br /><br />Also, if it's possible, is there anyone who can compile a list of necessary foods we should be eating, nutrient wise? I feel like this is a more logical way of compiling a healthy way to eat (i.e. eat liver once/twice a week, make sure to get eggs daily for choline, tubers for vit c..etc); the "goodness" (or badness) of calories seems to be determined by the nutrients they shuttle in, and the predominance of macronutrients (high/low carb) should be controlled by these very conditions (i.e. certain macros being more beneficial in their ability to transport certain micronutrients--indirectly through a mechanism such as insulin, or directly through the intrinsic nutrient stores of such foods)psychic24https://www.blogger.com/profile/02007506132069495095noreply@blogger.com