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  1. #1
    Rebelling in my psychosis thegymbum's Avatar
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    Glucagon/Lipolysis

    I was doing some reading and had a thought that's been on my mind. In contrast to a carbohyudrate rich meal, one major stimulus for glucagon secretion is a high fat/protein meal containing only negligible amounts of carbohydrate. With only negligible amounts of carbohydrate, insulin secretion is of course at a minimum, discounting the contribution of certain glucogenic amino acids and the direct insulin stimulation of some amino acids. So this sort of diet favors high postprandial levels of glucagon with very low insulin levels. Anyway, my point is, one of the major effects of glucagon is to increase lipolysis in adipose tissue. So I was wondering... how significant is this effect? Is it enough that it would promote a significant amount of lipolysis and contribute to decreased fat mass? Just a thought, if so it would give yet another reason that ketogenic diets can be beneficial.
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  2. #2
    Not Swimming. Emma-Leigh's Avatar
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    Originally Posted by thegymbum View Post
    I was doing some reading and had a thought that's been on my mind. In contrast to a carbohyudrate rich meal, one major stimulus for glucagon secretion is a high fat/protein meal containing only negligible amounts of carbohydrate. With only negligible amounts of carbohydrate, insulin secretion is of course at a minimum, discounting the contribution of certain glucogenic amino acids and the direct insulin stimulation of some amino acids. So this sort of diet favors high postprandial levels of glucagon with very low insulin levels. Anyway, my point is, one of the major effects of glucagon is to increase lipolysis in adipose tissue. So I was wondering... how significant is this effect? Is it enough that it would promote a significant amount of lipolysis and contribute to decreased fat mass? Just a thought, if so it would give yet another reason that ketogenic diets can be beneficial.
    Once again - as with ALL things that 'increase fat mobilisation' - at the end of the day it will do nothing unless total calorie intake is lower than what you need.

    Essentially: Fat loss is all about LOSING energy. So it is all well and good to promote LIPOLYSIS - but where is the fat going to go once it is in your system? So if you don't have a need for it - then it simply redeposits - be that in liver/ organs/ muscles or adipose stores (in addition to any extra fats you have eaten from your daily diet)!


    Also remember that having this higher FFA level in the body/ liver/ muscles has a generally negative health impact - among other things/ most notibly, contributes to NASH/NAFLD (Non-alcoholic fatty liver disease), is pro-inflammatory (stimulates TNF, among other things), and also contributes to insulin resistance.

    (pubmed: lipotoxicity if interested).
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  3. #3
    nevigsawkufelgnisaton in10city's Avatar
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    Originally Posted by thegymbum View Post
    I was doing some reading and had a thought that's been on my mind. In contrast to a carbohyudrate rich meal, one major stimulus for glucagon secretion is a high fat/protein meal containing only negligible amounts of carbohydrate. With only negligible amounts of carbohydrate, insulin secretion is of course at a minimum, discounting the contribution of certain glucogenic amino acids and the direct insulin stimulation of some amino acids. So this sort of diet favors high postprandial levels of glucagon with very low insulin levels. Anyway, my point is, one of the major effects of glucagon is to increase lipolysis in adipose tissue. So I was wondering... how significant is this effect? Is it enough that it would promote a significant amount of lipolysis and contribute to decreased fat mass? Just a thought, if so it would give yet another reason that ketogenic diets can be beneficial.
    Not significant at physiological concentrations.

    http://jcem.endojournals.org/cgi/content/full/86/5/2085
    It is the mark of an educated mind to be able to entertain a thought without accepting it.
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  4. #4
    Rebelling in my psychosis thegymbum's Avatar
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    Very interesting. Thanks for the feedback! I suppose I should have looked into it more before I opened my mouth, lol.
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  5. #5
    Registered User malibu2008's Avatar
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    Originally Posted by Emma-Leigh View Post
    Also remember that having this higher FFA level in the body/ liver/ muscles has a generally negative health impact - among other things/ most notibly, contributes to NASH/NAFLD (Non-alcoholic fatty liver disease), is pro-inflammatory (stimulates TNF, among other things), and also contributes to insulin resistance.

    (pubmed: lipotoxicity if interested).
    holy that is so untrue....unnatural fat, excess fructose, wheat and soy ae what case faty liver, please. do not try to pose that natural saturated and mono sat fat cause any sort of liver problems. even in excess

    http://wholehealthsource.blogspot.co...-reversal.html
    http://wholehealthsource.blogspot.co...grown-ups.html
    http://wholehealthsource.blogspot.co...l-part-ii.html
    http://wholehealthsource.blogspot.co...-ldl-part.html
    http://wholehealthsource.blogspot.co...-reversal.html
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  6. #6
    Not Swimming. Emma-Leigh's Avatar
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    Originally Posted by malibu2008 View Post
    holy that is so untrue....unnatural fat, excess fructose, wheat and soy ae what case faty liver, please. do not try to pose that natural saturated and mono sat fat cause any sort of liver problems. even in excess

    http://wholehealthsource.blogspot.co...-reversal.html
    http://wholehealthsource.blogspot.co...grown-ups.html
    http://wholehealthsource.blogspot.co...l-part-ii.html
    http://wholehealthsource.blogspot.co...-ldl-part.html
    http://wholehealthsource.blogspot.co...-reversal.html
    Yeah.... Cause THAT'S what I said in my post....

    *perfer et obdura; dolor hic tibi proderit olim*
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  7. #7
    Rebelling in my psychosis thegymbum's Avatar
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    Originally Posted by malibu2008 View Post
    holy that is so untrue....unnatural fat, excess fructose, wheat and soy ae what case faty liver, please. do not try to pose that natural saturated and mono sat fat cause any sort of liver problems. even in excess
    Uh huh. Excess of ANY fat causes health problems. FFA levels are detrimental in countless ways. It's not just "unnatural fat". "Natural" fat can be just as damaging in excess.
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  8. #8
    Registered User malibu2008's Avatar
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    beg to differ....it all depends whether you are talking about a glucose burnng metabolism or a fatty acid based metabolism.
    Let's look at glucose and lipid metabolism under a fast. There is no glucose uptake from the gut. The portal vein is no longer a glycation hot spot, the systemic circulation has only basal glucose too. Arterial endothelial cells are not undergoing hyperglycaemia induced apoptosis. This minimises the need for foam cell formation as there is essentially no damage needing repair.

    Chylomicrons are not being produced at all, the liver is depleted of carbohydrate and so puts out a minimum of VLDLs. However many VLDLs and subsequent LDLs are actually produced, they will not be exposed to aggressive glycation conditions. If the liver does continue to produce significant levels of VLDL, they will be based either on fats synthesised from residual glycogen stores or free fatty acids derived from adipose tissue. That is, mostly saturated with some monounsaturated. So VLDLs will be deficient in PUFA and not prone to glycoxidation. PUFA supply will be limited to hepatic stores and whatever is present in adipose tissue, ie not a lot.

    Bulk lipid for energy supply will be derived from adipose tissue lipolysis and be (a) mostly saturated fatty acids and (b) in free fatty acid form. You cannot glycate free fatty acids without direct free radical attack.

    No one stores lipids or glucose in their blood stream. It all goes in to short term storage. What comes out determines weight loss. Insulin determines what comes out.

    OLETF(Long-Evans Tokushima Fatty strain) rats, on high fat, fixed calorie diet of 28.7 joules per day put all of this energy in to storage but fail to extract as many of these calories/joules from storage as those OLETF rats on 28.7 joules of a high starch diet. What is going on?

    If you accept the insulin hypothesis of weight gain, the answer is that dietary fat is being trapped in adipocytes by excessive blood insulin. There must be excess insulin.

    Why is the insulin elevated when there is a reduced dietary stimulus for insulin production? These rats have peripheral, almost certainly muscle based, insulin resistance. But only on a high fat diet.

    High fat diets put lipids in to muscles, muscles full of lipid don't accept glucose. If the system works correctly the muscles run on lipids until there is a balance between fat supply rejecting glucose and fat depletion allowing glucose acceptance. A few billion years is ample time to get this system working correctly to maintain normoglycaemia in the face of varied macronutrient intakes from day to day.
    Well, if you can get lipids in to muscle cells but cannot then use that lipid for beta oxidation you would expect to develop muscle insulin resistance in proportion to the amount of fat you supply, ie if the fat enters the muscles but does not go any further those muscles will become insulin resistant and stay insulin resistant. If muscles are not accepting glucose because they are insulin resistant the glucose is going to have to be dealt with by increased levels of insulin. Hyperglycaemia is unacceptable.

    The extra insulin needed to maintain normoglycaemia then traps stored dietary fat in adipocytes. The rats get fat because they cannot get fat out of adipocytes. They will also do less running around and will probably feel colder than normal rats because they have no access to their fatty tissue for energy supplies. If they had access to food they would eat more, but 28.7 joules per day was the limit in this experiment. If they had access to more calories they would clearly eat more because no one likes the hunger and shivering produced by sequestering a chunk of your caloric fat intake in your adipocytes and locking it in there with insulin.

    Once your fat cells get full enough they will spill free fatty acids because they are now too full to listen to insulin any more. These FFAs join those intra cellular muscle tissue di and tri glycerides from the metabolic defect. Intra myocyte fatty acids still have no where to go, so muscle insulin resistance rockets, plasma glucose rockets and you have a superb model of fat induced obesity and peripheral insulin resistance.

    Glucose enters mitochondria as pyruvate. Fatty acids enter mitochondria as acyl CoA moieties. The place to be looking for explanations for the syndrome seen in the OLETF rat is in fatty acid processing. My guess is that lipid molecules get in to myocytes but never get effectively passed to the mitochondria.
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  9. #9
    "Full House" KLMARB's Avatar
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    Soooooo.....guess what? excess fat intake is detrimental when following a carb-based (sucrotic) nutritional pattern. Hyperinsulinemia anyone? The carb-fat NAD/western diet rears its ugly head again...
    I'll take arrogance and the inevitable hubris over self-doubt and lack of confidence, anyday.......
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    Registered User malibu2008's Avatar
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    Originally Posted by KLMARB View Post
    Soooooo.....guess what? excess fat intake is detrimental when following a carb-based (sucrotic) nutritional pattern. Hyperinsulinemia anyone? The carb-fat NAD/western diet rears its ugly head again...
    agreed
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