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kill Fat Cells

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    Quote Originally Posted by bluehealer View Post
    Thanks for posting these, Maxximal.

    I should have payed attention in school, then maybe I could understand the terminology in these studies.

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    Some very interesting reading. Thanks!
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    Quote Originally Posted by rulk22 View Post
    I use Quercetin to rid my gout and it works just as well as the meds im perscribed. I started to use NAC regularly last year and found out its best to add extremely high doses of Vit. C, other wise NAC will interfere with insulin sensitivity or something like that. As for Resveratrol I wish I could take Sustain Alpha year round...Perhaps Primordial Performance will release a Liquavade Trans-Resvertrol solo.
    Cissus will get rid of gout as well

    As far as NAC- the effects seem to be negligible on insulin sensitivity:

    J Physiol. 2010 May 1;588(Pt 9):1623-34. Epub 2010 Mar 22.

    N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans.
    Merry TL, Wadley GD, Stathis CG, Garnham AP, Rattigan S, Hargreaves M, McConell GK.

    Department of Physiology, The University of Melbourne, Parkville, Victoria, 3010, Australia. troy.merry@gmail.com

    Abstract
    There is evidence that reactive oxygen species (ROS) signalling is required for normal increases in glucose uptake during contraction of isolated mouse skeletal muscle, and that AMP-activated protein kinase (AMPK) is involved. The aim of this study was to determine whether ROS signalling is involved in the regulation of glucose disposal and AMPK activation during moderate-intensity exercise in humans. Nine healthy males completed 80 min of cycle ergometry at 62 +/- 1% of peak oxygen consumption ( V(O(2)peak).A 6,6-(2)H-glucose tracer was infused at rest and during exercise, and in a double-blind randomised cross-over design, N-acetylcysteine (NAC) or saline (CON) was co-infused. NAC was infused at 125 mg kg(1) h(1) for 15 min and then at 25 mg kg(1) h(1) for 20 min before and throughout exercise. NAC infusion elevated plasma NAC and cysteine, and muscle NAC and cysteine concentrations during exercise. Although neither NAC infusion nor exercise significantly affected muscle reduced or oxidised glutathione (GSH or GSSG) concentration (P > 0.05), S-glutathionylation (an indicator of oxidative stress) of a protein band of approximately 270 kDa was increased approximately 3-fold with contraction and this increase was prevented by NAC infusion. Despite this, exercised-induced increases in tracer determined glucose disposal, plasma lactate, plasma non-esterified fatty acids (NEFAs), and decreases in plasma insulin were not affected by NAC infusion. In addition, skeletal muscle AMPKalpha and acetyl-CoA carboxylase-beta (ACCbeta) phosphorylation increased during exercise by approximately 3- and approximately 6-fold (P < 0.05), respectively, and this was not affected by NAC infusion. Unlike findings in mouse muscle ex vivo, NAC does not attenuate skeletal muscle glucose disposal or AMPK activation during moderate-intensity exercise in humans.

    J Endocrinol Invest. 2009 Apr;32(4):352-6.

    N-acetylcysteine is able to reduce the oxidation status and the endothelial activation after a high-glucose content meal in patients with Type 2 diabetes mellitus.
    Masha A, Brocato L, Dinatale S, Mascia C, Biasi F, Martina V.

    Department of Internal Medicine, Division of Endocrinology, University of Turin, Corso A.M. Dogliotti 14, 10126 Turin, Italy.

    Abstract
    Post-prandial hyperglycemia seems to play a pivotal role in the pathogenesis of the cardiovascular complications of diabetes mellitus, as it leads to an oxidative stress which in turn causes a reduced NO bioavailability. These conditions produce an endothelial activation.

    AIM OF THE STUDY: The aim of this study was to assure that the administration of N-acetylcysteine (NAC), thiolic antioxidant, is able to decrease the oxidation status and endothelial activation after a high-glucose content meal.

    SUBJECTS AND METHODS: Ten patients with Type 2 diabetes mellitus (DMT2) (Group 1) and 10 normal subjects (Group 2) were studied. They assumed a high-glucose content meal without (phase A) or after (phase B) the administration of NAC. Glycemia, insulinemia, intercellular adhesion molecule 1, vascular adhesion molecule 1 (VCAM-1), E-selectin, malonaldehyde (MDA), and 4-hydroxynonenal (HNE) were assessed at -30, 0, +30, +60, +90, +120, and +180 min with respect to the meal consumption.

    RESULTS: During the phase A in Group 1, only HNE and MDA levels increased after the meal assumption; all parameters remained unchanged in Group 2. During the phase B, in Group 1, HNE, MDA, VCAM-1, and E-selectin levels after the meal were lower than those in phase A, while no change for all variables were observed in Group 2.

    CONCLUSIONS: A high-glucose meal produces an increase in oxidation parameters in patients with DMT2. The administration of NAC reduces the oxidative stress and, by doing so, reduces the endothelial activation. In conclusion, NAC could be efficacious in the slackening of the progression of vascular damage in DMT2.
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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    Quote Originally Posted by rms80 View Post
    Cissus will get rid of gout as well

    As far as NAC- the effects seem to be negligible on insulin sensitivity:

    J Physiol. 2010 May 1;588(Pt 9):1623-34. Epub 2010 Mar 22.

    N-Acetylcysteine infusion does not affect glucose disposal during prolonged moderate-intensity exercise in humans.
    Merry TL, Wadley GD, Stathis CG, Garnham AP, Rattigan S, Hargreaves M, McConell GK.

    Department of Physiology, The University of Melbourne, Parkville, Victoria, 3010, Australia. troy.merry@gmail.com

    Abstract
    There is evidence that reactive oxygen species (ROS) signalling is required for normal increases in glucose uptake during contraction of isolated mouse skeletal muscle, and that AMP-activated protein kinase (AMPK) is involved. The aim of this study was to determine whether ROS signalling is involved in the regulation of glucose disposal and AMPK activation during moderate-intensity exercise in humans. Nine healthy males completed 80 min of cycle ergometry at 62 +/- 1% of peak oxygen consumption ( V(O(2)peak).A 6,6-(2)H-glucose tracer was infused at rest and during exercise, and in a double-blind randomised cross-over design, N-acetylcysteine (NAC) or saline (CON) was co-infused. NAC was infused at 125 mg kg(1) h(1) for 15 min and then at 25 mg kg(1) h(1) for 20 min before and throughout exercise. NAC infusion elevated plasma NAC and cysteine, and muscle NAC and cysteine concentrations during exercise. Although neither NAC infusion nor exercise significantly affected muscle reduced or oxidised glutathione (GSH or GSSG) concentration (P > 0.05), S-glutathionylation (an indicator of oxidative stress) of a protein band of approximately 270 kDa was increased approximately 3-fold with contraction and this increase was prevented by NAC infusion. Despite this, exercised-induced increases in tracer determined glucose disposal, plasma lactate, plasma non-esterified fatty acids (NEFAs), and decreases in plasma insulin were not affected by NAC infusion. In addition, skeletal muscle AMPKalpha and acetyl-CoA carboxylase-beta (ACCbeta) phosphorylation increased during exercise by approximately 3- and approximately 6-fold (P < 0.05), respectively, and this was not affected by NAC infusion. Unlike findings in mouse muscle ex vivo, NAC does not attenuate skeletal muscle glucose disposal or AMPK activation during moderate-intensity exercise in humans.

    J Endocrinol Invest. 2009 Apr;32(4):352-6.

    N-acetylcysteine is able to reduce the oxidation status and the endothelial activation after a high-glucose content meal in patients with Type 2 diabetes mellitus.
    Masha A, Brocato L, Dinatale S, Mascia C, Biasi F, Martina V.

    Department of Internal Medicine, Division of Endocrinology, University of Turin, Corso A.M. Dogliotti 14, 10126 Turin, Italy.

    Abstract
    Post-prandial hyperglycemia seems to play a pivotal role in the pathogenesis of the cardiovascular complications of diabetes mellitus, as it leads to an oxidative stress which in turn causes a reduced NO bioavailability. These conditions produce an endothelial activation.

    AIM OF THE STUDY: The aim of this study was to assure that the administration of N-acetylcysteine (NAC), thiolic antioxidant, is able to decrease the oxidation status and endothelial activation after a high-glucose content meal.

    SUBJECTS AND METHODS: Ten patients with Type 2 diabetes mellitus (DMT2) (Group 1) and 10 normal subjects (Group 2) were studied. They assumed a high-glucose content meal without (phase A) or after (phase B) the administration of NAC. Glycemia, insulinemia, intercellular adhesion molecule 1, vascular adhesion molecule 1 (VCAM-1), E-selectin, malonaldehyde (MDA), and 4-hydroxynonenal (HNE) were assessed at -30, 0, +30, +60, +90, +120, and +180 min with respect to the meal consumption.

    RESULTS: During the phase A in Group 1, only HNE and MDA levels increased after the meal assumption; all parameters remained unchanged in Group 2. During the phase B, in Group 1, HNE, MDA, VCAM-1, and E-selectin levels after the meal were lower than those in phase A, while no change for all variables were observed in Group 2.

    CONCLUSIONS: A high-glucose meal produces an increase in oxidation parameters in patients with DMT2. The administration of NAC reduces the oxidative stress and, by doing so, reduces the endothelial activation. In conclusion, NAC could be efficacious in the slackening of the progression of vascular damage in DMT2.
    THANK YOU for posting that! I use nac everyday, and when I read his post, I was like, wtf i got to look this up! Thanks to both of you guys for the insight and info!

    Mike
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    Quote Originally Posted by criticalbench View Post
    THANK YOU for posting that! I use nac everyday, and when I read his post, I was like, wtf i got to look this up! Thanks to both of you guys for the insight and info!

    Mike
    Glad I could help
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    Yeah I can vouch for that, we never monitor blood glucose during APAP overdoses when giving mucomyst (NAC) and believe me some amazingly high doses are given.
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    "PPAR-gamma" and CLA?

    isnt the PPAR-gamma involved or influenced by TTA too?
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    Quote Originally Posted by rochabp View Post
    "PPAR-gamma" and CLA?

    isnt the PPAR-gamma involved or influenced by TTA too?
    TTA is a PPAR antagonist
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    Quote Originally Posted by rochabp View Post
    "PPAR-gamma" and CLA?

    isnt the PPAR-gamma involved or influenced by TTA too?
    Quote Originally Posted by MAxximal View Post
    TTA is a PPAR antagonist
    TTA hits all three isoforms to some degree.
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    I know it's not a supplement but it does kill fat cells...

    http://abcnews.go.com/Health/freezin...ry?id=11641994
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    Quote Originally Posted by monstermash View Post
    I know it's not a supplement but it does kill fat cells...

    http://abcnews.go.com/Health/freezin...ry?id=11641994
    http://www.getds.com/2010111294/Blog...-cryolipolysis
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    That is a bit ominous of a theory. What I have read does infer cell death and absorption into the body, but the idea that the release of fatty acid and absorption elsewhere as a 1 to 1 is a bit fatalist. If the body does have excess fats only so much will be absorbed by other fatty tissue, otherwise it will be passed as waste and one would enjoy the "Floaters" in their toilet bowl. One can not relegate AIDS victims that already enjoy a wasting disease to otherwise healthy people.
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    Fish oil also (specifically EPA DHA) are great for fat loss too and leucine don't forget.
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    Decreased fat storage by Lactobacillus paracasei


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    Anti-obesity effect of genistein, resveratrol and quercetin

    http://www.ncbi.nlm.nih.gov/pubmed/19053873
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    nice post.
    i use some of these off and am using CLA now only 4g ed though. also Resveratrol off and on
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    A Norwegian study says that CLA may increase thrombocytes, which is potentially dangerous for people with a history of pulmonary embolism.
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    Apoptosis appears to be a routine event....


    Well isn't possible to get rid of fat cells only shink them.... Wrong. Apoptosis appears to be a routine event.
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    Quote Originally Posted by MAxximal View Post
    Well isn't possible to get rid of fat cells only shink them.... Wrong. Apoptosis appears to be a routine event.
    Really not relevant unless you are dieting to a degree that will destroy muscle as well. The study cites extreme fat loss scenarios like anorexia or massive weight loss from an obese state as a significant context for adipocyte apoptosis.
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    HELIOS!!!!!
    The difference between who you are and who you want to be is what you do.
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    Quote Originally Posted by mr.cooper69 View Post
    Really not relevant unless you are dieting to a degree that will destroy muscle as well. The study cites extreme fat loss scenarios like anorexia or massive weight loss from an obese state as a significant context for adipocyte apoptosis.

    Atkins Diet
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    Quote Originally Posted by MAxximal View Post
    Atkins Diet
    Due to downregulation if IGF-1? The merit of destroying adipocytes is to reduce the hormonal response from empty adipocytes that generate cravings and the like. For many people including myself, low-carbing will have the same effect. If someone was obese and is now in-shape, then this study postulates that many adipocytes will have been destroyed; if someone has never been fat, then they don't have many adipocytes to begin with. Either way, the user already has a [lower] amount of fat cells, so no need to go through the torture that is the Atkins Diet .
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    Quote Originally Posted by rochabp View Post
    HELIOS!!!!!
    LOL
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