NAC and visceral fat loss

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    NAC and visceral fat loss


    N-acetylcysteine attenuates TNF-alpha induced changes in secretion of interleukin-6, plasminogen activator inhibitor-1 and adiponectin from 3T3-L1 adipocytes

    TNF-alpha is a key molecule in obesity-related metabolic disturbances. This study was designed to determine whether N-acetylcysteine (NAC), an antioxidant, prevents the activation of nuclear factor-kappaB (NF-kappaB) by exogenously administered TNF-alpha in adipocytes, and whether such change affects the production of adipocytokines. The treatment of well-differentiated 3T3-L1 cells with 20 mM of NAC significantly increased the reduced glutathione concentration up to 150% of control. The treatment with 10 ng/ml of TNF-alpha decreased antioxidant enzyme levels such as CuZn-superoxide dismutase (SOD), MnSOD and catalase, and activated NF-kappaB in 3T3-L1 adipocytes. The activation of NF-kappaB was significantly prevented by the pretreatment with 20 mM of NAC. TNF-alpha (1-10 ng/ml) dose-dependently increased interleukin (IL)-6 and plasminogen activator inhibitor-1 (PAI-1) secretion from 3T3-L1 adipocytes, while decreased adiponectin secretion. NAC (5-20 mM) attenuated the TNF-alpha-induced changes in these adipocytokine secretions in a dose-dependent manner. The effect of TNF-alpha and NAC on the adipocytokine productions was exerted at the m-RNA level, judging from results of the real time RT-PCR analysis. The present study revealed that NAC inhibited the TNF-alpha-mediated activation of NF-kappaB and improved the adverse changes in the levels of IL-6, PAI-1 and adiponectin in 3T3-L1 adipocytes. NAC may have the potential to improve the obesity-related abnormal adipocytokine metabolism by attenuating the TNF-alpha-induced oxidant-antioxidant imbalance in adipocytes.
    "The only good is knowledge and the only evil is ignorance." - Socrates


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    Looks like NAC+Vit C might be a good combo for fat loss?

    Association of anti-obesity activity of N-acetylcysteine with metallothionein-II down-regulation
    People with upper body or visceral obesity have a much higher risk of morbidity and mortality from obesity-related metabolic disorders than those with lower body obesity. In an attempt to develop therapeutic strategies targeting visceral obesity, depot-specific differences in the expression of genes in omental and subcutaneous adipose tissues were investigated by DNA array technology, and their roles in adipocyte differentiation were further examined. We found that levels of metallothionein-II (MT-II) mRNA and protein expression were higher in omental than in subcutaneous adipose tissues. The study demonstrates that MT-II may play an important role in adipocyte differentiation of 3T3L1 preadipocytes, and that N-acetylcysteine (NAC) inhibits the adipocyte differentiation of 3T3L1 cells by repressing MT-II in a time- and dose-dependent manner. Furthermore, the intraperitoneal administration of NAC to rats and mice resulted in a reduction of body weights, and a marked reduction in visceral fat tissues. These results suggest that MT-II plays important roles in adipogenesis, and that NAC may be useful as an anti-obesity drug or supplement.
    N-Acetylcysteine an Allium plant compound improves high-sucrose diet-induced obesity and related effects

    This study was designed to determine whether N-acetylcysteine (NAC, C5H9–NO3S), a compound from Allium species may be used as a complementary therapeutic agent, to inhibit high-sucrose induced-obesity and its effects on glucose tolerance, in vivo low-density lipoprotein (LDL)-oxidation and serum oxidative stress in rats. Initially, 24 male Wistar rats were divided into two groups: controls receiving standard chow (C, n=6) and those receiving high-sucrose diet (HS, n = 18). After 22 days, (HS) group was divided into three groups (n = 6/group); (HS-HS) continued to eat high-sucrose diet and water; (HS-N) continued to eat high-sucrose diet and received 2 mg l–1-NAC in its drinking water; (HS-CN) changing high-sucrose to standard chow and receiving 2 mg l 1-NAC in its drinking water. After 22 days of the HS-group division (44 days of experimental period) body weight, body mass index and surface area were enhanced in HS-HS rats (P < 0.001). HS-HS rats had glucose intolerance, increased serum triacylglycerol (TG), very low-density lipoprotein (VLDL), oxidized-LDL (ox-LDL) and lipid-hydroperoxide (LH) than the others (P < 0.01). NAC in HS-N and HS-CN rats reduced the obesity markers, feed efficiency, LH and ox-LDL, as well normalized glucose response, TG and VLDL (P < 0.01) in these groups compared with HS-HS. Total antioxidant substances, GSH/GSSG ratio and glutathione-reductase, were higher in HS-N than in HS-HS (P < 0.01). In conclusion, NAC improved high-sucrose diet-induced obesity and its effects on glucose tolerance, lipid profile, in vivo LDL-oxidation and serum oxidative stress, enhancing antioxidant defences. The application of this agent may be feasible and beneficial for high-sucrose diet-induced obesity, which certainly would bring new insights on obesity-related adverse effects control.
    N-acetylcysteine in high-sucrose diet-induced obesity: energy expenditure and metabolic shifting for cardiac health.

    To study the effects of N-acetylcysteine (NAC, C(5)H(9)-NO(3)S) on high-sucrose diet-induced obesity and its effects on energy metabolism and cardiac oxidative stress, male Wistar 24 rats were divided into four groups (n=6): (C) given standard chow and water; (N) receiving standard chow and 2g/l N-acetylcysteine in its drinking water; (HS) given standard chow and 30% sucrose in its drinking water, and (HS-N) receiving standard chow, 30% sucrose and N-acetylcysteine in its drinking water. After 30 days of the treatment, obesity was evidenced in HS rats from enhanced body weight, respiratory quotient, hypertriglyceridemia. As well depressed resting metabolic rate, and oxygen consumption per surface area. HS rats had triacylglycerol accumulation, oxidative stress and metabolic shifting in cardiac tissue. NAC enhanced fat oxidation and energy expenditure, normalizing these adverse effects, comparing HS-N and HS rats. The beta-hydroxyacyl coenzymne-A dehydrogenase activity was higher in HS-N animals, indicating higher heart fatty acid degradation than in HS. NAC normalized myocardial glycogen and lactate dehydrogenase activity, comparing HS-N and HS rats, but had no effects on calorimetric and biochemical parameters in standard-fed rats, comparing N and C groups. In conclusion, N-acetylcysteine offers promising therapeutic value in prevention of high-sucrose induced-obesity and its effect on cardiac tissue. N-acetylcysteine reduced the oxidative stress and prevented the metabolic shifting in cardiac tissue, enhancing fatty acid oxidation and reducing anaerobic metabolism in high-sucrose-fed conditions. The application of this agent in food system via exogenous addition may be feasible and beneficial for antioxidant protection and energy metabolism in cardiac tissue.
    Effects of N-acetylcysteine on sucrose-rich diet-induced hyperglycaemia, dyslipidemia and oxidative stress in rats

    This study examined whether sucrose-rich diet (SRD)-induced hyperglycaemia, dyslipidemia and oxidative stress may be inhibited by N-acetylcysteine (C5H9–NO3S), an organosulfur from Allium plants. Male Wistar 40 rats were divided into four groups (n = 10): (C) given standard chow and water; (N) receiving standard chow and 2 mg/l N-acetylcysteine in its drinking water; (SRD) given standard chow and 30% sucrose in its drinking water; and (SRD-N) receiving standard chow, 30% sucrose and N-acetylcysteine in its drinking water. After 30 days of treatment, SRD rats had obesity with increased abdominal circumference, hyperglycaemia, dyslipidemia and hepatic triacylglycerol accumulation. These adverse effects were associated with oxidative stress and depressed lipid degradation in hepatic tissue. The SRD adverse effects were not observed in SDR-N rats. N-Acetylcysteine reduced the oxidative stress, enhancing glutathione-peroxidase activity, and normalizing lipid hydroperoxyde, reduced glutathione and superoxide dismutase in hepatic tissue of SRD-N rats. The β-hydroxyacyl coenzyme-A dehydrogenase and citrate-synthase activities were increased in SRD-N rats, indicating enhanced lipid degradation in hepatic tissue as compared to SRD. SRD-N rats had reduced serum oxidative stress and diminished glucose, triacylglycerol, very-low-density lipoprotein (VLDL), oxidized low-density lipoprotein (ox-LDL) and cholesterol/high-density lipoprotein (HDL) ratio in relation to SRD. In conclusion, NAC offers promising therapeutic values in prevention of dyslipidemic profile and alleviation of hyperglycaemia in high-sucrose intake condition by improving antioxidant defences. N-Acetylcysteine had also effects preventing metabolic shifting in hepatic tissue, thus enhancing fat degradation and reducing body weight gain in conditions of excess sucrose intake. The application of this agent in food system via exogenous addition may be feasible and beneficial for antioxidant protection.
    3-day oral N-acetyl-cysteine supplementation alters metabolism but not performance of high intensity aerobic exercise in trained cyclists

    Redox homeostasis is essential for proper functioning of biological systems. Oxidative stress impairs contractile activity in skeletal muscle, and contributes to muscular fatigue during heavy exercise (Barclay & Hansel, 1991; Reid et al., 1992). Accordingly, antioxidant supplements may assist endogenous antioxidants to prevent deleterious effects associated with oxidative stress (Medved et al., 2004; Kelly et al., 2009). In this study we investigated the effect of oral N-acetyl-cysteine (NAC) supplementation on metabolism and high intensity cycling performance. Nine well-trained male cyclists (mean SD; 27 6 years of age, VO2peak 69.4 5.8 ml.kg−1.min−1) provided written informed consent. In a randomized, double-blind crossover design, subjects performed a 6 5 min High Intensity-Interval Training (HIT) cycling session at 82.5% of peak sustained power output, followed by a 10 minute self-paced Time Trial (TT) on two occasions 7 d apart. Prior to one session subjects consumed 5 750ml doses (2 2 d, 2 1 d, 1 1 hr pre-trial) of sports drink each containing 100mg.kg−1 NAC, which was repeated for the other session, but without NAC. Metabolic, electromyographic (EMG), performance data, and blood/plasma samples were collected for analysis before, during, and after the 6 5 min HIT bouts and subsequent TT. Respiratory Exchange Ratio (RER) was decreased in the NAC condition throughout HIT exercise, and was significant at bouts 1 and 5 (p < 0.05) as shown in The Figure. Compared to placebo, NAC decreased blood lactate during TT and recovery (p < 0.05). Both pH (p < 0.01), and HCO3 (p < 0.05) were reduced throughout exercise and recovery with NAC. In contrast NAC resulted in higher blood glucose concentration during HIT (p < 0.05). EMG median frequency of the vastus lateralis decreased in HIT bout 6 in the NAC condition (p < 0.05). No significant difference was observed in the total work performed in the 10-min TT (p = 0.16). These data indicate that NAC does not change performance in a self-paced 10-min TT, but induces a shift in muscle fibre-type recruitment and alters metabolism during high intensity interval exercise, which may provide a glycogen-sparing effect during prolonged exercise.
    But then we have

    Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after an acute muscle injury induced by eccentric exercise

    There has been no investigation to determine if the widely used over-the-counter, water-soluble antioxidants vitamin C and N-acetyl-cysteine (NAC) could act as pro-oxidants in humans during inflammatory conditions. We induced an acute-phase inflammatory response by an eccentric arm muscle injury. The inflammation was characterized by edema, swelling, pain, and increases in plasma inflammatory indicators, myeloperoxidase and interleukin-6. Immediately following the injury, subjects consumed a placebo or vitamin C (12.5 mg/kg body weight) and NAC (10 mg/kg body weight) for 7 d. The resulting muscle injury caused increased levels of serum bleomycin-detectable iron and the amount of iron was higher in the vitamin C and NAC group. The concentrations of lactate dehydrogenase (LDH), creatine kinase (CK), and myoglobin were significantly elevated 2, 3, and 4 d postinjury and returned to baseline levels by day 7. In addition, LDH and CK activities were elevated to a greater extent in the vitamin C and NAC group. Levels of markers for oxidative stress (lipid hydroperoxides and 8-iso prostaglandin F2α; 8-Iso-PGF2α) and antioxidant enzyme activities were also elevated post-injury. The subjects receiving vitamin C and NAC had higher levels of lipid hydroperoxides and 8-Iso-PGF2α 2 d after the exercise. This acute human inflammatory model strongly suggests that vitamin C and NAC supplementation immediately post-injury, transiently increases tissue damage and oxidative stress
    So the vitamin C is to mitigate the possible hypertension problem?
    "The only good is knowledge and the only evil is ignorance." - Socrates

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    I am a fan of the combo, but that last study you posted is why I never supplement with the pair around training; aside from when using nitrates.
    http://anabolicminds.com/forum/workout-logs/231713-rob112-3-means.html
    "Train like a beast, think like a human"-RTS

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    Quote Originally Posted by rob112 View Post
    I am a fan of the combo, but that last study you posted is why I never supplement with the pair around training; aside from when using nitrates.
    The issue is being caused by the excessive NAC dose in the study. Low-dosed NAC/Vit C (no more than a couple hundred mgs of each) might not be a bad idea.
    http://pescience.com/
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    The above is my own opinion and does not reflect the opinion of PES

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    Quote Originally Posted by mr.cooper69

    The issue is being caused by the excessive NAC dose in the study. Low-dosed NAC/Vit C (no more than a couple hundred mgs of each) might not be a bad idea.
    Yea, it is a higher dose than I use. When I first started taking NAC I found it really hard to figure out dosage in general. I now use a pretty standard dose of 600mgs(which is probably still a lot if near workout) and 500mg Vitamin
    http://anabolicminds.com/forum/workout-logs/231713-rob112-3-means.html
    "Train like a beast, think like a human"-RTS

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    Most people use 1.2 G (2 caps) for liver detox for MANY YEARS

    Wonder if the study does not necessary translate to "real world" otherwise, many PH and GEAR users would haver said/noticed something????
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    Quote Originally Posted by Whacked View Post
    Most people use 1.2 G (2 caps) for liver detox for MANY YEARS

    Wonder if the study does not necessary translate to "real world" otherwise, many PH and GEAR users would haver said/noticed something????
    These people usually aren't suffering from inflammatory conditions that can contribute to obesity and atherosclerosis
    http://pescience.com/
    http://selectprotein.com/
    The above is my own opinion and does not reflect the opinion of PES

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    Sup Coop

    Half the people I know using gear are just as fat and unhealthy as the general population. Not sure I agree.

    Additionally, gear and PH's in and of itself cause detrimental inflammatory processes, albeit more acute in nature.

    Quote Originally Posted by mr.cooper69 View Post
    These people usually aren't suffering from inflammatory conditions that can contribute to obesity and atherosclerosis
    A-Minds HYPE-SLAYER! All posts & feedback are guaranteed to be unsolicited and legit
    "The fear of the LORD is the beginning of knowledge. Fools despise wisdom & instruction"
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    Agreed with that.....

    And it's good to see you on AM....I remember you from the golden days of mindandmuscle.You should pop on in over on the Andro Factory subforum sometimes,we could use a guy like you who knows his ****

    Quote Originally Posted by Whacked View Post
    Sup Coop

    Half the people I know using gear are just as fat and unhealthy as the general population. Not sure I agree.

    Additionally, gear and PH's in and of itself cause detrimental inflammatory processes, albeit more acute in nature.

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