Ractopamine HCL use in humans??

[TexasLifter89]

Not sure where to put this since it is not a steroid, but it is in a class of nutrient repartioners and is being used on pigs & livestock to aid in growth. From the studies I read it shows nice results.

Does anyone know anyone who uses this and what are their results?

What is Ractopamine?
Ractopamine is a small compound belonging to a class of compounds called phenethanolamines. Ractopamine is not a steriod. Phenethanolamines are often referred to as repartitioning agents, because their mode of activity causes the shifting of nutrients from fat to lean muscle.

 

[JaredGalloway]

Very interested in seeing peoples experience with this...i would love to be a guinea pig but ive never even heard of this b4... good find...

 

[TexasLifter89]

Very interested in seeing peoples experience with this...i would love to be a guinea pig but ive never even heard of this b4... good find...

bump! I read on some bodybuilding sites about a few guys using it, but no one ever responded as to their results...

 

[Random181]

For advanced nutritent partitions why dont you give lr3 igf a try?

 

[DAdams91982]

bump! I read on some bodybuilding sites about a few guys using it, but no one ever responded as to their results...

Cause they have perished.

Adams

 

[TexasLifter89]

Cause they have perished.

Adams

oh man... hopefully that's not the case Adams...

 

[DAdams91982]

oh man... hopefully that's not the case Adams...

Naww... I am just bullshittin... now I will feel like a tool if any of them were harmed! :dunno:

Adams

 

[TexasLifter89]

haha Got me! It just seems interesting and produced good results for the cows & pigs, humans maybe a different story however.

 

[MuscleBound1337]

Lol, this **** is pretty dangerous apparently. I believe it works on the same receptors as clen (please don't quote me on this). It's used to increase lean mass while reducing fat in pigs. They feed the pigs are fed with ractopamine as an additive must be discountinued sometime prior to their slaughter to prevent contamination. I did a quick search and it seems a few people have raised the suspicion that it can be carcinogenic in humans. Malaysia has banned its use for this reason.

 

[MuscleBound1337]

This works on beta3 receptors I believe in the same way clen works. Humans don't have the same receptors as horses and swine, thats why clen doesn't act as an anabolic in humans like it does for animals. So i'm pretty sure if someone used this stuff they wouldn't experience any of that nutrient partitioning effect except fat loss/

 

[JaredGalloway]

Lol, this **** is pretty dangerous apparently. I believe it works on the same receptors as clen (please don't quote me on this). It's used to increase lean mass while reducing fat in pigs. They feed the pigs are fed with ractopamine as an additive must be discountinued sometime prior to their slaughter to prevent contamination. I did a quick search and it seems a few people have raised the suspicion that it can be carcinogenic in humans. Malaysia has banned its use for this reason.

please do not say that something is banned in malaysia... cause there are NO bans on any substance in malaysia or thailand...these countries might state that its banned but in reality u can get ANYTHING there...for very cheap and there are no consequences for being caught with them or distributing them...but thats obviously very off subject though...

i read in an MD magazine about beta3 receptors... i just can remember any of it... ill try to find the article and it might shed some light on how this stuff might work on humans...i just hope ur right about it working on beta-3 receptors because im sure clen works on the beta-2 receptors...

 

[JaredGalloway]

This article from md seems to show what beta-3 agonists will do in humans...im not sure if this is usefull but ill post it anyways...


Enhancing Fat Loss Through Beta-Adrenergic Mediated Stimulation
Written by Robbie Durand - From MD's Website - Part of Article


Enhancing Fat Mobilization During Rest
Many researchers have hypothesized that the ?-3 receptor to alpha-2adrenoceptor ratio is the key to the regulation of thermogenesis and adipose tissue lipolysis. What’s so special about this combination? Stimulation of the alpha-2 adrenoceptors is anti-lipolytic. It basically halts fat mobilization from adipose tissue. alpha-2 adrenoceptors are distributed differently in men and women, as men tend to contain more alpha-2 adrenoceptors in their abdomen whereas women tend to have more alpha-2 adrenoceptors located in their hips and buttocks. So how important are alpha-2 adrenoceptors for fat lipolysis? Well when you take a fat biopsy of adipose tissue ratios from a person’s butt, which is the hardest body part for many bodybuilders to get ripped up, you will find a three- to 10-fold higher concentration of alpha-2 adrenoceptors to beta receptors.38 It’s been demonstrated that epinephrine has a higher binding affinity than norepinephrine for the ?-2 adrenoceptors.6 In addition, at low concentrations (i.e., rest), it’s been reported that alpha-2 adrenoceptors are activated. However during exercise, high NE levels stimulate alpha-receptors which activate lipolysis.39 In human fat cells, after alpha-agonist administration, there’s marked down regulation of the ?-receptors, yet there’s no down regulation of the alpha-2 adrenoceptors.7 In fact, even after long term alpha-2 adrenoceptors agonist’s administration, there seems to be no down regulation of the alpha-2 adrenoceptors.7 If you’re trying to get ripped up adding some yohimbine to the supplement stack might be advantageous as alpha-2 adrenoceptors inhibits adenylyl cyclase activity, which in turn inhibits cAMP and turns off lipolysis!!! Another little benefit to men is that administration of yohimbine has been shown to enhance penile erections because the penis has a high density of alpha-2 adrenoceptors. alpha-2 adrenoceptors have the opposite effect from the beta receptors on intracellular cAMP levels.

beta-3 Agonists: A Great Start With a Poor Finish…
So what makes the beta-3 receptor so special? Gene studies of mass populations have shown that there’s strong evidence linking body mass index (BMI) and the beta-3 gene, which indicates that the beta-3 gene expression is a strong candidate for obesity.19 The beta-3 receptor has a low-binding affinity for epinephrine, yet a high binding affinity for norepinephrine.4 beta-3 receptors have a lower binding affinity for epinephrine compared to ?-1 and ?-2 receptors, however beta-3 receptors have a higher binding affinity for noradrenaline than ?-2 receptors, yet a lower binding affinity than ?-1. Administration of a beta-3 agonist has no effect on stimulating catecholamine release, which is quite different from many of the obesity drugs found on the market.12 White adipose tissue has a scarce number of beta-3 receptors, but a much larger number of beta-1 and beta-2 receptors.12 Another interesting feature about the beta-3 receptor is that in rat studies it’s highly resistant to down regulation, as are beta-2 receptors.32 The obesity treatment hypothesized by researchers was that if the beta-3 receptor is hard to down regulate and produces significant thermogenesis it might be a practical approach to stimulating fat loss. So here’s the study that started the beta-3 craze. Healthy volunteers were administered a dose of ephedrine, which stimulates all three beta- receptors in fat (beta-1, beta-2, beta-3), however they also administered nadolol. Nadolol inhibits both the beta-1 receptors, located chiefly in cardiac muscle and the beta-2 receptors, located chiefly in the bronchial and vascular musculature. What they found was nothing short of amazing. Even though beta-1and beta-2 receptors were blocked, there was a 43 percent increase in thermogenesis, which was entirely mediated by the beta-3 receptor. So the race was on…developing a beta-3 agonist could increase thermogenesis without the side effects of nervousness and tremors because beta-3 receptors are only located on adipose tissue.


The Mystery of White Adipose Tissue
In rats, the ?-3 agonist administration was a tremendous success; beta-3 agonist administration caused significant reductions in abdominal fat pads and a host of other beneficial mediators of fat lipolysis and was also found to be a potent anti-diabetic agent. beta-3 agonist in mice or rats approximates doubling of total body energy expenditure after an acute dose.14 beta-3 agonist administration also caused increases in hormone sensitive lipase (HSL) activity gene expression and also increases in uncoupling chain protein 1 (UCP-1) in adipose tissue. HSL is the major rate-limiting enzyme in adipose tissue lipolysis. By increasing HSL activity in adipose tissue more fatty acids are transported out of adipose to be used as an energy source. In fact, there’s an immediate increase in HSL gene activity that occurs with fasting.17 Your body is basically saying, “There’s no food coming so start mobilizing more adipose tissue as an energy source!”
So as stated before, there are very few beta-3 receptors located on white adipose tissue and there are very few brown adipocytes in humans, so how is there a decrease in white adipose tissue if there are few receptor sites? In fact, many studies have suggested that there’s an induction of brown adipose tissue into white adipose cell.20,21 That’s right!! White adipocytes tissue starts developing brown adipose tissue characteristics. Interestingly, beta-3 agonists have the ability to induce UCP-1 gene expression in white adipose tissue as well as brown adipose tissue.19 One study documented that four weeks of ?-3 agonists administration caused a 62-percent increase in UCP-1 expression at week two and a 132-percent increase at week four.25 UCP-1 is the major source of thermogenesis in brown adipose tissue. Take away UCP-1 and all you have is worthless brown adipose cells with no metabolic activity. Mice that are genetically engineered to be UCP-1 deficient suffer extreme hypothermia (i.e. decreased body core temperature) and are cold insensitive. Conversely mice that over-express UCP1 are hyperphagic (eat excessively) and obesity resistant.15,16 Here was a really cool experiment, which documents how UCP-1 regulates the brown adipose cell. Researchers took adipocytes from mice that were genetically modified so they didn’t produce UCP-1 or UCP-1 deficient mice. They exposed the brown adipocytes to norepinephrine, which is a potent stimulator of UCP-1, and guess what happened? Nothing!!! The brown adipocytes didn’t increase thermogenesis, demonstrating that UCP-1 is the major source of thermogenesis in adipose tissue.25

Did Someone Hear a Toilet Flush…
Okay…here’s where you hear a big toilet flush for ?-3 agonists. The research was overwhelming clear that beta-3 agonists can increase thermogenesis and reduce body fat in rats, but when humans were studied, the results were only marginal. When beta-3 agonists are administered acutely, there’s an increase in energy expenditure and lipolysis, with no effects on heart rate, catecholamines, or body core temperature.29 The problem is that long-term studies fail to show any change in fat lipolysis or changes in resting energy expenditure. When obese men were administered beta-3 agonists for 28 days, there was no change in 24-hour energy expenditure, body composition, catecholamines, or changes in fatty acid mobilization.12 The author concluded that unlike rat studies, which have shown beta-3 receptors to be resistant to down regulation, human beta-3 receptors are directly or indirectly down-regulated in response to beta-3 agonists. Another study, which lasted for 14 days, found no changes in resting energy expenditure or fat metabolism.30 Barbe et al.,27 investigated the effect of all beta-receptors (beta-1, beta-2 and beta-3) on a very low-calorie diet (382 calories a day) for 28 days. A microdialysis pump was inserted in the abdomen after 28 days on the low-calorie diet and three types of beta agonist drugs (i.e., Dobutamine beta-1 agonist], Terbutaline [beta-2 agonist] and CGP [partial-3 agonist]) were infused to measure changes to receptor sensitivity to fat tissue lipolysis. Results of the study concluded that there was a significant up-regulation of the beta-1 adrenergic pathway in adipose tissue. beta-2 receptors increased sensitivity to catecholamine, yet there were no changes in receptor number. There was only a mild increase in beta-3 receptor activity, further supporting that the beta-3 receptor is only weakly involved in the lipolytic process in humans. Another potential problem with ?-3 agonists is that brown adipose tissue decreases with age and beta-3 receptors are only sparsely located on white adipose tissue in humans (approximately 20 percent), whereas in rats, brown adipose tissue (approximately 90 percent) is abundant.31 Whether or not beta-3 agonists will be proven to be useful is debatable given the low receptor number found in human tissue. The research basically shows that beta-3 receptor is present in adipose tissue of both white and brown adipose tissue, yet its activation is only weakly involved in the lipolytic process in man. Based on the research, beta- receptors located on brown adipose tissue play a minor role in the lipolytic actions in humans, although highly thermogenic in rats. This effect is probably due to the fact that rats have a high abundance of brown adipose tissue compared to humans.24

Stimulating Fat Loss Through ?-Adrenergic System
In fat cells, it’s clearly established that agents increasing lipolysis also stimulate the beta-adrenergic system and increase cAMP levels. Catecholamines increase cAMP levels, whereas insulin decreases cAMP levels.22 No wonder ketogenic diets are so effective for getting ripped. Increases in cAMP increases lipolysis in both white and brown adipose tissue and also increases brown adipose tissue hypertrophy. In addition, UCP-1 is also stimulated by increasing cAMP levels.10 It seems that lipolysis is mainly dependent on the beta-1 and beta-2 receptors in adipose tissue; however these receptors are readily down-regulated.27 In fact, human fat cells have been shown to be 300 times more sensitive to Isoprenaline, which has beta-1 and beta-2 adrenoceptor activity, than beta-3 agonists.36 When it comes to supplements, that good ole ephedrine and caffeine stack was great for stimulating all three beta-receptors. For example, the caffeine, ephedrine and aspirin stack was so effective because ephedrine is a non-selective beta-agonist, while caffeine inhibited cAMP breakdown (keeps its activity high), and aspirin inhibited the negative feedback loop that reduces ?-agonist production. Ephedrine stimulates all three beta receptors located on adipose tissue. Researchers have suggested that beta-3 receptors may be a highly regulatory mechanism in fat cells after beta-1 and beta-2 receptors become desensitized. This may be the reason an increase in metabolic rate is seen after an ephedrine and caffeine stack is stopped, as subjects have been reported to continuously lose weight after discontinuation of caffeine and ephedrine.35 Another great thing about the caffeine-ephedrine stack is that it increases norepinephrine and norepinephrine and directly increases UCP-1 gene expression in both white and brown adipose tissue.24


Surprise, Surprise…
In conclusion, researchers once believed thermogenesis never occurs in white adipose tissue. Today, new research is questioning the validity of that claim. For example, a group of UCP-1 genetically deficient mice were exposed to a dose of beta-3 agonists. Based on what we know about UCP-1 as a potent stimulator of thermogenesis, researchers thought nothing should happen. How wrong they were!! There was still an increase in metabolic rate and body temperature that occurred in the UCP-1-deficient animals, which was mediated by white adipose tissue.34 The results demonstrate that white adipose tissue has the capacity to increase thermogenesis through the ?-3 receptor despite no effect on UCP-1. When reviewing the literature, it seems that in conjunction with consuming thermogenic supplements, you should also increase your consumption of polyunsaturated fats, as one study reported that in comparison to saturated fats with equal calories, a diet high in polyunsaturated fats increased mitochondrial activity and higher UCP-1 content than with saturated fats.26 Researchers are looking into pharmaceutical drugs that can counteract obesity by increasing UCP-1 expression in other organs (i.e., white adipose tissue). Muscle might be the better alternative to increasing thermogenesis as muscle is the major site of free fatty acid utilization. Of the beta-1 and beta-2 receptors located in muscle, the ?-2 receptor is the only receptor sub-type of importance for the adrenergic regulation of lipolysis in skeletal muscle and blood flow.28 Another positive benefit of increasing epinephrine during exercise is that epinephrine will cause vasodilatation of muscle, causing greater muscle swelling (a.k.a. pump) primarily mediated thru beta-2 receptors located on skeletal muscle.

 

[isoc]

I dont know the science behind all this, but it has been available for a few years, if it was really that impressive we would all know about it. IMHO, dont mess with it, probably doesnt work well, or any better than stuff we know a lot more about, including the risks.

 

[JohnnieFreeze]

I "researched" it..it worked for about a week and research subject quickly adapted to it..no more effect therafter.

 

[crazyfool405]

bump! I read on some bodybuilding sites about a few guys using it, but no one ever responded as to their results...

ive seen some studies on trecadrine b3 agonisst which works similiar,

ill see waht i can dig up on this thouhg

 

[crazyfool405]

only things i found on my data base are:

reduces adipose tissue in pigs

reduces adipoise tissue in cat fish and increases lean mass

 

[crazyfool405]

Introduction

A number of β-adrenergic receptor (β-AR) agonists have been shown to decrease body fat and increase muscle mass with oral administration in rodents, cattle, swine and sheep, although there appear to be species differences in responsiveness to different β-AR agonists [1, 2 and 3]. The mechanism for the decreased body fat in β-AR agonist treated animals is not fully understood. Although increased lipolysis has been demonstrated after β-AR agonist treatment of adipocytes in vitro, studies carried out in vivo have not consistently demonstrated increased lipolysis, even with a reduction in carcass fat [2].

The effects of clenbuterol have been previously demonstrated in mice [4], while the effects of previous termractopaminenext term have not. Since it has been suggested that these compounds target different β-AR subtypes and may have different mechanisms whereby they decrease adipose tissue mass, we wished to establish whether both were effective in decreasing adipose tissue mass and whether increased adipose tissue apoptosis contributed to the decrease in adipose tissue mass in normal mice.
2. Materials and methods
2.1. Animals

Five-week-old male (N=20) and female (N=20) ICR mice (Harlan Research Laboratories, Indianapolis, IN) were allowed to acclimate for 1 week prior to the experiment start date. Animals were housed singly in suspended wire cages and were provided ground rodent chow (ProLab® RMH 2500; Purina Mills, St. Louis, MO) and water ad libitum. Ambient room temperature was maintained and the light/dark cycle was 06:00/18:00 h, respectively. Animals were cared for in accordance with the Guide for the Care and Use of Laboratory Animals [5]. Prior to the start of the study, animals were briefly anesthetized with isofluorane and an IPPT-200 transponder (programmable ID and temperature, BMDS, Seaford, DE) was implanted subcutaneously between the scapulae.
2.2. Materials

Test articles included clenbuterol (Sigma Chemical Company, St. Louis, MO, item# C5423) and previous termractopaminenext term hydrochloride—Paylean® 9 (Elanco Animal Health, Indianapolis, IN). Clenbuterol is available as a pure product, and previous termractopaminenext term is readily available as a type A medicated article. Paylean® 9 contains 20 g previous termractopaminenext term hydrochloride per kilogram in a ground corncob base. In order to achieve doses of 200 and 800 ppm it was necessary to add 20 and 80 g of product per kilogram of diet. Control and clenbuterol diets were prepared with 80 g of alphacel, which is a diluent used to mimic the effect of the corncob in the previous termractopaminenext term product. The dose of clenbuterol used in this experiment was similar to those used in previous experiments with mice [6, 7, 8, 9 and 10].
2.3. Daily observations

Food intake (FI) was measured daily, while body weight (BW) and body temperatures (BT) were measured on days 0, 3, 7, 10, 14, 17, and 20 at approximately the same time of day (1300 h) during the treatment period. At 9 weeks of age (day 21), a final body weight measurement was obtained approximately 1 h prior to euthanasia, and animals were sacrificed by decapitation following CO2 asphyxiation.

Body composition analysis was performed after the mice had been decapitated, using a PIXImus® densitometer (GE Lunar Corporation; Waukesha, WI), which uses dual-energy X-ray absorptiometry to measure whole body (subcranial) bone mineral density, bone mineral content, percent lean tissue and percent fat tissue [11 and 12]. Brown intrascapular adipose tissue (BAT), inguinal (Ing), retroperitoneal (Rp), and epididymal (Epi) or parametrial (Par) white adipose tissues were harvested. Heart, liver, and kidney, as well as the right-side gastrocnemius (GC), semitendinosus, biceps femoris, triceps brachii, and longissimus dorsi muscles were removed, weighed individually, flash frozen in liquid nitrogen and then stored at −80 °C. Tissue weights were recorded for statistical analysis.
2.4. DNA isolation and apoptosis assay

Only the Epi and Par fat pads had sufficient tissue for the apoptosis assay. Apoptosis was assayed in two ways: DNA isolated from fat tissue was separated into two fractions: fragmented and genomic DNA. First, the fragmented DNA was run on an agarose gel in order to identify a ladder pattern of internucleosomal DNA degradation that is characteristic of apoptosis [13 and 14]. Second, apoptosis was quantified as the ratio of fragmented- to total-DNA, multiplied by 100 [15]. Briefly, approximately 50 mg of the Epi or Par white adipose tissue was homogenized in lysis buffer (10 mM Tris–HCl, pH 8.0; 10 mM EDTA, pH 8.0; 0.5% Triton X-100) and centrifuged at 14,000×g for 15 min to separate fragmented DNA from genomic DNA. The supernatant, containing fragmented DNA, was extracted with phenol–chloroform–isoamyl alcohol (25:24:1), and the DNA was precipitated by adding polyacryl carrier (Molecular Research Center, Inc., Cincinnati, OH) and ethanol. Genomic (non-fragmented) DNA was extracted from the pellet with DNAzol and the polyacryl carrier. DNA in each fraction was quantified by the PicoGreen method (Molecular Probes, Inc., Eugene, OR) and fluorescence was measured using a SpectroMax Gemini (Molecular Devices).
2.5. Statistical analysis

Analysis of variance (SAS) was used to determine significance of treatment and gender effects. Significance among means was determined by Tukey’s test. Statistically significant differences are defined at the 95% confidence interval.
3. Results
3.1. Food Intake, body weight, body composition and body temperature

There were no significant gender, treatment or gender×treatment effects on body weight, weight gain, food intake, feed efficiency or body temperature. Densitometry indicated no significant gender, treatment or gender×treatment differences in body composition (Table 1).

Table 1. Effects of 21-day oral treatment with control, 200 ppm clenbuterol, 200 ppm previous termractopaminenext term and 800 ppm previous termractopaminenext term on body weight, food intake, feed efficiency, body temperature and body composition in mice
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Full-size table (<1K)

There were no significant differences among treatment means. Data shown are treatment means. TSE: Treatment standard error.

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3.2. Tissue weights

There were significant gender effects for weights of Rp adipose tissue, biceps brachialis muscle, heart, kidney and liver, and significant treatment effects for Rp and Epi/Par adipose tissue and BAT (Table 2 and Fig. 1). There was a significant gender×treatment interaction for the Epi/Par fat pad (P<0.05; Table 3). Overall, Rp and Epi/Par fat pad weights were reduced in both 800 ppm previous termractopaminenext term and clenbuterol treated mice compared to control (P<0.05; Fig. 1), but for the Epi/Par fat pads, the effect occurred only in females ( Table 3). BAT mass was significantly increased (P<0.05) in the clenbuterol-treated group compared to control (Fig. 1).

Table 2. Effects of 21-day oral treatment with control, 200 ppm clenbuterol, 200 ppm previous termractopaminenext term and 800 ppm previous termractopaminenext term on selected tissue weights (g) in male and female mice
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Full-size table (<1K)

Data shown are treatment means. S.E.M.: Standard error of the mean.

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Fig. 1. Retroperitoneal fat pad (Rp) weight, epididymal/parametrial fat pad (Epi/Par) weight and intrascapular brown adipose tissue (BAT) weight for control, 200 ppm clenbuterol, 200 ppm previous termractopaminenext term and 800 ppm previous termractopaminenext term treated mice. Data are means±S.E.M. a, b, c: Means with different letters are different, P<0.05.

View Within Article



Table 3. Effects of 21-day oral treatment with control, 200 ppm clenbuterol, 200 ppm previous termractopaminenext term and 800 ppm previous termractopaminenext term on Epi and Par weights in male and female mice (N=5)

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Full-size table (<1K)

Means with different letters are different, P<0.05.

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3.3. Adipose tissue apoptosis

There was no significant gender effect on % DNA fragmentation in the Epi/Par fat pad, but there was a significant treatment effect (F(3,30)=4.0; P=0.017). Percent DNA fragmentation in the Epi/Par fat pad in the 200 ppm clenbuterol-treated group was increased compared to control and 200 ppm previous termractopaminenext term-treated groups (P<0.05; Fig. 2). There was also a significant increase in % DNA fragmentation in the 800 ppm previous termractopaminenext term treatment group compared to control (P<0.05; Fig. 2). Neither clenbuterol nor previous termractopaminenext term treatments increased DNA fragmentation in retroperitoneal or inguinal fat pads.



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Fig. 2. Percent DNA fragmentation (apoptosis) in epididymal/parametrial (Epi/Par) fat pads in control, 200 ppm clenbuterol, 200 ppm previous termractopaminenext term and 800 ppm previous termractopaminenext term treated mice. Data are means±S.E.M. a, b, c: Means with different letters are different, P<0.05.

View Within Article


4. Discussion
Treatment of male and female mice with either 200 ppm clenbuterol or 800 ppm previous termractopaminenext term in the diet resulted in a significant increase in apoptosis in the epididymal and parametrial adipose tissues, a finding that has not been previously reported. This finding suggests that activation of β-ARs can trigger the apoptotic process in adipose tissue. Although we did not specifically identify the cell type involved, these results are similar to those in previous experiments in which leptin administration was shown to increase apoptosis of adipocytes [14] and decrease the number of adipocytes in fat pads in which apoptosis was found [16]. Clenbuterol has been shown to have direct effects on mouse adipocytes in previous studies. For example, clenbuterol stimulated lipolysis and inhibited insulin-induced lipolysis in mouse adipocytes in vitro [17], and clenbuterol decreased insulin binding to mouse adipocytes in vitro [18]. These findings suggest that the effects of clenbuterol and previous termractopaminenext term on adipocyte apoptosis may also be direct effects.

Clenbuterol treatment also resulted in increased BAT mass in both males and females and decreased mass of Rp and Epi/Par fat pads in females only, findings that are similar to those of a previous study with mice [19]. We also found that 800 ppm previous termractopaminenext term resulted in decreased Rp and Epi/Par fat pad mass. The increase in BAT mass in clenbuterol treated mice is consistent with the increase that occurs as a result of increased sympathetic nervous system (SNS) stimulation during cold exposure [20] and after exogenous administration of specific β-AR agonists [21]. Phosphorylation of the mitogen-activated protein kinase ERK1/2 has been shown to be involved in the hyperplastic effect of β-AR stimulation of BAT [20].

Body composition, food intake, feed efficiency, body weight, and body temperature were not significantly affected by either previous termractopaminenext term or clenbuterol in our study. Likewise, neither β-AR agonist increased muscle mass, although this was a prominent effect in other studies in mice [17] and rats [22]. In rats, oral administration of previous termractopaminenext term also had little effect on body weight, while intraperitoneal administration caused an increase [23]. Studies with pigs, however, have shown increased body weight and food intake following administration of previous termractopaminenext term [24 and 25]. Whether these differences are a result of differences in mouse strain or species used is not known. It is possible that the use of densitometry to measure body composition did not provide sufficient sensitivity to detect differences. However, Nagy and Clair [12] and Brommage [11] both found a consistent linear relationship between densitometry-derived lean mass and fat mass and those obtained by chemical analysis. It is unlikely that these small differences would have affected the results of our study. Thus, it is unclear why we did not find differences in body composition in mice treated with clenbuterol or previous termractopamine.next term

The effect of clenbuterol and previous termractopaminenext term on adipose apoptosis is interesting. Clenbuterol has been shown to protect against apoptosis in both brain and liver [26, 27 and 28], and in BAT, β-AR stimulation also protects against adipocyte apoptosis [20]. In contrast, norepinephrine, a β-AR agonist, was found to induce apoptosis of cardiac myocytes via β1-AR stimulation [29 and 30]. However, the effect of β-AR agonists on apoptosis of white adipose tissue has not previously been reported.

Apoptosis of white adipose tissue can be induced by a variety of factors, some of which act directly on adipocytes, such as tumor necrosis factor-α [31], galectin-12 [32] and conjugated linoleic acids [33]. Adipose tissue apoptosis can also be induced by leptin, acting via central nervous system receptors [14 and 34]. The mechanisms and central pathways involved in leptin-induced adipose apoptosis have not yet been determined, but Neuropeptide Y (NPY) may be a negative downstream effector, because administration of an NPY receptor blocker resulted in increased adipose tissue apoptosis [35]. Both NPY and leptin have been shown to influence SNS activity. Leptin acts centrally to increase SNS activity in brown and white adipose tissue [36], while intracerebroventricular injection of NPY suppressed SNS stimulation of brown adipose tissue (BAT) [37]. NPY is also co-localized with norepinephrine in sympathetic nerve terminals and can act prejunctionally to suppress the release of norepinephrine [38]. The effects of these two peptides on SNS activity and adipose tissue apoptosis are interesting in light of our current findings of increased adipose apoptosis in response to β-AR stimulation. Our demonstration of adipose apoptosis induced by β-AR stimulation suggests a mechanism by which centrally active neuropeptides and neurotransmitters could affect adipose tissue cellularity.
Acknowledgements

This study was supported in part by the Georgia Research Alliance Eminent Scholar endowment held by C.A.B.
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[crazyfool405]

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[JadeSnowe]

PLEASE READ BEFORE TRYING RACTOPAMINE! IMPORTANT

PLEASE CHECK THIS OUT BEFORE TRYING THIS SO CALLED SUPPLEMENT OR WHATEVER YOU WANT TO CALL IT!!
Since I have not been a member long enough I cannot post the source I got this from or my email address for more info. I will say that if you google Dr. Mercola and Ractopmine you should be able to find this article. I will copy the majority of the article here. Please read, very important. This stuff is dangerous.
Be Safe & Blessed
~BELLE (JADESNOWE)

Banned in 160 Nations… Yet U.S. FDA Regards it as Safe?
Posted by Dr. Mercola | March 06 2010 | 71,614 views

cattle, livestockA livestock drug banned in 160 nations and responsible for hyperactivity, muscle breakdown and 10 percent mortality in pigs has been approved by the FDA.

The beta agonist ractopamine, a repartitioning agent that increases protein synthesis, was recruited for livestock use when researchers found the drug, used in asthma, made mice more muscular.

Ractopamine is started as the animal nears slaughter.

How does a drug marked, "Not for use in humans. Individuals with cardiovascular disease should exercise special caution to avoid exposure. Use protective clothing, impervious gloves, protective eye wear, and a NIOSH-approved dust mask" become "safe" in human food? With no washout period?

The drug is banned in Europe, Taiwan and China, and more than 1,700 people have been "poisoned" from eating pigs fed the drug since 1998, but ractopamine is used in 45 percent of U.S. pigs and 30 percent of ration-fed cattle.

 

[JadeSnowe]

((MORE INFO CONCERNING RACTOPAMINE, I HOPE IT HELPS.))

Ractopamine, aka Paylean and Optaflexx, is banned in 160 countries, including Europe, Taiwan and China. If imported meat is found to contain traces of the drug, it is turned away, while fines and imprisonment result for its use in banned countries.

Yet, in the United States 45 percent of pigs, 30 percent of ration-fed cattle, and an unknown percentage of turkeys are pumped full of this drug in the days leading up to slaughter.

Why?

This drug, manufactured by Elanco Animal Health, increases protein synthesis. In other words, it makes animals more muscular … and this increases food growers’ bottom line.

Adding insult to injury, up to 20 percent of ractopamine remains in the meat you buy from the supermarket, according to veterinarian Michael W. Fox. Yet this drug is marked “Not for use in humans,” and is known to increase death and disability in livestock.

Why is Ractopamine Allowed in U.S. Meat?

While other drugs require a clearance period of around two weeks to help ensure the compounds are flushed from the meat prior to slaughter (and therefore reduce residues leftover for human consumption), there is no clearance period for ractopamine.

In fact, food growers intentionally use the drug in the last days before slaughter in order to increase its effectiveness.

“How does a drug marked, "Not for use in humans. Individuals with cardiovascular disease should exercise special caution to avoid exposure. Use protective clothing, impervious gloves, protective eye wear, and a NIOSH-approved dust mask" become "safe" in human food? With no washout period?” asks columnist Martha Rosenberg.

She answers:

“The same way Elanco's other two blockbusters, Stilbosol (diethylstilbestrol or DES), now withdrawn, and Posilac or bovine growth hormone (rBST), bought from Monsanto in 2008, became part of the nation's food supply: shameless corporate lobbying.

A third of meetings on the Food Safety and Inspection Service's public calendar in January 2009 were with Elanco, a division of Eli Lilly -- or about ractopamine.”

Massive Industry Lobbying Gets Agribusiness What it Wants … at Your Expense

Industrial agriculture lobbyists wield incredible power in Congress, and the fact that ractopamine is in U.S. meat is a shining testimony to this.

Time magazine put it quite well when they described current farm policy as "a welfare program for the megafarms that use the most fuel, water and pesticides; emit the most greenhouse gases; grow the most fattening crops; hire the most illegals; and depopulate rural America."

There are too many conflicts of interest to name, but, for example, you may be surprised to learn that former Iowa Governor Tom Vilsack is now the Secretary of Agriculture, an appointment that took place despite massive public outcry.

What was needed for an effective Secretary of Agriculture was someone who would develop and implement a plan that promotes family-scale farming and a safe and nutritious food system with a sustainable and organic vision.

What we got was yet another politician who’s already made room in his bed for the industry lobby. Overall, Vilsack’s record is one of aiding and abetting Concentrated Animal Feeding Operations (CAFOs) or factory farms (the ones that use chemicals like ractopamine) and promoting animal cloning.

Cozy Connections Allowed rbGH Hormones in Your Dairy Products, Too

Michael Taylor, a former vice president of public policy and chief lobbyist at Monsanto Company, is now the senior advisor for the U.S. Food and Drug Administration (FDA).

Who is Michael Taylor?

He is the person who not only “oversaw the creation of GMO policy,” according to Jeffrey Smith, the leading spokesperson on the dangers of GM foods, but also oversaw the policy regarding Monsanto’s genetically engineered bovine growth hormone (rbGH/rbST).

This growth hormone, which has been banned in Canada, Europe, Japan, Australia and New Zealand because of cancer risks and other health concerns, was approved in the United States while Taylor was in charge at the FDA. Smith writes:

“Taylor also determined that milk from injected cows did not require any special labeling. And as a gift to his future employer Monsanto, he wrote a white paper suggesting that if companies ever had the audacity to label their products as not using rbGH, they should also include a disclaimer stating that according to the FDA, there is no difference between milk from treated and untreated cows.”

Taylor’s white paper, which again was untrue as even FDA scientists acknowledged differences in the rbGH milk, allowed Monsanto to sue dairies that labeled their products rbGH-free!

In a similar vain, the FDA's Center for Veterinary Medicine's Office of Surveillance and Compliance sent a 14-page warning letter to Elanco regarding ractopamine three years after its approval for use in pigs. They accused the company of withholding information about "safety and effectiveness" and "adverse animal drug experiences.”

Nonetheless, the next year the FDA decided to approved ractopamine for use in cattle, too, and later for turkeys as well.

What Should You do if You Don’t Want Drugs and Chemicals in Your Food?

As the U.S. agriculture industry now stands, antibiotics, pesticides, GM ingredients, hormones and countless other drugs are fair game in your food. So if you purchase your food from a typical supermarket, you are taking your chances that your food is teeming with chemicals and drugs -- even those that have been banned in other countries.

So please do your health a favor and support the small family farms in your area. You’ll receive nutritious food from a source that you can trust, and you’ll be supporting the honest work of a real family farm.

It all boils down to this: if you want to optimize your health, you must return to the basics of healthy food choices. Put your focus on WHOLE foods -- foods that have not been processed or altered from their original state -- food that has been grown or raised as nature intended, without the use of chemical additives, drugs, hormones, pesticides and fertilizers.

It’s as simple as that!

It is not nearly as daunting a task as it may seem to find a local farmer that can supply your family with healthy, humanely raised animal products and produce. At LocalHarvest.org, for instance, you can enter your zip code and find farmers' markets, family farms, and other sources of sustainably grown food in your area, all with the click of a button.

Once you make the switch from supermarket to local farmer, the choice will seem natural, and you can have peace of mind that the food you’re feeding your family is safe.