Melanotan II

[Talo]

Does anyone have experience with this ?

[spiderman7]

I have a bit. Seemed to help with libido, appetite, and the tan. The appetite effects disappear after a few weeks of use for me.

[Talo]

How long did you use it for ?
How long did the tan last ?
How often and how much did you take ?
Any negative sides ?

[spiderman7]

How long did you use it for ?
I used it for about two weeks. Off and on now thought for awhile.
How long did the tan last ?
It allowed me to get a darker tan then usual. It would last about a week if I would stop.
How often and how much did you take ?
I took about 200 mcg eod. The goal was to aid in fat loss. I was not concerned about a tan.
Any negative sides ?

I get a flushing feeling shortly after with some nausea. This went away fairly quickly. Some say if you take a antihistamine prior to the shot it reduces the effect.

[Talo]

Thanks

[#8]

It helps with fat loss?

[spiderman7]

It helps with fat loss?

Yes. I believe so. There are a couple of studies that say so. Here is one...



The Effects of the Melanocortin Agonist (MT-II) on Subcutaneous and Visceral Adipose Tissue in Rodents, April D. Strader, Haifei Shi, Ryuichi Ogawa, Randy J. Seeley and Ofer Reizes, JPET September 2007 vol. 322 no. 3 1153-1161

Abstract

The melanocortin system is a critical pathway in the regulation of energy balance. In this study, we analyzed the peripheral effects of the synthetic melanocortin agonist melanotan-II (MT-II) in rodents fed a low-fat or high-fat diet. MT-II-treated high-fat diet-induced obese (DIO) mice lost weight and body fat, whereas MT-II-treated low-fat-fed mice maintained their original body weight. Specifically, MT-II treatment led to a general reduction in both visceral and subcutaneous adipose tissue in high-fat-fed mice compared with Vehicle (ad libitum) controls. Vehicle-treated pair-fed DIO mice lost an equivalent amount of body weight compared with MT-II-treated mice but retained more adipose tissue. Pair-fed mice showed a reduction in visceral adipose tissue and no effect on subcutaneous adipose tissue compared with MT-II-treated mice. It is surprising that subcutaneous lean mass was significantly reduced in the pairfed mice. The data were replicated in DIO rats and indicated that MT-II treatment led to a generalized reduction in adipose tissue. These results indicate that peripheral MT-II treatment leads to weight loss that affects both the visceral and subcutaneous fat compartments. This finding illustrates the complexity of analyzing weight-reducing compounds. Although the present data suggest that the anorectic effect of MT-II is primarily a consequence of reduced food intake, the body composition data suggest that other mechanisms are involved.


Introduction

The melanocortin system is a critical neuronal signaling pathway for the actions of peripheral adiposity signals, such as leptin and insulin (Seeley et al., 2004). Energy balance regulated by the central melanocortin system relies on a balance in signaling between the endogenous melanocortin-3 and melanocortin-4 receptor (MC3R and MC4R) antagonist agouti-related peptide (AgRP) and the agonist a-melanocyte-stimulating hormone (a-MSH) derived from the pro-opiomelanocortin peptide. Central administration of AgRP results in long-lasting food intake in rats (Hagan et al., 2000), whereas both central and peripheral administration of a-MSH and the synthetic melanocortin receptor agonist melanotan-II (MT-II) reduces food intake (Hwa et al., 2001; Obici et al., 2001; Cettour-Rose and Rohner-Jeanrenaud, 2002; Hamilton and Doods, 2002; Pierroz et al., 2002; Choi et al., 2003a; Raposinho et al., 2003; Blüher et al., 2004; Seeley et al., 2005). The vital role of the MC3R and MC4R in maintaining melanocortin tone and energy balance is evident in melanocortin-receptor knockout mice. Both the MC3R and MC4R knockout mice exhibit increased adiposity due to the lack of receptor signaling by a-MSH (Chen et al., 2000a,b).

Although it is widely accepted that peripheral administration of MT-II results in a reduction in overall body fat (Pierroz et al., 2002; Choi et al., 2003a; Seeley et al., 2005), few studies have examined reductions in specific fat compartments. For example, peripheral MT-II-treatment in rats selectively reduced visceral adipose tissue, such as the retroperitoneal and epididymal fat pads, (Choi et al., 2003a) but no changes in subcutaneous fat. The use of a pair-fed control group suggests that the weight-reducing effects of MT-II are primarily a consequence of reduced food intake, because pair-fed and MT-II-treated groups show similar body weights at the end of treatment (Pierroz et al., 2002). In contrast to MT-II, central administration of AgRP or the synthetic antagonist SHU9119 results in a general increase in adipose tissue, such as the epididymal, retroperitoneal, and inguinal fat pads (Raposinho et al., 2000; Obici et al., 2001; Small et al., 2001; Korner et al., 2003). Even rats given central AgRP and pair-fed the same number of calories as vehicle-treated controls exhibited a specific increase in the weight of the inguinal fat pad (Korner et al., 2003).

Increased adiposity raises the levels of leptin and insulin. Leptin is secreted primarily from subcutaneous fat, and plasma levels correlate best with total subcutaneous adipose tissue (Montague et al., 1997; Van Harmelen et al., 1998). Unlike leptin, insulin levels are closely correlated with visceral adiposity (Pouliot et al., 1992; Ross et al., 1996). Central administration of AgRP and SHU9119 results in a disproportionate increase in leptin in ad libitum fed rodents compared with AgRP and SHU9119-pair-fed rodents, which may be explained by an increase in subcutaneous fat (Adage et al., 2001; Korner et al., 2003). These data indicate that melanocortin signaling can regulate peripheral adipose stores and that some of their effects may be independent of ingestion. Evidence for this shows that melanocortin receptor ligands alter oxygen consumption, body temperature, and lipolysis (Murphy et al., 2000; Hamilton and Doods, 2002; Choi et al., 2003a; Bradley et al., 2005; Song et al., 2005).

Over-consumption of a high-fat (HF) diet results in generalized increased adiposity (Woods et al., 2003) that can be partially reversed when rodents are given MT-II (Pierroz et al., 2002; Seeley et al., 2005). MT-II-induced anorexia is most pronounced when animals are obese or have been made obese after consumption of a high-fat diet compared with a low-fat diet (Hwa et al., 2001; Cettour-Rose and Rohner-Jeanrenaud, 2002; Hamilton and Doods, 2002; Pierroz et al., 2002; Blüher et al., 2004). Traditionally, it is believed that the accumulation of visceral adipose tissue poses a greater risk for comorbid conditions, such as type-2 diabetes and heart disease, whereas the presence of subcutaneous adipose tissue is viewed as less harmful (Després, 1993; Lebovitz, 2003). Therefore, an important effect of MT-II treatment or behavioral methods, such as caloric restriction, is the determination of what fat compartment is actually being reduced. Because weight loss induced by MT-II in rodents exposed to a high-fat diet is incomplete and never results in a level of adiposity possessed by rodents having never been on a high-fat diet, we hypothesized that the adipose tissue loss during MT-II treatment is a result of differential loss from the two main adipose compartments, visceral and subcutaneous. To test this hypothesis, we implanted mice and rats with 14-day osmotic mini-pumps and examined depot-specific weight loss using nuclear magnetic resonance.

..

Discussion

Weight loss through chronic administration of the melanocortin receptor agonist MT-II is readily achieved in rodents (Obici et al., 2001; Pierroz et al., 2002; Choi et al., 2003a,b; Seeley et al., 2005). The current findings support existing data and extend the literature in many ways. The data corroborate previous studies in that MT-II elicits weight loss most effectively in DIO rodents (Hwa et al., 2001; Cettour-Rose and Rohner-Jeanrenaud, 2002; Pierroz et al., 2002; Seeley et al., 2005). In contrast, rodents raised on low-fat diets are less sensitive to peripheral MT-II (Cettour-Rose and Rohner-Jeanrenaud, 2002; Pierroz et al., 2002). One of the primary mechanisms for MT-II-induced weight loss is reduced food intake. A critical point in understanding the mechanism for weight loss maintenance during chronic MT-II delivery is that once a new adiposity level is reached and plasma leptin has fallen, food intake increases to reflect the reduced inhibitory signaling of leptin on CNS circuits that regulate food intake. Specifically, AgRP neurons are targets for leptin, and when leptin levels are low, the inhibitory effect of leptin on AgRP is reduced, which allows AgRP to be more effective in increasing intake. In the present study, high-fat-fed rodents given MT-II reduced food intake for a period of time shorter than the length of delivery by the mini-pump. At the time-point during which food intake increases, weight loss had already reached its peak; therefore, the increase in food intake that followed, while the rodents maintained a lowered body weight, is a behavioral response that reflects a new lowered level of leptin signaling, rather than a waning of the anorectic effect of MT-II. This effect of MT-II and other peptides, such as amylin, on food intake has been reported by others (Hamilton and Doods, 2002; Raposinho et al., 2003; Seeley et al., 2005; Roth et al., 2006). To summarize, MT-II reduces food intake until lowered leptin levels are attained, and once a new body fat level is reached, food intake returns to normal (Seeley et al., 2005). Likewise, if adipose stores are low, as in the rodents on the low-fat diets, MT-II is relatively ineffective in reducing food intake and lowering body fat.

An important contribution of the present study is the identification of specific adipose compartments reduced by peripheral MT-II and that the weight loss is partially independent of food intake. Many studies have examined the effects of peripheral and central melanocortin agonists and antagonists on adiposity. For example, in separate studies, peripheral and central administration of MT-II or α-MSH decreased visceral adipose tissue (Obici et al., 2001; Choi et al., 2003a,b). Interestingly, Choi et al. (2003a,b) identified a decrease in subcutaneous fat following central administration of MT-II. In contrast, central administration of SHU9119 or AgRP increased retroperitoneal, epididymal, and inguinal fat (Adage et al., 2001; Obici et al., 2001; Small et al., 2001), an effect partially independent of food intake because antagonist-treated pair-fed rats had more total body fat than vehicle controls. In contrast to central administration, we show for the first time that chronic peripheral MT-II reduced visceral and subcutaneous adipose compartments. The present data are consistent with previous findings in that peripheral MT-II reduced visceral fat in MT-II-treated rodents. Interestingly, the effect on body fat was greatest in the MT-II-treated groups compared with pair-fed controls. In fact, in our rat study and in the study by Choi et al. (2003a), visceral fat was not reduced in the pair-fed controls as it was in the mouse study. Similar effects have been noted by Chen and Heiman (2000) in which leptin-induced weight loss was examined in rats and fat loss in pair-fed and ad libitum vehicle groups was identical. Only leptin treatment resulted in a loss of visceral fat in the above-mentioned study. One explanation for the discrepancy in visceral weight loss in the pair-fed controls between rats and mice may be a difference in metabolic rate. When pair-fed rodents are given a single allocation of food, they typically consume the majority of that food shortly after presentation. Because mice have a higher metabolic rate compared with rats, during the period when the pair-feeding allocation is totally consumed and fuel stores need to be mobilized, mice may be more adept at mobilizing fat stores from the visceral adipose depot than rats. In spite of this, the present study identified a generalized additional decrease in subcutaneous fat in both mice and rats. The current findings also identified a decrease in the epididymal fat only in MT-II-treated rats, which corroborates previous studies (Choi et al., 2003a).

This study highlights the utility of the NMR for analyzing total and specific fat compartments. Most studies assess fat depot changes by dissection and weighing each specific fat pad. By comparison, utilization of the NMR to assess compartmental fat and lean mass is more accurate and complete. Not only were all of the specific fat pads contained within each compartment but nondissectible fat, such as intramyocellular, epidermal, or organ adipose tissue, was included as well. Lastly, the utilization of the NMR technology is powerful in that it revealed potential confounding effects of the pair-feeding control group.

Mice that were pair-fed to the MT-II-treated group displayed reduced lean body mass compared with the ad libitum fed vehicle-treated controls despite achieving similar final body weights. Pair-fed mice not only lost visceral body fat, they also lost lean mass in the subcutaneous compartment. This finding highlights the complexities of parceling out the respective contribution of a therapeutic weight loss treatment, e.g., food intake-dependent and independent effects. These data and recent data from other studies (Larsen et al., 2001; Roth et al., 2006) suggest that pair-feeding may not be an optimal control for anorectic pharmacological agents. For example, in a recent paper by Roth et al. (2006), amylin was chronically infused via a mini-pump into rats as in the current study and significant reductions in fat was observed. In this study, a pair-fed control group was included, and total adipose and lean body mass were reduced. Although pair-feeding is the current standard for dissociating the anorectic versus metabolic effects of a compound, the physiological relevance of this control group must be evaluated carefully.

The depot-specific reduction in adipose tissue also parallels the plasma levels of two adiposity signals, leptin and insulin (Woods and Seeley, 2001). In both the mouse and rat study, visceral fat was decreased following MT-II treatment. It is known that central administration of SHU9119 and α-MSH affects insulin secretion (Adage et al., 2001; Obici et al., 2001). Centrally administered SHU9119 resulted in a 3-fold increase in plasma insulin compared with pair-fed SHU9119-treated controls, but because the pair-fed SHU9119-treated rats were leaner than the ad libitum fed SHU9119-treated rats, the increased adipose tissue in the SHU9119-treated ad libitum rats was the cause of the increase in plasma insulin rather than SHU9119 treatment itself. In contrast, we observed a decrease in plasma insulin in MT-II-treated and vehicle-treated pair-fed rats. This finding is in agreement with the peripheral administration of MT-II in the study by Choi et al. (2003a), in which a similar decrease in plasma insulin was noted in both the MT-II and pair-fed rats. In the present study, despite reduced insulin, pair-fed rats did not differ from ad libitum fed controls with respect to visceral fat mass.

In contrast to insulin, plasma leptin levels are increased in the SHU9119-treated group independent of body weight in the study by Adage et al. (2001). SHU9119 treatment in ad libitum and pair-fed rats resulted in significant increases in circulating leptin, 6- and 2-fold, respectively. Because leptin is traditionally associated with subcutaneous fat, it is tempting to speculate that SHU9119 increased subcutaneous adipose tissue and consequently resulted in an increase in plasma leptin. However, only visceral and epididymal adipose tissue changes were measured, and both were increased (Adage et al., 2001). In support of this speculation, Obici et al. (2001) infused SHU9119 centrally and found increased visceral and subcutaneous fat in rats. These findings combined with the present data support the hypothesis that changes in subcutaneous fat predict circulating leptin levels. We show that MT-II treatment resulted in a selective decrease in subcutaneous adipose mass in both mice and rats, and in the rat study, plasma leptin was lowest in the MT-II versus pair-fed and ad libitum controls. These findings are consistent with data by Choi et al. (2003a,b) who demonstrated that central MT-II treatment results in a decrease in subcutaneous fat (Choi et al., 2003b) and that peripheral MT-II resulted in nondetectable levels of leptin (Choi et al., 2003a).

To determine whether MT-II could be acting directly upon adipocytes, it is important to anatomically link melanocortin receptors to specific adipose compartments. In the present study, epididymal and inguinal adipose showed expression of the MC4R. These data are consistent with a previous study that also found that MC4R is expressed in inguinal adipose (Hoggard et al., 2004), but because MT-II is a nonselective agonist, it is possible that MT-II may be acting on other melanocortin receptors and that some of these are expressed on adipocytes (Boston and Cone, 1996; Hoch et al., 2007). Furthermore, α-MSH or MT-II treatment results in adipocyte lipolysis (Bradley et al., 2005). Although melanocortin receptors are on adipocytes, this does not definitively mean that lipolysis is a direct effect of MT-II. Recently, MC4R mRNA was extensively mapped to neural sites responsible for sympathetic outflow to the inguinal fat pad (Song et al., 2005). Together, these findings suggest that MT-II may act on peripheral or central substrates to reduce levels of subcutaneous fat.

The melanocortin system is arguably a promising target for the development of a pharmacological treatment for obesity; however, many studies demonstrate dramatic weight loss through nonconventional delivery methods, such as intracranial injections. The present data are significant because they provide evidence for peripherally delivered MT-II to reduce both compartments of adipose tissue, which when reduced undeniably result in a more promising healthy outcome.

References

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[Feenom]

What about beauty marks...freckles? I heard it increases them. I have very pale skin. Will it be an issue?

[JonnyO]

Dont use it and expect any fat loss though. Ive used it many time. Dont do the loading many suggest, just start off with .25-.5 and you'll be fine. I usually take it at night before bed because it makes my stomach upset. I dont hit the tanning beds though, but I have before and you dont need much, Id suggest 2x a week then once a week to maintain the desired color.

Usually after a montho r so I'll have a decent color going then its just a maintenece dosage a few times per week.

[Talo]

I think the fat loss would just be an added bonus ( if noticed ) with the tan being the main reason for this .

[ubcpower]

an asian friend of mine used it and got quite dark, he need to fake and bake on top of using it though

[Average 270lb Guy]

I used it 1 1/2 years ago, dosing as JohhnyO said and it worked great. Though it made my freckles turn almost black but they fade over time. When I tan or go into the sun now my freckles darken up pretty quick but it has increased my tolerance for burning. It also darkened my hair (the little I have) and made my goatee turn almost black as well. I usually have blondish to brown hair. Stomach pain was tolerable, lasted about 5-10 mins and the libido was like taking a cialis but having no control over it.

[Not2Big]

I've used the Melanotan II a couple of times and would definitely do it again. The dosage is largely based on body size. For most people, 1 mg per day is more than enough to get a deep, dark tan. I would recommend starting with a smaller dose .25 and graduating up from there as it can cause some nauseau and flushing (very similar to a niacin flush) for the first short while. You do need to have some degree of UV to 'activate' the process. Usually 1 tan per week on the tanning beds is enough.

You would continue on this dose until you reach the desired level of color (usually takes 2-3 weeks). Maintenance would be 1-2 shots per week. The tan seems to last longer than a 'normal' tan. Initially you might find, depending on your skin type, that existing moles and freckles may appear to get darker while using it. For myself, this has subsided when I discontinued it. The appearance of new moles is also a possibility. It's great for people who don't ordinarily tan easily or people who burn quite easily.

I've toyed around with taking it in the morning, taking it in a divided dose and taking it at night. I've found that when I take it before bed, the 'nausea' feeling was much more tolerable.

[Beachmuscle]

How long did you use it for ?
2 weeks at a time. No tanning beds.
How long did the tan last ?
Almost same as a tan.
How often and how much did you take ?
1mg a day
Any negative sides ?
Not for me, my girlfriend had a spot develop but it went away after 2 months from our trip.

We didn't hit the tanning beds. Just melanotan 2. We darkened up and we noticed we tanned SUPER FAST our first few days.

[juced_porkchop]

just started it up myself for first time. going .23-0.5mg ed.
herd about fatloss so i guess witht he igf1lr3 and this it will be better.

[japh]

Can you let us know how it goes juced porkchop?

Before and after pics of forearm, leg, abdomen maybe?

I'm a little bit ginger myself so I'm going to give it a try this spring/summer during my diet.

I've seen how it works firsthand through a buddy and it does definitely work!

[troy_trinity]

The stuff makes you tan no question.

It gives you a color that you can't get naturally. DARK.

used 0.5 mg's 3x per week before tanning 3x per week. Upset stomach- immensely decreases appetite while dieting.

[juced_porkchop]

Can you let us know how it goes juced porkchop?

Before and after pics of forearm, leg, abdomen maybe?

I'm a little bit ginger myself so I'm going to give it a try this spring/summer during my diet.

I've seen how it works firsthand through a buddy and it does definitely work!
no pics.

but ill post how i liked it once its done. :popc2

[tony_canuck]

whatever you do, start small!! I got a bunch of friggin freckles because I started off with more than I should've, and I thought I was using a very tiny amount.

[japh]

Cool, thanks jp.

A quick written review would be just as good.