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Antaeus Labs Introduces: Lipomorph


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#1 henryv

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Posted 25 June 2014 - 06:38 AM

Antaeus Labs are proud to present LipoMorph, a weight-management supplement at the cutting edge of scientific understanding of human physiology. LipoMorph is the first “fat burner” supplement to specifically target all known modifiable mechanisms of white fat browning, and both brown and beige fat activation.

 

White Fat
Ordinary white fat stores energy in the form of fat droplets, one droplet per adipocyte, which can be broken down by lipolysis into free fatty acids which are circulated into the blood stream and transported to the fuel-requiring tissue where they undergo beta-oxidation to acetyl-CoA which can be used to generate energy through the Krebs cycle. The energy stored in white fat, when liberated, is primarily burned to produce ATP to power cells.
Unfortunately, modern Western diet and lifestyle habits (consisting of excessive caloric intake typically coupled with insufficient physical activity) can cause an excessive accumulation of both subcutaneous and visceral white adipose tissue (WAT) that can have numerous adverse effects on health and health markers.

 

Brown Fat
Brown fat is a thermogenic tissue that turns energy (stored as triglycerides) into heat. It’s found in abundance in hibernating mammals. When the temperature drops, animals like bears “go to sleep for the winter”. They’re able to survive by burning reserves of energy which have been stored as white and brown fat. The heat produced by the brown fat, which is activated by the cold, maintains the essential core body temperature of the animal through the winter months.

It’s also found in high quantities in babies, but is present in much smaller amounts in adult humans.
Unlike adults, babies are unable to regulate their own temperature by, say, putting on a coat or moving to a warmer room, so their ability to regulate their own temperature is more vital to their survival. Accordingly, they have greater amounts of brown fat which is widely distributed viscerally and subcutaneously, decreasing as age increases until as adults brown fat is largely limited to small deposits in the lower neck and supraclavicular region. These deposits are suspected to be useful in cold weather for warming blood as it flows to the brain. Brown fat appears brown in color because of the high density of mitochondria and excellent blood supply. Certain natural conditions, like endurance exercise and cold temperatures, can encourage the human body to produce and/or activate brown fat.

Thermogenesis in brown fat is mediated by thermogenin, also known as uncoupling protein 1 (UCP1). UCP1 is specific to the mitochondria of brown fat, and functions as a proton transporter, uncoupling oxidative phosphorylation from ATP synthesis and allowing the resulting energy to dissipate in the form of heat. The thermogenic effect of UCP1 is known as “non-shivering thermogenesis”.

 

Beige fat
In addition to classical brown fat, which originates from the same progenitor cells as muscle tissue, brown-like fat expressing the same thermogenic genes as brown fat can be made from regular mature white fat cells and their precursors. This brown-from-white fat is variously termed “brite” or “beige” fat, and the process of its creation known as “browning” of white fat. Whereas excessive white adipose tissue (WAT) impairs health, the recruitment and activation of brown and beige adipose tissue is currently being investigated as being potentially beneficial in the fight against obesity and metabolic disorders.

 


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#2 henryv

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Posted 25 June 2014 - 06:44 AM

Regulators of brown and beige fat

Natural regulators of brown and beige fat include external conditions like cold temperatures, and exercise, as well as internal mechanisms like thyroid hormones, beta-adrenergic hormones, retinoids, PPARγ and PPARα agonists, and the liver X receptor.

 

Exercise and peroxisome proliferator-activated receptors

Exercise has a number of positive health benefits, particularly regular, sustained aerobic exercise. One of the mediators of the positive metabolic effects of endurance exercise is peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). PGC-1α is a transcriptional coactivator that binds to and activates transcription factors that regulate the genes involved in energy metabolism. It has a number of functions in the body, including influencing muscle fiber type determination, controlling lactate metabolism, and increasing amino acid breakdown in response to exercise stimulus.

One of the products of amino acid breakdown in muscle tissue is β-aminoisobutyric acid (BAIBA), arising from the degradation of thymine and valine. BAIBA is believed to act as a messenger signalling molecule, released into the blood stream by exercise, that helps the body respond to demands for more energy by increasing β-oxidation of fatty acids.
It’s also recently been discovered that BAIBA can induce white adipose tissue (WAT) to express brown fat-specific genes – including the all-important thermogenic UCP1.

 

β-aminoisobutyric acid

What is it?
BAIBA is a naturally occurring amino acid, a product of the metabolism of thymine and valine. [1][2]
Levels of BAIBA are increased significantly by endurance exercise, a result of PGC1α-mediated amino acid breakdown. [3]

 

Target(s):

  • BAIBA exerts its effects on hepatocytes (liver cells) and white adipocytes (fat cells) through PPARalpha (PPARα). [4] PPARα regulates the use of fat as a source of energy. [5]

Research summary:

  • Activation of PPARα in the liver and adipose tissue promotes lipolysis and beta oxidation of fatty acids. [5]
  • PPARα activation stimulates white fat cell precursors to differentiate into beige/brite adipocytes. [4]
  • PPARα agonism also induces mature white adipocytes to develop a beige/brite phenotype. [4]
  • PPARα agonists increase UCP-1 mRNA levels in brown fat. [6]
  • PPARα agonism in the small intestine is thought to be involved in the regulation of satiety (lack of hunger). [7][8]
  • Coadministered PPARα and β3 adrenoceptor agonists may have a synergistic effect on the browning of white fat and UCP1-mediated thermogenesis. [9]
  • BAIBA induces human stem cells, under conditions that would normally result in white adipocyte differentiation, instead to express brown-fat specific genes like UCP-1. [4]
  • BAIBA induced increased expression of brown/beige fat-specific genes in an in vivo experiment on mice. [4]
  • BAIBA levels are increased after endurance exercise, and may be responsible for some of the metabolic benefits of exercise. [4]
  • BAIBA increases hepatic fatty acid oxidation and decreases fat mass in mice [10]
  • Some of the fat-loss effects of thymine-based prescription drugs in humans may be due to an increase in utilization of free fatty acids resulting from the production of BAIBA as a metabolite. [10]
  • Rats and mice treated with BAIBA and other PPARα agonists lose more body fat and gain less body weight than control animals. [11][7][9][10][4]

 

 


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#3 henryv

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Posted 25 June 2014 - 06:49 AM

Cold Temperatures and beta-adrenergic hormones

The thermogenic effects of brown fat can be activated in several ways; in hibernating animals and babies the trigger is cold temperatures. Cold temperatures trigger a release of norepinephrine into the blood stream, an adrenergic hormone which has several important roles, one of which is to activate brown fat via the beta-3 adrenergic receptor (β3 adrenoreceptor).

Unlike other beta adrenergic receptors, which are widely distributed about the body, being found in cardiac tissue, skeletal and smooth muscle, and adipose tissue, distribution of β3 receptors are restricted to a few tissues – including brown fat, where activation increases energy expenditure.

Brown fat also expresses heat-sensing receptors of its own. The receptor that detects cold temperatures is the cold and menthol receptor 1 (CMR1), more formally known as the transient receptor potential cation channel subfamily M member 8 (TRPM8).The transient receptor potential channels (TRPs) help the peripheral nervous system detect important variations in temperature; TRPV1 detects and regulates heat, but can also be activated by things like capsaicin (which is why chili peppers taste hot), and TRPM8 detects cold but can also be activated by compounds like menthol (which is why peppermint tastes cold).

Thermogenesis in brown fat can be triggered by TRPM8 activation or norepinephrine release (β3 adrenoreceptor agonism). Human white adipose tissue also expresses the cold-sensing receptor TRPM8, which, when activated, transdifferentiates to a brown-like phenotype expressing UCP-1.

 

Octopamine

What is it?
Octopamine is a naturally-occurring endogenous amine found in plants such as bitter orange as well as vertebrates and invertebrates. [12][13]

 

Target(s):

  • Octopamine is a selective agonist of the mammalian beta-3 adrenergic receptor (β3 adrenoreceptor). [14][15]
  • Beta-3-adrenoceptor agonism is one of the primary regulators of brown fat activation and beige fat recruitment. [16]

Research summary:

  • Beta-3-adrenoceptor activation is believed to be required for the transdifferentiation of mature white fat cells into brite/beige adipocytes. [16]
  • Octopamine stimulates lipolysis in white fat cells and increased oxidation in brown fat cells in several mammal species. [15]
  • Octopamine stimulates fatty acid oxidation in the liver, which may help prevent free fatty acids being reabsorbed into adipocytes. [17]

Menthol

What is it?

(−)-Menthol is a naturally-occurring compound found in wild mint and peppermint.

 

Target(s):

  • Menthol is an agonist of the TRPM8 receptor, also known as the cold and menthol receptor.
  • TRPM8 activation triggers thermogenesis in brown fat by mimicking long-term cold exposure. [18]
  • Menthol is also an agonist of transient receptor potential A1 (TRPA1) in humans, [19] another thermosensitive (cold-sensing) receptor that has been linked to brown fat activation in animal models. [20]

Research summary:

  • Dietary menthol induced non-shivering thermogenesis in mice without influencing metabolic markers such as heart rate or thyroid hormone levels. [18]
  • Human white adipose tissue also expresses the cold-sensing receptor TRPM8, which, when activated by menthol, transdifferentiates to a brown-like phenotype expressing UCP-1. [21]
  • A human clinical trial is currently recruiting participants to determine the metabolic effects of menthol. [22]

 


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#4 henryv

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Posted 25 June 2014 - 06:51 AM

Retinoids and LXR

 

Ilex Kudingcha Extract

 

What is it?

Ilex Kudingcha (Ilex kaushue) is a species of the holly genus of plants. In China the leaves are dried and brewed into a tea called Kuding. The bitter-tasting Kuding tea has been used for millennia as a traditional chinese medicine (TCM) for a variety of ailments.

 

Target(s):
  • Kuding has the ability to suppress the activity of the Liver X Receptor beta (LXRβ) through antagonist activity. [23]
  • LXRβ antagonism results in decreased transcriptional activity of the enzyme sterol regulatory element-binding protein-1c (SREBP-1c), which is required for lipogenesis. [24]

Research summary:

  • LXRβ is believed to be a regulator (repressor) of UCP-1 activity. [25]
  • LXRβ antagonism may cause UCP1 transcription to be activated through an increase in PGC1α expression. [25]

Vitamin A

What is it?

One of the forms of vitamin A is retinol. This animal-derived retinoid is essential for healthy skin, bone, and teeth. The main active metabolite of vitamin A is retinoic acid.

 

Target(s):
  • Retinoic acid binds to and activates the retinoic acid receptor (RAR).
  • The vitamin A metabolite 9-cis-retinoic acid is an endogenous ligand of the retinoid X receptor (RXR)
Research summary:
  • Retinoic acid activates transcription of uncoupling protein-1 (UCP-1) both in vitro and in vivo. [26][27]
  • Retinoic acid is necessary for induction of human UCP1 by beta-adrenergic agonists. [28]
  • Retinal (retinaldehyde), another retinol metabolite, induces browning of white fat through activation of the retinoic acid receptor (RAR). [29]


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#5 henryv

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Posted 25 June 2014 - 06:55 AM

Other regulators of beige and brown fat

 

Fucoxanthin

What is it?
Fucoxanthin is a naturally-occurring xanthophyll found in brown algae and edible seaweed.

 

Target(s):
Some of fucoxanthin’s putative anti-obesity effects may be via downregulation of PPAR-γ. [30]

 

Research summary:

  • Fucoxanthin increases the metabolic rate, induces the browning of white fat, and upregulates UCP1 (thermogenin) expression in mice. [31]
  • Mice fed a high fat diet and supplemental fucoxanthin had increased expression of β3-adrenergic receptor mRNA in white fat tissue. [32]
  • In in vitro experiments, fucoxanthin and its metabolites suppress adipogenesis via downregulation of PPAR-γ. [30]
  • Fucoxanthin increases phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) and decreases the expression of SREBP1c in mouse adipose tissue, promoting β-oxidation of fatty acids and reducing lipogenesis [33]
  • A human study on obese non-diabetic women given a commercial product containing fucoxanthin and pomegranate seed oil found that it increase the resting energy expenditure of the participants and promoted weight loss. [34]

Stearoyl Vanillylamide

What is it?

Stearoyl vanillylamide is a naturally-occurring capsaicin analogue found in red pepper species. Capsaicin is responsible for the hot/burning feeling caused by chili peppers. Unlike capsaicin, stearoyl vanillylamide is nonpungent, meaning it does not impart the “spicy” or irritative effects of capsaicin.

 

Target(s):

Stearoyl vanillylamide, capsaicin and similar compounds activate the transient receptor potential cation channel V1 (TRPV1).

 

Research summary:

  • TRPV1 activation stimulates the release of catecholamines such as adrenaline and noradrenaline from the adrenal medulla. [35] Noradrenaline is a major regulator of brown fat activation, through β3 adrenoreceptor activation.
  • Nonpungent capsaicin analogs have been demonstrated to activate brown adipose tissue and increase energy expenditure in a human clinical trial. [36]
  • A systematic review of human clinical trials observed that regular consumption of capsaicinoids increased energy expenditure, and significantly reduced abdominal adipose tissue levels. [37]
  • Chronic TRPV1 activation by dietary TRPV1 agonists can increase phosphorylated levels of protein kinase A (PKA) and endothelial NO synthase (eNOS), causing peripheral vasodilation and a decrease in blood pressure in hypertensive rats. [38]
  • The oral administration of TRPV1 agonists prevents adipogenesis and obesity in mice fed a high-fat diet. [39]
  • Stearoyl vanillylamide increased lipolysis and oxidation of free fatty acids in rats, resulting in increased capacity for exercise [40]
  • Some non-pungent capsinoids have also been found to activate TRPA1, another receptor that may be involved in cold detection. [41]


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#6 henryv

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Posted 25 June 2014 - 07:01 AM

LipoMorph encapsulates the most cutting-edge scientific understanding of nutritional manipulation of metabolic regulation, and as such represents the most complete natural thermogenic formula on the market. A simplified overview of the physiological mechanisms by which the LipoMorph ingredients are believed to act is shown below.

This supplement is not suitable for WADA-tested athletes, as octopamine appears on the current WADA banned substance list.

If you are an athlete subjected to testing for PEDs please check with your governing body before purchasing this supplement.

 

These statements have not been evaluated by the Food and Drug Administration.
This product is not intended to diagnose, treat, cure, or prevent any disease.

 

References:
[1] Nielsen, H.R., Sjølin, K.-E., Nyholm, K., Baliga, B.S., Wong, R., and Borek, E. (1974). β-Aminoisobutyric Acid, a New Probe for the Metabolism of DNA and RNA in Normal and Tumorous Tissue. Cancer Res 34, 1381–1384.
[2] Hillcoat, B.L. (1961). The excretion of beta-aminoisobutyric acid following thymine and dihydrothymine administration to man. Aust J Exp Biol Med Sci 39, 423–427.
[3] Hatazawa, Y., Tadaishi, M., Nagaike, Y., Morita, A., Ogawa, Y., Ezaki, O., Takai-Igarashi, T., Kitaura, Y., Shimomura, Y., Kamei, Y., et al. (2014). PGC-1α-Mediated Branched-Chain Amino Acid Metabolism in the Skeletal Muscle. PLoS ONE 9, e91006.
[4] Roberts, L.D., Boström, P., O’Sullivan, J.F., Schinzel, R.T., Lewis, G.D., Dejam, A., Lee, Y.-K., Palma, M.J., Calhoun, S., Georgiadi, A., et al. (2014). β-Aminoisobutyric Acid Induces Browning of White Fat and Hepatic β-Oxidation and Is Inversely Correlated with Cardiometabolic Risk Factors. Cell Metabolism 19, 96–108.
[5] Rakhshandehroo, M., Knoch, B., Müller, M., and Kersten, S. (2010). Peroxisome proliferator-activated receptor alpha target genes. PPAR Res 2010.
[6] Barbera, M.J., Schluter, A., Pedraza, N., Iglesias, R., Villarroya, F., and Giralt, M. (2001). Peroxisome proliferator-activated receptor alpha activates transcription of the brown fat uncoupling protein-1 gene. A link between regulation of the thermogenic and lipid oxidation pathways in the brown fat cell. J. Biol. Chem. 276, 1486–1493.
[7] Fu, J., Gaetani, S., Oveisi, F., Lo Verme, J., Serrano, A., Rodríguez de Fonseca, F., Rosengarth, A., Luecke, H., Di Giacomo, B., Tarzia, G., et al. (2003). Oleylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-α. Nature 425, 90–93.
[8] Lo Verme, J., Gaetani, S., Fu, J., Oveisi, F., Burton, K., and Piomelli, D. (2005). Regulation of food intake by oleoylethanolamide. Cell. Mol. Life Sci. 62, 708–716.
[9] Suárez, J., Rivera, P., Arrabal, S., Crespillo, A., Serrano, A., Baixeras, E., Pavón, F.J., Cifuentes, M., Nogueiras, R., Ballesteros, J., et al. (2014). Oleoylethanolamide enhances β-adrenergic-mediated thermogenesis and white-to-brown adipocyte phenotype in epididymal white adipose tissue in rat. Dis Model Mech 7, 129–141.
[10] Maisonneuve, C., Igoudjil, A., Begriche, K., Lettéron, P., Guimont, M.-C., Bastin, J., Laigneau, J.-P., Pessayre, D., and Fromenty, B. (2004). Effects of zidovudine, stavudine and beta-aminoisobutyric acid on lipid homeostasis in mice: possible role in human fat wasting. Antivir. Ther. (Lond.) 9, 801–810.
[11] Guzmán, M., Lo Verme, J., Fu, J., Oveisi, F., Blázquez, C., and Piomelli, D. (2004). Oleoylethanolamide stimulates lipolysis by activating the nuclear receptor peroxisome proliferator-activated receptor alpha (PPAR-alpha). J. Biol. Chem. 279, 27849–27854.
[12] Tang, F., Tao, L., Luo, X., Ding, L., Guo, M., Nie, L., and Yao, S. (2006). Determination of octopamine, synephrine and tyramine in Citrus herbs by ionic liquid improved “green” chromatography. J Chromatogr A 1125, 182–188.
[13] David, J.C., and Coulon, J.F. (1985). Octopamine in invertebrates and vertebrates. A review. Prog. Neurobiol. 24, 141–185.
[14] Carpéné, C., Galitzky, J., Fontana, E., Atgié, C., Lafontan, M., and Berlan, M. (1999). Selective activation of beta3-adrenoceptors by octopamine: comparative studies in mammalian fat cells. Naunyn Schmiedebergs Arch. Pharmacol. 359, 310–321.
[15] Fontana, E., Morin, N., Prévot, D., and Carpéné, C. (2000). Effects of octopamine on lipolysis, glucose transport and amine oxidation in mammalian fat cells. Comp. Biochem. Physiol. C Toxicol. Pharmacol. 125, 33–44.
[16] Barbatelli, G., Murano, I., Madsen, L., Hao, Q., Jimenez, M., Kristiansen, K., Giacobino, J.P., De Matteis, R., and Cinti, S. (2010). The emergence of cold-induced brown adipocytes in mouse white fat depots is determined predominantly by white to brown adipocyte transdifferentiation. Am. J. Physiol. Endocrinol. Metab. 298, E1244–1253.
[17] De Oliveira, A.L., de Paula, M.N., Comar, J.F., Vilela, V.R., Peralta, R.M., and Bracht, A. (2013). Adrenergic Metabolic and Hemodynamic Effects of Octopamine in the Liver. Int J Mol Sci 14, 21858–21872.
[18] Ma, S., Yu, H., Zhao, Z., Luo, Z., Chen, J., Ni, Y., Jin, R., Ma, L., Wang, P., Zhu, Z., et al. (2012). Activation of the cold-sensing TRPM8 channel triggers UCP1-dependent thermogenesis and prevents obesity. J Mol Cell Biol mjs001.
[19] Xiao, B., Dubin, A.E., Bursulaya, B., Viswanath, V., Jegla, T.J., and Patapoutian, A. (2008). Identification of the Transmembrane Domain Five as a Critical Molecular Determinant of Menthol Sensitivity in Mammalian TRPA1 Channels. J Neurosci 28, 9640–9651.
[20] Tamura, Y., Iwasaki, Y., Narukawa, M., and Watanabe, T. (2012). Ingestion of cinnamaldehyde, a TRPA1 agonist, reduces visceral fats in mice fed a high-fat and high-sucrose diet. J. Nutr. Sci. Vitaminol. 58, 9–13.
[21] Rossato, M., Granzotto, M., Macchi, V., Porzionato, A., Petrelli, L., Calcagno, A., Vencato, J., De Stefani, D., Silvestrin, V., Rizzuto, R., et al. (2014). Human white adipocytes express the cold receptor TRPM8 which activation induces UCP1 expression, mitochondrial activation and heat production. Molecular and Cellular Endocrinology 383, 137–146.
[22] Effects and Safety of Menthol on Blood Pressure and Metabolic Parameters in Prehypertensive and Mild Hypertensive Patients (ESMAB) ClinicalTrials.gov Identifier: NCT01408446
[23] Fan, S., Zhang, Y., Hu, N., Sun, Q., Ding, X., Li, G., Zheng, B., Gu, M., Huang, F., Sun, Y.-Q., et al. (2012). Extract of Kuding tea prevents high-fat diet-induced metabolic disorders in C57BL/6 mice via liver X receptor (LXR) β antagonism. PLoS ONE 7, e51007.
[24] Schultz, J.R., Tu, H., Luk, A., Repa, J.J., Medina, J.C., Li, L., Schwendner, S., Wang, S., Thoolen, M., Mangelsdorf, D.J., et al. (2000). Role of LXRs in control of lipogenesis. Genes Dev. 14, 2831–2838.
[25] Korach-André, M., Archer, A., Barros, R.P., Parini, P., and Gustafsson, J.-Å. (2011). Both liver-X receptor (LXR) isoforms control energy expenditure by regulating Brown Adipose Tissue activity. PNAS 108, 403–408.
[26] Puigserver, P., Vazquez, F., Bonet, M.L., Pico, C., and Palou, A. (1996). In vitro and in vivo induction of brown adipocyte uncoupling protein (thermogenin) by retinoic acid. Biochem J 317, 827–833.
[27] Alvarez, R., de Andrés, J., Yubero, P., Viñas, O., Mampel, T., Iglesias, R., Giralt, M., and Villarroya, F. (1995). A novel regulatory pathway of brown fat thermogenesis. Retinoic acid is a transcriptional activator of the mitochondrial uncoupling protein gene. J. Biol. Chem. 270, 5666–5673.
[28] Del Mar Gonzalez-Barroso, M., Pecqueur, C., Gelly, C., Sanchis, D., Alves-Guerra, M.C., Bouillaud, F., Ricquier, D., and Cassard-Doulcier, A.M. (2000). Transcriptional activation of the human ucp1 gene in a rodent cell line. Synergism of retinoids, isoproterenol, and thiazolidinedione is mediated by a multipartite response element. J. Biol. Chem. 275, 31722–31732.
[29] Kiefer, F.W., Vernochet, C., O’Brien, P., Spoerl, S., Brown, J.D., Nallamshetty, S., Zeyda, M., Stulnig, T.M., Cohen, D.E., Kahn, C.R., et al. (2012). Retinaldehyde dehydrogenase 1 regulates a thermogenic program in white adipose tissue. Nat. Med. 18, 918–925.
[30] Maeda, H., Hosokawa, M., Sashima, T., Takahashi, N., Kawada, T., and Miyashita, K. (2006). Fucoxanthin and its metabolite, fucoxanthinol, suppress adipocyte differentiation in 3T3-L1 cells. Int. J. Mol. Med. 18, 147–152.
[31] Maeda, H., Hosokawa, M., Sashima, T., Funayama, K., and Miyashita, K. (2005). Fucoxanthin from edible seaweed, Undaria pinnatifida, shows antiobesity effect through UCP1 expression in white adipose tissues. Biochem. Biophys. Res. Commun. 332, 392–397.
[32] Maeda, H., Hosokawa, M., Sashima, T., Murakami-Funayama, K., and Miyashita, K. (2009). Anti-obesity and anti-diabetic effects of fucoxanthin on diet-induced obesity conditions in a murine model. Mol Med Rep 2, 897–902.
[33] Kang, S.-I., Shin, H.-S., Kim, H.-M., Yoon, S.-A., Kang, S.-W., Kim, J.-H., Ko, H.-C., and Kim, S.-J. (2012). Petalonia binghamiae extract and its constituent fucoxanthin ameliorate high-fat diet-induced obesity by activating AMP-activated protein kinase. J. Agric. Food Chem. 60, 3389–3395.
[34] Abidov, M., Ramazanov, Z., Seifulla, R., and Grachev, S. (2010). The effects of XanthigenTM in the weight management of obese premenopausal women with non-alcoholic fatty liver disease and normal liver fat. Diabetes, Obesity and Metabolism 12, 72–81.
[35] Watanabe, T., Kawada, T., Kato, T., Harada, T., and Iwai, K. (1994). Effects of capsaicin analogs on adrenal catecholamine secretion in rats. Life Sciences 54, 369–374.
[36] Yoneshiro, T., Aita, S., Kawai, Y., Iwanaga, T., and Saito, M. (2012). Nonpungent capsaicin analogs (capsinoids) increase energy expenditure through the activation of brown adipose tissue in humans. Am. J. Clin. Nutr. 95, 845–850.
[37] Whiting, S., Derbyshire, E., and Tiwari, B.K. (2012). Capsaicinoids and capsinoids. A potential role for weight management? A systematic review of the evidence. Appetite 59, 341–348.
[38] Yang, D., Luo, Z., Ma, S., Wong, W.T., Ma, L., Zhong, J., He, H., Zhao, Z., Cao, T., Yan, Z., et al. (2010). Activation of TRPV1 by Dietary Capsaicin Improves Endothelium-Dependent Vasorelaxation and Prevents Hypertension. Cell Metab 12, 130–141.
[39] Zhang, L.L., Yan Liu, D., Ma, L.Q., Luo, Z.D., Cao, T.B., Zhong, J., Yan, Z.C., Wang, L.J., Zhao, Z.G., Zhu, S.J., et al. (2007). Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity. Circ. Res. 100, 1063–1070.
[40] Kim, K.-M., Kawada, T., Ishihara, K., Inoue, K., and Fushiki, T. (1998). Swimming Capacity of Mice Is Increased by Oral Administration of a Nonpungent Capsaicin Analog, Stearoyl Vanillylamide. J. Nutr. 128, 1978–1983.
[41] Shintaku, K., Uchida, K., Suzuki, Y., Zhou, Y., Fushiki, T., Watanabe, T., Yazawa, S., and Tominaga, M. (2012). Activation of transient receptor potential A1 by a non-pungent capsaicin-like compound, capsiate. Br J Pharmacol 165, 1476–1486.


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#7 henryv

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Posted 25 June 2014 - 07:08 AM

You may also find this article on one of the key ingredients pertinent and interesting: What is BAIBA?


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#8 henryv

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Posted 25 June 2014 - 07:30 AM

Lipomorph: 5 reasons why BETA is BETTER
  •   Beta-aminoisobutyric acid

    Antaeus Labs LipoMorph is the only supplement to contain this exciting new ingredient that is believed to function as an exercise mimetic and fat browning agent. 

  •    Beta-oxidation

    In addition to liberating fatty acids from fat cells through lipolysis, LipoMorph ingredients stimulate beta-oxidation to prevent free fatty acids being reabsorbed into adipocytes.

  •     Beta-3-adrenoceptors

    Octopamine is one of the only known selective agonists of the mammalian beta-3 adrenergic receptor (β3 adrenoreceptor). β3 adrenoreceptors on adipocytes are key activators of brown and beige fat potential. 

  •   Liver X Receptor Beta (LXRβ)

    The Kuding in LipoMorph suppresses lipogenesis through antagonism of LXRβ.

  •     Beta-hydroxybutyrate

    BAIBA stimulates the production of ketone bodies like beta-hydroxybutyrate in the liver. Not only are ketone bodies an excellent fuel source for the body and brain, but they may also contribute to the browning of white fat themselves.

These statements have not been evaluated by the Food and Drug Administration.
This product is not intended to diagnose, treat, cure, or prevent any disease.


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#9 bashman

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Posted 25 June 2014 - 07:41 AM

1st get me shredded


"Sometimes you bust and sometimes you flush. When your up its never as good as it seems and when your down you never think your going to be up again"

#10 Mr Taco

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Posted 25 June 2014 - 07:59 AM

I'm assuming this will be stim free... will it have any stimulant like properties? I'd prefer not personally but I'm interested either way.


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#11 andrewmccloskey

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Posted 25 June 2014 - 08:18 AM

Looks like octopamine will be a stim? Not sure.

#12 Right Hook

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Posted 25 June 2014 - 08:33 AM

I will have to sit down and read this all after some Demiurge. It looks like one of those old Spook/Par write ups for Avant.

Capsaicin on paper is very good. But I've never been able to "stomach" any product with it (pun intended). I notice reference #36 uses the following:

Capsinoids (capsiate, dihydrocapsiate, and nordihydrocapsiate) are capsaicin-like compounds found in a nonpungent type of red pepper, “CH-19 Sweet” (8, 9). Although capsinoids are much less pungent than capsaicin, they are as potent as capsaicin at increasing sympathetic nerve activity, thermogenesis, EE, and fat oxidation and in reducing body fat both in small rodents and humans (10–16).

Is Stearoyl Vanillylamide another name for one of these? Is the label going to disclose the doses of each ingredient?

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#13 Bodock

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Posted 25 June 2014 - 09:54 AM

very interdasting, thats alot to cipher, yall gonna do any sponsored logs? :doitfaggot:



#14 hellsgatekeeper

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Posted 25 June 2014 - 10:12 AM

I'm interested, looks alot more promising then your usual "we put lots of caffeine in with a bunch of random ingredients that probably don't do shit" fat burner lol.
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#15 bossman523

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Posted 25 June 2014 - 10:24 AM

in for the shredz



#16 henryv

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Posted 25 June 2014 - 12:41 PM

I will have to sit down and read this all after some Demiurge. It looks like one of those old Spook/Par write ups for Avant.

Capsaicin on paper is very good. But I've never been able to "stomach" any product with it (pun intended). I notice reference #36 uses the following:

Capsinoids (capsiate, dihydrocapsiate, and nordihydrocapsiate) are capsaicin-like compounds found in a nonpungent type of red pepper, “CH-19 Sweet” (8, 9). Although capsinoids are much less pungent than capsaicin, they are as potent as capsaicin at increasing sympathetic nerve activity, thermogenesis, EE, and fat oxidation and in reducing body fat both in small rodents and humans (10–16).

Is Stearoyl Vanillylamide another name for one of these? Is the label going to disclose the doses of each ingredient?

 

Those capsinoids from CH-19 are proprietary, patented, and expensive. And because they're patented, that's where research is funded (because the patent-holders Ajinomoto bankroll it). Since no other MOA has been suggested for their effects than TRPV1 activation, and those effects are commensurate with those to be expected of TRPV1 activation, I think it reasonable to draw a parallel to other TRPV1-activating nonpungent capsaicin analogues.


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#17 henryv

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Posted 25 June 2014 - 12:50 PM

I'm assuming this will be stim free... will it have any stimulant like properties? I'd prefer not personally but I'm interested either way.

 

Looks like octopamine will be a stim? Not sure.

 

If there is a stim effect I would expect it to be very mild.

 

very interdasting, thats alot to cipher, yall gonna do any sponsored logs? :doitfaggot:

 

I dunno about sponsored logs. We'll give some bottles away for sure though. 


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#18 eaglefan

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Posted 25 June 2014 - 12:52 PM

I would love to get one of those give away bottles, have you tried this at all Henry??



#19 henryv

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Posted 25 June 2014 - 12:55 PM

I'm interested, looks alot more promising then your usual "we put lots of caffeine in with a bunch of random ingredients that probably don't do shit" fat burner lol.

 

There's a lot of interesting research going on into this "browning" phenomena at the moment. This is probably the first (or second) of many supplement products in this area, and eventually there may well be pharmaceuticals.

I would love to get one of those give away bottles, have you tried this at all Henry??

No-one's tried it yet. The product should be available to purchase from the 1st.


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#20 henryv

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Posted 25 June 2014 - 12:58 PM

We'll give some bottles away for sure though. 

By which I mean we'll do one of our usual puzzle-type competitions as a giveaway. Sponsored logs tend to be quite biased.


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#21 gtsmike

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Posted 25 June 2014 - 01:16 PM

in for free stuff...

 

 

 

and a product label. 



#22 henryv

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Posted 25 June 2014 - 01:29 PM

Is the label going to disclose the doses of each ingredient?

 

in for...

a product label.

 


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#23 Right Hook

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Posted 25 June 2014 - 01:47 PM

Those capsinoids from CH-19 are proprietary, patented, and expensive. And because they're patented, that's where research is funded (because the patent-holders Ajinomoto bankroll it). Since no other MOA has been suggested for their effects than TRPV1 activation, and those effects are commensurate with those to be expected of TRPV1 activation, I think it reasonable to draw a parallel to other TRPV1-activating nonpungent capsaicin analogues.


Ok. Thanks. Looks good on paper. Browning of WAT and brite seem more interesting than actually activating existing BAT. BAT is actually quite minimal in men, especially lean men it seems. Studied BAT a lot before they were even talking about brite as much.

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#24 henryv

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Posted 25 June 2014 - 01:52 PM

Ok. Thanks. Looks good on paper. Browning of WAT and brite seem more interesting than actually activating existing BAT. BAT is actually quite minimal in men, especially lean men it seems. Studied BAT a lot before they were even talking about brite as much.

If you want to read any of the refs let me know.


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#25 bossman523

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Posted 25 June 2014 - 02:07 PM

back in for complimentary bottle


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