Carb blocker supplements

Do these actually work or is it more of a marketing tactic? If they do work, how do they differ from a GDA?

2 Likes

Prepare for a lot of info!

4 Likes

hahah I’m ready!!

If you want one —> Defuse by Evomuse.
Take that on a cheat meal, and you will lose weight.
Dunno how Matt did it, but that stuff is liquid gold.

If you want a good GDA
Glucasatrol (Ketogenics)
Glycoshield (HPS)

Would be the 2 I would recommend.

1 Like

Defuse? Never taken it. Thanks for giving me something to research during my post w/o cardio.

1 Like

Everyone who has tried it, or who I have given it to has loved it.
For example when I went to visit my client Kelsey in NJ a few weeks ago.
We split 3 pints of ice cream between us and mexican.
We both woke up a pound lighter the next morning.

If you ever have a time where you are going to go ape shit on food, that stuff works wonders.
Matt has a hard time keeping it in stock because he is a one man team. But his gut health and BMP 2.0 are amazing products.

4 Likes

Probably all the Clen and Cytomel. ; )

2 Likes

Have not used either, so I can’t comment on that.

1 Like

Haha. Just kidding my friend.

Glucose disposal agents can be useful for shuttling carbohydrates whereas “carb-blockers” are gimmicky and a waste of money. I’ve had great experiences with SNS Glycophase as a GDA.

1 Like

Hmm this is something I need to snag up for my traveling trips. Noted

1 Like

thank you for the recommendation! I’m more so interested in the research aspect/difference between the two but I’ll look into Defuse too!

@TheSolution have you logged or plan to with Revive MD Glucose?

No plans at all
Glucasatrol and Glycoshield suit me well, and it reflects on my BG Readings.

1 Like

Here is the write up for defuse

The science behind Defuse is thick, but very digestible if you understand some key physiological terms. Give this pre-glossary a quick read, then as you go through the write up and come across one of these terms you may want to revisit the definition to get a better grasp. Or if you’re already a super science nerd, feel free to skip over this section and get right to the meat.
Pre-adipocytes & pre-adipocyte differentiation
Pre-adipocytes are immature fat cells that have not yet developed distinguishing characteristics. Basically like the Army Reserve, they’re called upon when needed, but instead of going into battle they are transformed into full-fledged fat cells through a process called differentiation. At this point they can start storing lipid droplets containing fats, cholesterol, and various metabolic machinery.

Peroxisome proliferator-activated receptor gamma (PPARy)
Of the three known PPAR subtypes (alpha, delta, gamma), PPARy is the only one that encourages nutrient storage upon activation. It is intricately involved in the uptake of carbohydrate and fat into adipose tissue, as well as being a key signal to trigger adipocyte differentiation.
CCAAT-enhancer binding proteins (C/EBP’s)
C/EBP’s include a family of six transcription factors, for our purposes we are just concerned with C/EBPa and C/EBPb. Both of these are directly involved in pre-adipocyte differentiation and work in conjunction with PPARy.
AMP-activated protein kinase (AMPk)
AMPk is a major regulator of cellular energy signaling. Upregulation triggers skeletal muscle fatty acid oxidation (fat burning), increased insulin sensitivity, and glucose uptake.

Normally, AMPk is triggered during conditions of low cellular energy (low glycogen storage, energy depletion during exercise, calorie restriction, etc). During times of caloric excess (which is exactly when you’ll be using Defuse), AMPk is significantly downregulated, which is quite detrimental for fat loss; hence the inclusion of AMPk activators in the formula.
Transient receptor potential vanilloid receptor 1 (TrpV1)
A few years ago some groundbreaking research came out implicating this receptor as a major player in obesity. This is the receptor that capsaicin from chili peppers interacts with, and quite a bit of research has demonstrated that triggering TrpV1 has a significant effect on fat burning.
Hormone Sensitive Lipase (HSL)
HSL is crucial for the initial phase of fat loss. It is imperative for breaking down the stored triglyceride in a fat cell into free fatty acids (FFA’s) so they can be transported for oxidation (burning). The breakdown of stored triglyceride into FFA’s (before transport and oxidation of the fat even occur) is a three-step process, and HSL governs the first step, and is also the rate-limiting step. Boosting HSL allows the other two steps to do more work, which allows for more fat to be burned.
Fatty Acid Synthase (FAS)
Think of FAS as the anti-HSL, basically performing the opposite function, encouraging the storage of fat. It is comprised of a group of enzymes regulated upstream by SREBP-1c, which is triggered by insulin. Research shows a significant upregulation of FAS in obesity, coupled with suppressed HSL.
Brown Adipose Tissue (BAT)
BAT is structurally and functionally different from white adipose tissue (WAT). BAT contains several, small lipid droplets surrounding the large nuclear machinery in the middle, whereas WAT contains one huge lipid droplet with a small nucleus near the cell wall. That right there gives some indication of the function of the BAT cell, along with its high mitochondria density and UCP1 expression. BAT’s main function is generating heat by burning calories; the numerous small lipid droplets release their fat in response to cold in order to elevate body temperature. People with higher BAT levels (or better BAT signaling) take longer to start shivering in the cold, as their bodies are able to maintain better homeostatic thermoregulation.

Acacia Catechins
Where does it come from?
Found growing in various parts of China and India, Acacia Catechu is a tall thorny tree. It was selected for inclusion in Defuse as a source of epicatechin and EGCG.
Primary Effects
PPARy and C/EBP
Acacia Catechins have been shown to suppress pre-adipocyte differentiation through the blockade of two important fat storage proteins, C/EBP and PPARy, which has a downstream inhibition on the master fat storing gatekeeper, FAS (1).

Platycodon saponins
Where does it come from?
Platycodin d. is isolated from the roots of the Platycodon grandiflorum plant, found in East Asia.
Primary Effects
AMPk Activation
Fat loss and fat gain are moderated by numerous complex mechanisms, and AMPk is a key player in this flux. Generally speaking, bolstering AMPk activation is great for fat loss, in the right amount. Platycodin d. has been shown in multiple studies to significantly inhibit fat gain and increase fat burning through AMPk activation. Downstream, this AMPk activation attenuates activation of SREBP-1 and fatty acid synthase (FAS), two hormones responsible for fat storage. This is done in a novel way by triggering SIRT1 and CaMMK-b (2–4).

PPAR-y and C/EBPa Modulation
Platycon d. has been shown to reduce abdominal and whole body fat accumulation in mice fed an obesogenic diet by PPAR-y and C/EBPa (3). Basically they gave mice Platycodon d., tried to make them fat, and couldn’t do it.

Adipokine and Glucose Management
Another recent study trying to fatten up mice found that Platycodon d. was able to kick-start adiponectin (a fat burning adipokine) locally in fat cells while keeping it stable in serum compared to the placebo group. It was also able to suppress TNFa (an inflammatory cytokine) locally in fat cells. This resulted in reduced food intake and reduced fat accumulation while increasing glucose uptake in skeletal muscle (5). With regards to glucose, another study showed it was able to reduce blood sugar without stimulating insulin release, which is great for enhancing fat burning as well as long term health (6).

Baicalin
Where does it come from?
Baicalin is a flavone found in the herb blue skullcap.
Primary Effects
AKt, CaMKKb, AMPk, ACC, PPARy, C/EBP, FAS, KLF-2 & KLF-15
Baicalin has been shown to downregulate PPAR-y and C/EBPs; it does this by suppressing Akt phosphorylation through inhibition of PDK1 (7,8). The net result of this, among other things, is going to be inhibiting fat accumulation by attenuating preadipocyte differentiation.

Baicalin is another AMPk activator, which does so through the favorable CaMMK pathway like Platycodin d. (9). Researchers in Shanghai conducted a profound study in mice fed a high fat diet (HFD) with or without baicalin supplementation (10). Keep in mind that mice don’t normally eat a high fat diet, and their metabolic machinery is ill adapted to do so. After 16 weeks, the bicalin group saw the following effects:
Suppression of body weight gain normally caused by the HFD
Reduced visceral fat
Decreased cholesterol
Decreased circulating FFA’s (a sign of increased fat oxidation)
Decreased circulating insulin
Reduced TNF-a (a potent inflammatory cytokine)
Reduced liver fat gain
Stimulation of AMPk and ACC
Decreased SREBP-1c and FAS

Another study out of Korea supported the previously seen fat loss potential and concluded that baicalin upregulates anti-fat storage regulators (KLF-2) and downregulates pro-fat storing regulators (KLF-15) which results in an inhibition of cellular fat accumulation (8). This is a perfect storm for prevention of fat gain.

Methyl Cinnamate
Where does it come from?
Methyl Cinnimate (MC) is an ester of cinnamic acid found in several plants and spices.
Primary Effects
MC again targets pre-adipocytes through modulation of PPAR-y, SREBP-1, and C/EBPa, CaMMK2, and AMPk, thereby reducing the ability of the body to accumulate fat storage (11).

Salvia miltiorrhiza
Where does it come from?
Salvia miltiorrhiza is an Asian perennial plant from the Salvia genus.
Primary Effects
DGAT, Glucose Sensitivity, Hepatic Lipid Metabolism
Diglyceride acetyltransferase (DGAT) is the enzyme responsible for the third and final step in producing a triglyceride from glycerol and fatty acids. Inhibit DGAT, which Salvia m. has been shown to do, and you reduce fat accumulation and increase leptin sensitivity significantly (12) . If your body wants to store more fat; it cranks up DGAT activity.

Salvia m. has also been shown in research to improve uptake of glucose in skeletal muscle, thereby reducing fat storage through a 2nd angle (13).

When feeding two groups of rats a fattening diet for six weeks, the control group showed increased body fat accumulation, hyperinsulinemia, hyperlipidemia, and increased liver enzymes. The group fed the same diet in conjunction with Salvia m. did not show any of these negative effects from the high fat diet (14).

Raspberry Ketone
Where does it come from?
Raspberry Ketone (RK) is a natural phenolic, aromatic compound found in raspberries, cranberries and blackberries.
Primary Effects

TRPV1, NE, HSL
Activating the Transient Receptor Potential Vanilloid Type 1 protein (TRPV1) offers numerous benefits for fat loss and general health, including prevention of adipogenesis and obesity (15).

Through modulation of norepinephrine (NE) and hormone sensitive lipase (HSL), RK appears to be a powerhouse for encouraging fat loss and prevention of fat gain. When mice were fed fattening diet, RK prevented visceral and liver fat accumulation as well as reversing the fat gain in previously obese mice (16). Recently liver fat has been implicated in metabolic disturbances to an even greater degree than the previous villain, visceral fat, so this is a benefit of great magnitude for overall health (17).

18b-glycyrrhetinic acid
Where does it come from?
18b-glycyrrhetinic acid (18b-GA) is a metabolite of glycyrrhetinic acid with very unique properties found in the licorice herb.
Primary Effects
While high doses of licorice/glycyrrhetinic acid have been shown to inhibit the enzyme 11b-HSD, which is responsible for converting cortisol to the inactive form cortisone (18), the low dose of this specific 18b metabolite have some important yet unrelated effects.

PPARy, C/EBPa, HSL, HbA1c, Inflammation
18b-GA is another ingredient in DeFuse selected for its potent inhibitory effect on the likely now familiar PPARy and C/EBPa pathway. A recent university study out of South Korea found that 18b-GA was able to decrease lipid accumulation by downregulation of PPARy and C/EBPa in maturing pre-adipocytes. In addition to this effect on pre-adipocytes, it was also able to increase fat release, upregulate HSL, adipose TG lipase and perilipin in mature fat cells (19). So basically 18b-GA is going to prevent immature fat cells from becoming fat cells, and increase lipolysis in mature fat cells, a perfect two pronged attack.

Another study out of India showed that 18b-GA was able to control blood glucose and HbA1c in diabetic rats on par with the potent pharmaceutical glibenclamide (20). It also appears to have a significant effect on preventing free fatty acid induced lipid accumulation and lipotoxicity by stabilizing mitochondrial lysosomes and improving liver function (21). Finally, 18b-GA has also been shown to be anti-inflammatory by reducing IL-8 (22). Current research shows that inflammation is likely a major contributing factor to fat gain, so by reducing inflammatory interleukins we can help create a more optimal hormonal environment.

6-gingerol
Where does it come from?
Gingerol, found in ginger, is chemically similar to capsaicin and piperine. Once cooked, gingerol becomes zingerone.
Primary Effects
PPARy, C/EBPa, FAS, SREBP-1c, Acetyl-CoA, Akt, AP2/4, ROS, Inflammation
In a university study out of Tokyo, researchers looked at the effect of gingerol on rats fed a fattening diet to see if it could alleviate any of the damage. They found it was able to reduce plasma insulin, SREBP-1c, and liver acetyl-CoA carboxylase, which attenuated both body weight gain and fat accumulation (23).

6-gingerol is also an effective player in our main theme of targeting pre-adipocyte differentiation. Both in vitro and in vivo, we see anti-adipogenic properties through reduction in PPARy, C/EBPa and FAS (24,25). The researchers performing these studies also found that it was able to reduce levels of something called adipocyte-specific fatty acid binding protein (aP2, also called FABP4), which is a carrier protein for fatty acids and has become an emerging target protein for treating diabetes and obesity (26,27).
In addition to the direct anti-adipogenic effects, gingerol can also control oxidative damage by reducing intracellular ROS and boosting glutathione, as well as reduce inflammation by blocking TNF-a, NF-kB and PKC signaling (28,29).

Cinchonine
Where does it come from?
Cinchonine is a natural compound found in Cinchona bark, indigenous to the Western Andes.
Primary Effects
During overfeeding, cinchonine supplemented subjects gained 40% less weight, 25% less visceral fat, and had lower levels of triglycerides, glucose, serum cholesterol and free fatty acids (30). It also inhibited the diet induced upregulation of inflammatory cytokines by inhibiting Toll Like Receptor 2 (TLR2). In summary, it was shown to reduce fat gain and inflammation compared to control groups when given a fattening diet.

(-)Hydroxycitric acid
Where does it come from?
Hydroxycitric Acid (HCA) is found in the tropical plant Garcinia cambogia.
Primary Effects
HCA has been shown to favorably alter the expression of genes that regulate adipogenesis and lipolysis, which makes it a great addition to the Defuse formula (31). New research shows that it appears to do so by blocking a key enzyme called atp-citratelyase (32). In a previous study, HCA was also shown to reduce fatty acid synthesis from glucose (33).

Anthocyanins/betalains
Where does it come from?
Anthocyanins and betalains are a class of pigmentations found in various plants, fruits and flowers, with numerous health-promoting effects.
Primary Effects
PPARy, Adiponectin, NPY, Glucose, Leptin, Resistin
Once again, we’re targeting inhibition of PPARy to suppress fat storage. Anthocyanins have been shown to do just this, causing suppressed pre-adipocyte differentiation and lipid accumulation (34). A brand new university study out of Korea looked at rats on a normal diet vs. rats on a normal diet plus anthyocyanins for 40 days (35). Here’s what they found in the supplemented group:
Significantly lower body weight
Reduced fat cell size
Reduced expression of neuropeptide Y (a neurotransmitter that signals increased food intake and fat storage) and of protein kinase A (a regulator of cellular energy storage).

Another study looked at the effects of anthocyanin supplementation over 10 weeks and found that it lowered total cholesterol, triglycerides, serum leptin and resistin. The researchers concluded that anthocyanins “…posess a preventative potential for obesity-associated diseases” (36).

Other studies have shown an anti-obesity effect as well, demonstrating resistance to fat gain with supplementation (37,38). Betalains specificaly have been shown to boost adiponectin, act as an antioxidant, and prevent LDL oxidation (39–41).

Loranthus
Where does it come from?
Loranthus is a parasitic plant found growing on branches of woody trees, from the Loranthaceae family.
Primary Effects
FAS inhibition, glucose
Loranthus has several studies supporting its ability to potently inhibit FAS, making it a perfect choice to prevent fat gain, and a key ingredient in the formula.

Initially, Tian et. al, discovered that loranthus potently inhibits FAS to a greater extent than cerulenin and C75 (currently used to inhibit FAS in a laboratory setting), and also reduced body weight in tested subjects (42). Next, they established an IC50 value (a measurement used to determine the inhibitory potency of a compound) and found that loranthus has both a fast acting and long acting effect on FAS inhibition (43). Finally, they determined that the FAS inhibitory activity of loranthus comes from a specific family (Loranthaceae), so it is important to use this form, which we have done in Defuse (44).

At least two other studies have shown the ability of loranthus to favorably regulate blood glucose levels, in diabetic and non-diabetic subjects (45,46).

Citrus aurantium
Where does it come from?
Citrus aurantium (CA) refers to a citrus tree and its fruit, which contains N-methyltyramine, octopamine and synephrine.
Primary Effects
PPARy, C/EBP (a&b), FAS, aP2
Quite a bit of research has been done on CA, for now we just want to focus on a couple of studies that make it highly relevant for its inclusion in the Defuse formula.

The first noteworthy study looked at CA’s effect on pre-adipocyte differentiation, and it turned out to do pretty much everything we want in an anti-fat gain compound. It was shown to downregulate PPARy, C/EBPb and C/EBPa (expression of C/EBPa makes fat cells more sensitive to insulin). In addition to this, it also dramatically decreased FAS and aP2, as well as other fat signaling pathways. This demonstrates CA’s ability to positively manipulate the fat storage vs. fat burning pathway and inhibit adipocyte differentiation (47).

Finally, a recent meta-analysis looking at a combination of 20 published and unpublished studies including 360 human subjects concluded that supplemental CA increases resting metabolic rate and energy expenditure (48).

Lotus leaf
Where does it come from?
Lotus leaf comes from the aquatic lotus plant in the Nelumbonaceae family.
Primary Effects
SREBP-1c, REE, a-glucosidase, GLUT4, AGEs
Keeping with the recurring theme of attacking pre-adipocyte differentiation, lotus leaf could be a potentially big player in this assault. Research has demonstrated the ability of lotus to decrease SREBP-1c and triglyceride accumulation during adipogenesis, increase lipolysis, and decrease adipocyte differentiation capacity (49).

In a study out of Japan, researchers took the now hopefully familiar route of trying to fatten up mice and rats with and without lotus supplementation and measured various obesity related parameters. They found that the supplemented group was able to prevent fat gain as well as hepatic triglycerides, coupled with an inhibited ability to absorb lipids and an accelerated rate of fat oxidation and resting energy expenditure (50).

A 2013 study out of Korea looked at the effect of lotus supplementation for 7 weeks in animals with diabetes. They found that lotus was an extremely potent inhibitor of an enzyme called a-glucosidase, which lowers the rate of glucose absorption and extends digestion time, leading to a lower post-prandial glucose response (51). The same study also demonstrated the ability of lotus to lower plasma triglycerides and total cholesterol. Inhibition of a-glucosidase has been shown to reduce triglyceride uptake into fat cells, decrease hepatic lipogenesis, favorably effect skeletal muscle GLUT4 receptor density density, and diminish the production of Advanced Glycation End products (AGEs) (52).

Olive Leaf extract
Where does it come from?
Olive leaf extract (OLE) is derived from the leaves of the olive plant; we have selected an extract with a high potency of oleuropein, a phenolic compound with some interesting properties relating to prevention of fat gain.
Primary Effects
PPARy, C/EBPa, RQ, AGEs, Insulin, Glucose
We’ll kick this one off with the current theme, OLE is yet another ingredient in the Defuse formula that prevents adipocyte differentiation through inhibition/downregulation of PPARy and C/EBPa (53).

A study published in the Journal of Nutrition found that OLE supplementation increased V02, reduced myocardial oxidative stress, and lowered respiratory quotient (RQ- lower levels indicate more fat oxidation vs. carbohydrate oxidation) (54). In another study published in Nutrition, researchers overfed two groups of rats for eight weeks, then gave one group OLE and continued to overfeed both groups for another eight weeks. The non-supplemented group developed metabolic syndrome, including elevated abdominal and liver fat, collagen accumulation in the heart and liver, elevated oxidative stress markers, abnormal cholesterol and impaired glucose tolerance. The group supplemented with OLE either improved or normalized all of those parameters, demonstrating a potent protective effect against overfeeding (53).

In a brand new human study out of The University of Aukland, overweight men at risk for metabolic syndrome were given supplementation with OLE for 12 weeks; researchers noted a 15% improvement in insulin sensitivity along with an almost 30% improvement in pancreatic beta cell responsiveness (the cells that produce insulin) (55). An improvement in fasting insulin and HbA1c was also noted in a previous human study with 79 diabetic adults (56).

Finally, OLE is another ingredient in the formula that acts as an anti-glycation agent, reducing production of AGEs (57).

Galega officionalis
Where does it come from?
Galega officinalis is an herbaceous plant in the Faboideae family native to the Middle East, containing a potent compound called guanidine.
Primary Effects
AMPK, FAS, Acetyl-CoA, GLUT4, Glucose
Galega is going to contribute to fat gain inhibition through some familiar mechanisms, and looks to be quite a promising compound. It has been shown to activate AMPk, increase GLUT4 translocation, and increase skeletal muscle glucose uptake in vitro and in vivo (58,59).

An animal study out of Glasgow again demonstrated AMPk activation, as well as inhibition of Acetyl-CoA carboxylase and FAS, increased fat oxidation, and a reduction in body weight (60).

The most impressive research on galega looked at the effect of supplementation for 28 days on normal and obese mice and measured several parameters. In normal mice, supplementation caused weight loss and a voluntary reduction of food intake. Interestingly, after cessation of the supplement, food intake increased back to normal but the weight loss was maintained. The obese mice supplementing with galega also showed reduced food intake, and the researchers noted a “striking absence of body fat” during post-mortem examinations. Both groups showed a reduction in fasting blood glucose, and the obese group also showed a reduction in serum insulin (61).
Panax ginseng berry extract
Where does it come from?
Panax ginseng berry extract (GBE) comes from Ginseng; a perennial plant from the Araliaceae family.
Primary Effects
AMPk, FAS, glucose, SREBP-1c
GBE has been shown to inhibit lipogenesis during overfeeding by suppressing FAS and SREBP-1c, while upregulating AMPk. Supplementation was also shown to reverse diet-induced blood sugar cholesterol elevations, while reducing hepatic glucose output (62). Several studies in obese and/or diabetic animals have demonstrated a favorable modulation of blood glucose, loss of body weight, and even pancreatic beta cell regeneration (63–66).

Forskolin 60%
Where does it come from?
Forskolin is a diterpene from the Coleus forskohlii plant.
Primary Effects
Forskolin is well known to effectively target cAMP in adipose tissue, which, among other things, mimics exercise and caloric restriction.

A 12 week randomized, double-blind placebo study out of the University of Kansas found that forskolin supplementation caused a decrease in body fat and an increase in lean body mass compared to the placebo group (67). The even better news is that this study only used a 10% extract; we have obtained a far more potent 60% extract for Defuse. It has also been suggested to help mitigate weight gain in overweight human subjects (68).

Silibinin
Where does it come from?
Silibinin comes from milk thistle seeds, and is the main active component of silymarin.
Primary Effects
Most people are well aware of Milk Thistle’s profound effect on liver health, but silibinin is included in Defuse for a different reason.

ATGL, Insulin, FFA’s, Resistin, TNFa, oxLDL
Silibinin is the first ingredient in the formula to upregulate something called adipose triglyceride lipase (ATGL), which is an enzyme responsible for initiating the breakdown of stored fat (triglyceride) inside the adipocyte (69). Silibinin has also been shown to reduce serum fatty acids, improve skeletal muscle insulin resistance, reduce visceral fat, downregulate resistin, and improve glucose metabolism by downregulating gluconeogenesis genes and supporting the Akt pathway (69–71).

And for some bonus points, silibinin also inhibits oxidation of LDL particles, decreases lipid peroxidation and lowers TNFa (71,72)

Rosemary Leaf Extract (carnosic acid)
Where does it come from?
Rosemary is a Mediterranean perennial herb; the leaf extract is a source of a natural diterpene called carnosic acid.
Primary Effects
PPARy, C/EBP, Glucose, Gastric Lipase, Hepatic Lipase
Carnosic acid (CA) does pretty much everything you could ask from an anti-adipogenic compound. Again we’re going after PPARy and C/EBPa inhibition, and CA has a unique effect on restructuring the ratios of different forms of C/EBPb, the combined result being inhibition of adipogenesis (73,74).

A recent study out of Switzerland boasted some impressive results in overfed mice supplemented with Rosemary leaf extract for 50 days, showing almost a 60% reduction in fat gain and 40% reduction in hepatic triglyceride levels. The researchers determined this effect was likely due to an inhibition of pancreatic lipase activity, and concluded Rosemary extract “…can limit weight gain induced by a high-fat diet and protect against obesity-related liver steatosis” (75).

CA has been shown in several other studies to significantly reduce body weight and body fat in lean and obese individuals, lower triglycerides, total cholesterol and insulin, reduce visceral fat, improve liver enzymes, favorably modulate glucose and glucose tolerance, inhibit gastric lipase (thereby reducing fat absorption), and inhibit pre-adipocyte differentiation (74,76–78).

Stearoyl Vanillylamide (capsaicin analogue)
Where does it come from?
Stearoyl Vanillylamide (SV) is a non-pungent analogue of capsaicin, the active component of chili peppers.
Primary Effects
TrpV1, BAT, REE
If you’ve been paying attention to obesity research the past few years, you’ve likely heard of the transient receptor potential vanilloid (TrpV1). See the description in the intro of the article if you need a quick explanation. Multiple studies have demonstrated SV/capsaicin’s ability to act as a potent TrpV1 agonist leading to decreases in body fat and increases in energy expenditure (80,81).
Brown Adipose Tissue (BAT) has taken an interesting journey in the research over the years, and for a long time was suspected to be negligible in adult humans, and therefore an unfruitful target for obesity and weight loss. However, new research is showing we were likely wrong all along, and that BAT is indeed a “…regulator of whole-body energy expenditure and body fat in humans as in small rodents, and a hopeful target combating obesity and related disorders” (82). SV has been shown to have a profound effect in several studies on BAT upregulation through TrpV1 binding (80–83). The net effect of this BAT activation is a significant increase in fat oxidation and energy expenditure. Two recent meta-analyses looking at the summation of the data determined that capsaicin supplementation increases VO2, energy expenditure and fat loss in humans (84,85).

Summary
Psychologically and emotionally we need time off, and often that time off involves eating and drinking large meals with friends and family. While we want, and need, to participate we can often find our other, fitness-related, goals compromised.

Defuse gives us a much-needed tool for physique enhancement. Defuse helps prevent fat gain that happens with occasional caloric surplus (vacation and Holidays), and short burst muscle gaining cycles. Incorporating Defuse strategically as directed will minimize fat gain and help to maintain your much-desired leanness.

Bibliography

5 Likes
  1. Furuyashiki T, Nagayasu H, Aoki Y, Bessho H, Hashimoto T, Kanazawa K, et al. Tea catechin suppresses adipocyte differentiation accompanied by down-regulation of PPARgamma2 and C/EBPalpha in 3T3-L1 cells. Biosci. Biotechnol. Biochem. [Internet]. 2004 Nov [cited 2013 Oct 7];68(11):2353–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15564676

  2. Hwang YP, Choi JH, Kim HG, Khanal T, Song GY, Nam MS, et al. Saponins, especially platycodin D, from Platycodon grandiflorum modulate hepatic lipogenesis in high-fat diet-fed rats and high glucose-exposed HepG2 cells. Toxicol. Appl. Pharmacol. [Internet]. 2013 Mar 1 [cited 2013 Oct 4];267(2):174–83. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23319015

  3. Lee EJ, Kang M, Kim YS. Platycodin D inhibits lipogenesis through AMPKα-PPARγ2 in 3T3-L1 cells and modulates fat accumulation in obese mice. Planta Med. [Internet]. 2012 Sep [cited 2013 Oct 4];78(14):1536–42. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22872592

  4. Hwang YP, Choi JH, Kim HG, Lee H-S, Chung YC, Jeong HG. Saponins from Platycodon grandiflorum inhibit hepatic lipogenesis through induction of SIRT1 and activation of AMP-activated protein kinase in high-glucose-induced HepG2 cells. Food Chem. [Internet]. 2013 Sep 1 [cited 2013 Oct 4];140(1-2):115–23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23578622

  5. Ahn Y-M, Kim SK, Kang J-S, Lee B-C. Platycodon grandiflorum modifies adipokines and the glucose uptake in high-fat diet in mice and L6 muscle cells. J. Pharm. Pharmacol. [Internet]. 2012 May [cited 2013 Oct 4];64(5):697–704. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22471365

  6. Zheng J, He J, Ji B, Li Y, Zhang X. Antihyperglycemic effects of Platycodon grandiflorum (Jacq.) A. DC. extract on streptozotocin-induced diabetic mice. Plant Foods Hum. Nutr. [Internet]. 2007 Mar [cited 2013 Oct 4];62(1):7–11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17226070

  7. Kwak DH, Lee J-H, Song KH, Ma JY. Inhibitory effects of baicalin in the early stage of 3T3-L1 preadipocytes differentiation by down-regulation of PDK1/Akt phosphorylation. Mol. Cell. Biochem. [Internet]. 2013 Oct 4 [cited 2013 Oct 7]; Available from: http://www.ncbi.nlm.nih.gov/pubmed/24091917

  8. Lee H, Kang R, Hahn Y, Yang Y, Kim SS, Cho SH, et al. Antiobesity effect of baicalin involves the modulations of proadipogenic and antiadipogenic regulators of the adipogenesis pathway. Phytother. Res. [Internet]. 2009 Nov [cited 2013 Oct 7];23(11):1615–23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19813240

  9. Ma Y, Yang F, Wang Y, Du Z, Liu D, Guo H, et al. CaMKKβ is involved in AMP-activated protein kinase activation by baicalin in LKB1 deficient cell lines. PLoS One [Internet]. 2012 Jan [cited 2013 Oct 7];7(10):e47900. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3478266&tool=pmcentrez&rendertype=abstract

  10. Guo H, Liu D, Ma Y, Liu J, Wang Y, Du Z, et al. Long-term baicalin administration ameliorates metabolic disorders and hepatic steatosis in rats given a high-fat diet. Acta Pharmacol. Sin. [Internet]. 2009 Nov [cited 2013 Oct 7];30(11):1505–12. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19890358

  11. Chen Y-Y, Lee M-H, Hsu C-C, Wei C-L, Tsai Y-C. Methyl cinnamate inhibits adipocyte differentiation via activation of the CaMKK2-AMPK pathway in 3T3-L1 preadipocytes. J. Agric. Food Chem. [Internet]. 2012 Feb 1 [cited 2013 Oct 7];60(4):955–63. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22273148

  12. Ko JS, Ryu SY, Kim YS, Chung MY, Kang JS, Rho M-C, et al. Inhibitory activity of diacylglycerol acyltransferase by tanshinones from the root of Salvia miltiorrhiza. Arch. Pharm. Res. [Internet]. 2002 Aug [cited 2013 Nov 4];25(4):446–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12214853

  13. Tao W, Deqin Z, Yuhong L, Hong L, Zhanbiao L, Chunfeng Z, et al. Regulation effects on abnormal glucose and lipid metabolism of TZQ-F, a new kind of Traditional Chinese Medicine. J. Ethnopharmacol. [Internet]. 2010 Apr 21 [cited 2013 Nov 4];128(3):575–82. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20123010

  14. Tan Y, Lao W, Xiao L, Wang Z, Xiao W, Kamal MA, et al. Managing the combination of nonalcoholic Fatty liver disease and metabolic syndrome with chinese herbal extracts in high-fat-diet fed rats. Evid. Based. Complement. Alternat. Med. [Internet]. 2013 Jan [cited 2013 Nov 4];2013:306738. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3588405&tool=pmcentrez&rendertype=abstract

  15. Zhang LL, Yan Liu D, Ma LQ, Luo ZD, Cao TB, Zhong J, et al. Activation of transient receptor potential vanilloid type-1 channel prevents adipogenesis and obesity. Circ. Res. [Internet]. 2007 Apr [cited 2010 Sep 6];100(7):1063–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17347480

  16. Morimoto C, Satoh Y, Hara M, Inoue S, Tsujita T, Okuda H. Anti-obese action of raspberry ketone. Life Sci. [Internet]. 2005 May [cited 2010 Sep 12];77(2):194–204. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15862604

  17. Fabbrini E, Magkos F, Mohammed BS, Pietka T, Abumrad NA, Patterson BW, et al. Intrahepatic fat, not visceral fat, is linked with metabolic complications of obesity. Proc. Natl. Acad. Sci. U. S. A. [Internet]. 2009 Sep [cited 2010 Aug 11];106(36):15430–5. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2741268&tool=pmcentrez&rendertype=abstract

  18. Krähenbühl S, Hasler F, Frey BM, Frey FJ, Brenneisen R, Krapf R. Kinetics and dynamics of orally administered 18 beta-glycyrrhetinic acid in humans. J. Clin. Endocrinol. Metab. [Internet]. 1994 Mar [cited 2013 Oct 29];78(3):581–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8126129

  19. Moon M-H, Jeong J-K, Lee Y-J, Seol J-W, Ahn D-C, Kim I-S, et al. 18β-Glycyrrhetinic acid inhibits adipogenic differentiation and stimulates lipolysis. Biochem. Biophys. Res. Commun. [Internet]. 2012 Apr 20 [cited 2013 Oct 29];420(4):805–10. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22465130

  20. Kalaiarasi P, Pugalendi KV. Antihyperglycemic effect of 18 beta-glycyrrhetinic acid, aglycone of glycyrrhizin, on streptozotocin-diabetic rats. Eur. J. Pharmacol. [Internet]. 2009 Mar 15 [cited 2013 Oct 29];606(1-3):269–73. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19374864

  21. Wu X, Zhang L, Gurley E, Studer E, Shang J, Wang T, et al. Prevention of free fatty acid-induced hepatic lipotoxicity by 18beta-glycyrrhetinic acid through lysosomal and mitochondrial pathways. Hepatology [Internet]. 2008 Jun [cited 2013 Oct 29];47(6):1905–15. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18452148

  22. Kang O-H, Kim J-A, Choi Y-A, Park H-J, Kim D-K, An Y-H, et al. Inhibition of interleukin-8 production in the human colonic epithelial cell line HT-29 by 18 beta-glycyrrhetinic acid. Int. J. Mol. Med. [Internet]. 2005 Jun [cited 2013 Oct 29];15(6):981–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15870903

  23. Okamoto M, Irii H, Tahara Y, Ishii H, Hirao A, Udagawa H, et al. Synthesis of a new [6]-gingerol analogue and its protective effect with respect to the development of metabolic syndrome in mice fed a high-fat diet. J. Med. Chem. [Internet]. 2011 Sep 22 [cited 2013 Oct 29];54(18):6295–304. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21851089

  24. Tzeng T-F, Liu I-M. 6-gingerol prevents adipogenesis and the accumulation of cytoplasmic lipid droplets in 3T3-L1 cells. Phytomedicine [Internet]. 2013 Apr 15 [cited 2013 Oct 29];20(6):481–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23369342

  25. Tzeng T-F, Chang CJ, Liu I-M. 6-Gingerol Inhibits Rosiglitazone-Induced Adipogenesis in 3T3-L1 Adipocytes. Phytother. Res. [Internet]. 2013 Mar 21 [cited 2013 Oct 29]; Available from: http://www.ncbi.nlm.nih.gov/pubmed/23519881

  26. Furuhashi M, Tuncman G, Görgün CZ, Makowski L, Atsumi G, Vaillancourt E, et al. Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2. Nature [Internet]. 2007 Jun 21 [cited 2013 Nov 5];447(7147):959–65. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17554340

  27. Maeda K, Cao H, Kono K, Gorgun CZ, Furuhashi M, Uysal KT, et al. Adipocyte/macrophage fatty acid binding proteins control integrated metabolic responses in obesity and diabetes. Cell Metab. [Internet]. 2005 Feb [cited 2013 Nov 5];1(2):107–19. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16054052

  28. Lee C, Park GH, Kim C-Y, Jang J-H. [6]-Gingerol attenuates β-amyloid-induced oxidative cell death via fortifying cellular antioxidant defense system. Food Chem. Toxicol. [Internet]. 2011 Jun [cited 2013 Oct 29];49(6):1261–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21396424

  29. Lee T-Y, Lee K-C, Chen S-Y, Chang H-H. 6-Gingerol inhibits ROS and iNOS through the suppression of PKC-alpha and NF-kappaB pathways in lipopolysaccharide-stimulated mouse macrophages. Biochem. Biophys. Res. Commun. [Internet]. 2009 Apr 24 [cited 2013 Oct 29];382(1):134–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19268427

  30. Jung SA, Choi M, Kim S, Yu R, Park T. Cinchonine Prevents High-Fat-Diet-Induced Obesity through Downregulation of Adipogenesis and Adipose Inflammation. PPAR Res. [Internet]. 2012 Jan [cited 2013 Oct 29];2012:541204. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3362995&tool=pmcentrez&rendertype=abstract

  31. Lau FC, Bagchi M, Sen C, Roy S, Bagchi D. Nutrigenomic analysis of diet-gene interactions on functional supplements for weight management. Curr. Genomics [Internet]. 2008 Jun [cited 2013 Oct 29];9(4):239–51. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2682937&tool=pmcentrez&rendertype=abstract

  32. Vasques CAR, Schneider R, Klein-Júnior LC, Falavigna A, Piazza I, Rossetto S. Hypolipemic Effect of Garcinia cambogia in Obese Women. Phytother. Res. [Internet]. 2013 Oct 17 [cited 2013 Oct 29]; Available from: http://www.ncbi.nlm.nih.gov/pubmed/24133059

  33. Hood RL, Beitz DC, Johnson DC. Inhibition by potential metabolic inhibitors of in vitro adipose tissue lipogenesis. Comp. Biochem. Physiol. B. [Internet]. 1985 Jan [cited 2013 Oct 29];81(3):667–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/4028683

  34. Kim H-K, Kim JN, Han SN, Nam J-H, Na H-N, Ha TJ. Black soybean anthocyanins inhibit adipocyte differentiation in 3T3-L1 cells. Nutr. Res. [Internet]. 2012 Oct [cited 2013 Oct 29];32(10):770–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23146774

  35. Badshah H, Ullah I, Kim SE, Kim T-H, Lee HY, Kim MO. Anthocyanins attenuate body weight gain via modulating neuropeptide Y and GABAB1 receptor in rats hypothalamus. Neuropeptides [Internet]. 2013 Jul 2 [cited 2013 Oct 29]; Available from: http://www.ncbi.nlm.nih.gov/pubmed/23830691

  36. Graf D, Seifert S, Jaudszus A, Bub A, Watzl B. Anthocyanin-Rich Juice Lowers Serum Cholesterol, Leptin, and Resistin and Improves Plasma Fatty Acid Composition in Fischer Rats. PLoS One [Internet]. 2013 Jan [cited 2013 Oct 22];8(6):e66690. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3688949&tool=pmcentrez&rendertype=abstract

  37. Prior RL, E Wilkes S, R Rogers T, Khanal RC, Wu X, Howard LR. Purified Blueberry Anthocyanins and Blueberry Juice Alter Development of Obesity in Mice Fed an Obesogenic High-Fat Diet (dagger). J. Agric. Food Chem. [Internet]. 2010 Feb 11; Available from: http://www.ncbi.nlm.nih.gov/pubmed/20148514

  38. Tsuda T. Regulation of adipocyte function by anthocyanins; possibility of preventing the metabolic syndrome. J. Agric. Food Chem. [Internet]. 2008 Mar 13 [cited 2013 Oct 29];56(3):642–6. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18211021

  39. Tsuda T, Ueno Y, Aoki H, Koda T, Horio F, Takahashi N, et al. Anthocyanin enhances adipocytokine secretion and adipocyte-specific gene expression in isolated rat adipocytes. Biochem. Biophys. Res. Commun. [Internet]. 2004 Mar 26 [cited 2013 Oct 29];316(1):149–57. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15003523

  40. Tesoriere L, Butera D, D’Arpa D, Di Gaudio F, Allegra M, Gentile C, et al. Increased resistance to oxidation of betalain-enriched human low density lipoproteins. Free Radic. Res. [Internet]. 2003 Jun [cited 2013 Oct 29];37(6):689–96. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12868496

  41. Tesoriere L, Butera D, Allegra M, Fazzari M, Livrea MA. Distribution of betalain pigments in red blood cells after consumption of cactus pear fruits and increased resistance of the cells to ex vivo induced oxidative hemolysis in humans. J. Agric. Food Chem. [Internet]. 2005 Mar 23 [cited 2013 Oct 29];53(4):1266–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15713051

  42. Tian W-X, Li L-C, Wu X-D, Chen C-C. Weight reduction by Chinese medicinal herbs may be related to inhibition of fatty acid synthase. Life Sci. [Internet]. 2004 Mar 26 [cited 2013 Oct 29];74(19):2389–99. Available from: http://www.ncbi.nlm.nih.gov/pubmed/14998716

  43. Wang Y, Zhang S-Y, Ma X-F, Tian W-X. Potent inhibition of fatty acid synthase by parasitic loranthus [Taxillus chinensis (dc.) danser] and its constituent avicularin. J. Enzyme Inhib. Med. Chem. [Internet]. 2006 Mar [cited 2013 Oct 29];21(1):87–93. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16570511

  44. Wang Y, Deng M, Zhang S-Y, Zhou Z-K, Tian W-X. Parasitic loranthus from Loranthaceae rather than Viscaceae potently inhibits fatty acid synthase and reduces body weight in mice. J. Ethnopharmacol. [Internet]. 2008 Aug 13 [cited 2013 Oct 29];118(3):473–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18583073

  45. Osadebe PO, Okide GB, Akabogu IC. Study on anti-diabetic activities of crude methanolic extracts of Loranthus micranthus (Linn.) sourced from five different host trees. J. Ethnopharmacol. [Internet]. 2004 Dec [cited 2013 Oct 28];95(2-3):133–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15507325

  46. Obatomi DK, Bikomo EO, Temple VJ. Anti-diabetic properties of the African mistletoe in streptozotocin-induced diabetic rats. J. Ethnopharmacol. [Internet]. 1994 Jun [cited 2013 Oct 29];43(1):13–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/7967645

  47. Kim G-S, Park HJ, Woo J-H, Kim M-K, Koh P-O, Min W, et al. Citrus aurantium flavonoids inhibit adipogenesis through the Akt signaling pathway in 3T3-L1 cells. BMC Complement. Altern. Med. [Internet]. 2012 Jan [cited 2013 Nov 5];12:31. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3350436&tool=pmcentrez&rendertype=abstract

  48. Stohs SJ, Preuss HG, Shara M. A review of the human clinical studies involving Citrus aurantium (bitter orange) extract and its primary protoalkaloid p-synephrine. Int. J. Med. Sci. [Internet]. 2012 Jan [cited 2013 Oct 29];9(7):527–38. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3444973&tool=pmcentrez&rendertype=abstract

  49. Siegner R, Heuser S, Holtzmann U, Söhle J, Schepky A, Raschke T, et al. Lotus leaf extract and L-carnitine influence different processes during the adipocyte life cycle. Nutr. Metab. (Lond). [Internet]. 2010 Jan [cited 2013 Oct 29];7:66. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2922297&tool=pmcentrez&rendertype=abstract

  50. Ono Y, Hattori E, Fukaya Y, Imai S, Ohizumi Y. Anti-obesity effect of Nelumbo nucifera leaves extract in mice and rats. J. Ethnopharmacol. [Internet]. 2006 Jun 30 [cited 2013 Oct 29];106(2):238–44. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16495025

  51. Kim A-R, Jeong S-M, Kang M-J, Jang Y-H, Choi H-N, Kim J-I. Lotus leaf alleviates hyperglycemia and dyslipidemia in animal model of diabetes mellitus. Nutr. Res. Pract. [Internet]. 2013 Jun [cited 2013 Oct 29];7(3):166–71. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3679324&tool=pmcentrez&rendertype=abstract

  52. Bischoff H. The mechanism of alpha-glucosidase inhibition in the management of diabetes. Clin. Invest. Med. [Internet]. 1995 Aug [cited 2013 Nov 6];18(4):303–11. Available from: http://www.ncbi.nlm.nih.gov/pubmed/8549017

  53. Drira R, Chen S, Sakamoto K. Oleuropein and hydroxytyrosol inhibit adipocyte differentiation in 3 T3-L1 cells. Life Sci. [Internet]. 2011 Nov 7 [cited 2013 Nov 1];89(19-20):708–16. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21945192

  54. Ebaid GMX, Seiva FRF, Rocha KKHR, Souza GA, Novelli ELB. Effects of olive oil and its minor phenolic constituents on obesity-induced cardiac metabolic changes. Nutr. J. [Internet]. 2010 Oct 19 [cited 2010 Oct 21];9(1):46. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20958965

  55. De Bock M, Derraik JGB, Brennan CM, Biggs JB, Morgan PE, Hodgkinson SC, et al. Olive (Olea europaea L.) leaf polyphenols improve insulin sensitivity in middle-aged overweight men: a randomized, placebo-controlled, crossover trial. PLoS One [Internet]. 2013 Jan [cited 2013 Nov 1];8(3):e57622. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3596374&tool=pmcentrez&rendertype=abstract

  56. Wainstein J, Ganz T, Boaz M, Bar Dayan Y, Dolev E, Kerem Z, et al. Olive leaf extract as a hypoglycemic agent in both human diabetic subjects and in rats. J. Med. Food [Internet]. 2012 Jul [cited 2013 Nov 1];15(7):605–10. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22512698

  57. Kontogianni VG, Charisiadis P, Margianni E, Lamari FN, Gerothanassis IP, Tzakos AG. Olive leaf extracts are a natural source of advanced glycation end product inhibitors. J. Med. Food [Internet]. 2013 Sep [cited 2013 Nov 1];16(9):817–22. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24044491

  58. Lui T-N, Tsao C-W, Huang S-Y, Chang C-H, Cheng J-T. Activation of imidazoline I2B receptors is linked with AMP kinase pathway to increase glucose uptake in cultured C2C12 cells. Neurosci. Lett. [Internet]. 2010 May 3 [cited 2013 Nov 4];474(3):144–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/20298750

  59. Chang C-H, Tsao C-W, Huang S-Y, Cheng J-T. Activation of imidazoline I(2B) receptors by guanidine to increase glucose uptake in skeletal muscle of rats. Neurosci. Lett. [Internet]. 2009 Dec 25 [cited 2013 Nov 4];467(2):147–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19822195

  60. Mooney MH, Fogarty S, Stevenson C, Gallagher AM, Palit P, Hawley SA, et al. Mechanisms underlying the metabolic actions of galegine that contribute to weight loss in mice. Br. J. Pharmacol. [Internet]. 2008 Apr [cited 2013 Nov 4];153(8):1669–77. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2438274&tool=pmcentrez&rendertype=abstract

  61. Palit P, Furman BL, Gray AI. Novel weight-reducing activity of Galega officinalis in mice. J. Pharm. Pharmacol. [Internet]. 1999 Nov [cited 2013 Nov 4];51(11):1313–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/10632090

  62. Quan H-Y, Yuan H-D, Jung MS, Ko SK, Park YG, Chung SH. Ginsenoside Re lowers blood glucose and lipid levels via activation of AMP-activated protein kinase in HepG2 cells and high-fat diet fed mice. Int. J. Mol. Med. [Internet]. 2012 Jan [cited 2013 Nov 4];29(1):73–80. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21971952

  63. Dey L, Xie JT, Wang A, Wu J, Maleckar SA, Yuan CS. Anti-hyperglycemic effects of ginseng: comparison between root and berry. Phytomedicine [Internet]. 2003 Jan [cited 2013 Nov 4];10(6-7):600–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/13678250

  64. Xie JT, Zhou YP, Dey L, Attele AS, Wu JA, Gu M, et al. Ginseng berry reduces blood glucose and body weight in db/db mice. Phytomedicine [Internet]. 2002 Apr [cited 2013 Nov 4];9(3):254–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12046868

  65. Attele AS, Zhou Y-P, Xie J-T, Wu JA, Zhang L, Dey L, et al. Antidiabetic effects of Panax ginseng berry extract and the identification of an effective component. Diabetes [Internet]. 2002 Jun [cited 2013 Nov 4];51(6):1851–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/12031973

  66. Park E-Y, Kim H-J, Kim Y-K, Park S-U, Choi J-E, Cha J-Y, et al. Increase in Insulin Secretion Induced by Panax ginseng Berry Extracts Contributes to the Amelioration of Hyperglycemia in Streptozotocininduced Diabetic Mice. J. Ginseng Res. [Internet]. 2012 Apr [cited 2013 Nov 4];36(2):153–60. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3659577&tool=pmcentrez&rendertype=abstract

  67. Godard MP, Johnson BA, Richmond SR. Body composition and hormonal adaptations associated with forskolin consumption in overweight and obese men. Obes. Res. [Internet]. 2005 Aug [cited 2013 Nov 4];13(8):1335–43. Available from: http://www.ncbi.nlm.nih.gov/pubmed/16129715

  68. Henderson S, Magu B, Rasmussen C, Lancaster S, Kerksick C, Smith P, et al. Effects of coleus forskohlii supplementation on body composition and hematological profiles in mildly overweight women. J. Int. Soc. Sports Nutr. [Internet]. 2005 Jan [cited 2013 Nov 4];2:54–62. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2129145&tool=pmcentrez&rendertype=abstract

  69. Yao J, Zhi M, Gao X, Hu P, Li C, Yang X. Effect and the probable mechanisms of silibinin in regulating insulin resistance in the liver of rats with non-alcoholic fatty liver. Braz. J. Med. Biol. Res. [Internet]. 2013 Mar 15 [cited 2013 Nov 4];46(3):270–7. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23532271

  70. Zhang Y, Hai J, Cao M, Zhang Y, Pei S, Wang J, et al. Silibinin ameliorates steatosis and insulin resistance during non-alcoholic fatty liver disease development partly through targeting IRS-1/PI3K/Akt pathway. Int. Immunopharmacol. [Internet]. 2013 Sep 13 [cited 2013 Nov 3];17(3):714–20. Available from: http://www.ncbi.nlm.nih.gov/pubmed/24036369

  71. Haddad Y, Vallerand D, Brault A, Haddad PS. Antioxidant and hepatoprotective effects of silibinin in a rat model of nonalcoholic steatohepatitis. Evid. Based. Complement. Alternat. Med. [Internet]. 2011 Jan [cited 2013 Nov 4];2011:nep164. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3136786&tool=pmcentrez&rendertype=abstract

  72. Wallace S, Vaughn K, Stewart BW, Viswanathan T, Clausen E, Nagarajan S, et al. Milk thistle extracts inhibit the oxidation of low-density lipoprotein (LDL) and subsequent scavenger receptor-dependent monocyte adhesion. J. Agric. Food Chem. [Internet]. 2008 Jun 11 [cited 2013 Nov 4];56(11):3966–72. Available from: http://www.ncbi.nlm.nih.gov/pubmed/18476698

  73. Gaya M, Repetto V, Toneatto J, Anesini C, Piwien-Pilipuk G, Moreno S. Antiadipogenic effect of carnosic acid, a natural compound present in Rosmarinus officinalis, is exerted through the C/EBPs and PPARγ pathways at the onset of the differentiation program. Biochim. Biophys. Acta [Internet]. 2013 Jun [cited 2013 Nov 4];1830(6):3796–806. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23541989

  74. Ibarra A, Cases J, Roller M, Chiralt-Boix A, Coussaert A, Ripoll C. Carnosic acid-rich rosemary (Rosmarinus officinalis L.) leaf extract limits weight gain and improves cholesterol levels and glycaemia in mice on a high-fat diet. Br. J. Nutr. [Internet]. 2011 Oct [cited 2013 Nov 4];106(8):1182–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21676274

  75. Harach T, Aprikian O, Monnard I, Moulin J, Membrez M, Béolor J-C, et al. Rosemary (Rosmarinus officinalis L.) leaf extract limits weight gain and liver steatosis in mice fed a high-fat diet. Planta Med. [Internet]. 2010 Apr [cited 2013 Nov 4];76(6):566–71. Available from: http://www.ncbi.nlm.nih.gov/pubmed/19918713

  76. Romo Vaquero M, Yáñez-Gascón M-J, García Villalba R, Larrosa M, Fromentin E, Ibarra A, et al. Inhibition of gastric lipase as a mechanism for body weight and plasma lipids reduction in Zucker rats fed a rosemary extract rich in carnosic acid. PLoS One [Internet]. 2012 Jan [cited 2013 Nov 4];7(6):e39773. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3382157&tool=pmcentrez&rendertype=abstract

  77. Wang T, Takikawa Y, Satoh T, Yoshioka Y, Kosaka K, Tatemichi Y, et al. Carnosic acid prevents obesity and hepatic steatosis in ob/ob mice. Hepatol. Res. [Internet]. 2011 Jan [cited 2013 Nov 4];41(1):87–92. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21199201

  78. Takahashi T, Tabuchi T, Tamaki Y, Kosaka K, Takikawa Y, Satoh T. Carnosic acid and carnosol inhibit adipocyte differentiation in mouse 3T3-L1 cells through induction of phase2 enzymes and activation of glutathione metabolism. Biochem. Biophys. Res.

2 Likes

Legend - putting in the work there with the education.

Thanks, Bob!

2 Likes

thank you!!