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USPowders Q & A: VAT Attack!
VAT attack! is without a doubt one of the most innovative powders to hit the weight loss scene. USPowders, a subsidiary of USPlabs is the forefront of the innovative side of the bulk powder game. It’s rarely seen in our industry that a company releases innovation at an economical and cost effective way.
I’m about to tell you why you need VAT Attack! the ONLY Non-Hormonal way to combat visceral adipose tissue (VAT). VAT is the "blubber" deep down that when reduced is the only way to get the deep ripped defined physique!
Glucocorticoids are recognized as stress hormones that mediate a myriad of physiological pathways that are implicated in inflammatory, metabolic, and cardiovascular processes. An excessive expression of glucocorticoids can lead to obesity, hypertension (and other cardiovascular dysfunctions), dyslipidemia, impaired insulin metabolism, and other inflammatory states.
Now, cortisol (corticosterone), a catabolic hormone released in the adrenal cortex, is the main (active) glucocorticoid form in humans. Two proteins are known to mediate glucocorticoid action. One is corticosteroid-binding globulin (CBG), and the other is 11ß-hydroxysteroid dehydrogenase. The protein, 11ß-HSD has two isoenzymes that regulate the interconversion of cortisol and cortisone at the endoplasmic reticulum.
These two isoenzymes, 11ß-HSD type 1 and 11ß-HSD type 2, are not only produced by different genes, but also have different tissue distribution. More specifically, 11ß-HSD1 is primarily distributed in the liver, the kidneys, the brain, and in adipose cells; while 11ß-HSD2 is mainly found in the kidney and the salivary glands. In humans, 11ß-HSD1 is responsible for the conversion of inactive cortisone to cortisol, while 11ß-HSD2 is mediates the catalysis of the opposite reaction. Cortisol is primarily converted into the inert glucocorticoid, cortisone, in the kidney. Cortisol accumulation occurs via a combination of tissue 11ß-HSD1 activity and plasma diffusion. Plasma glucocorticoid levels are mediated by the activity of the hypothalamic-pituitary-adrenal (HPA) axis, and can be triggered by stress, both physical and psychological.
The glucocorticoid receptor mediates glucocorticoid action and, consequently, activates or deactivates target genes involved in such physiological processes as adipocyte differentiation, inflammation, and gluconeogenesis. Examples of these target genes include glucose-6-phosphatase [G6Pase], tyrosine aminotransferase (TAT), leptin, hormone sensitive lipase (HSL), lipoprotein lipase (LPL), corticotrophin-releasing hormone (CRH), interleukin 6 (IL-6), prolactin, and so on.
Clearly, 11ß-HSD1 activity is important for the regulation of cortisol levels. In particular, 11ß-HSD1 inhibition leads to a series of effects including increased fat loss, reduction in hyperglycemia and hepatic glucose output (via reduced expression of glucose-6-phosphatase [G6Pase] and phosphoenolpyruvate carboxykinase [PEPCK], the rate-limiting enzymes in gluconeogenesis), reduced hepatic fat accumulation (via reduction in the differentiation of pre-adipocytes to adipocytes, reduction of the activities of enzymes involved in fatty-acid synthesis and triglyceride accumulation), improved peripheral insulin sensitivity (via reversal of glucocorticoid antagonism of insulin-stimulated glucose disposal), reduction of visceral adipose tissue fat accumulation, and favorable changes in other metabolic indicators. Note that fat accumulation can occur either via increase in the size of individual adipocytes (large adipose cells are more insulin insensitive), or an increase in the number of adipocytes (via adipose differentiation from pre-adipocytes to adipocytes). Or both!
We have seen that cortisol management is desirable to mitigate metabolic disturbances. We have also established that 11ß-HSD1 is the key regulatory enzyme for cortisol synthesis, and that the inhibition of this enzyme, in the presence of physiological and psychological stress stimuli, will favorably induce a myriad of beneficial results, including improved (visceral) fat loss, improved insulin sensitivity, improved cardiovascular state, and enhanced lean mass preservation.
But how can we achieve 11ß-HSD1 via non-hormonal means?
Enter VAT Attack! Contained in VAT Attack!, Coffee (Coffea Arabica L.) extract is known to support lipid and glucose metabolism via selectively inhibiting the action of 11ß-HSD1 (but not that of 11ß-HSD2), leading to physiological processes enumerated earlier. Elevated cortisol levels are known to induce breakdown of muscle tissue.
Essentially, cortisol exerts a metabolic action by elevating glucose levels during exercise, for instance, via inducing protein (amino acid) and lipid mobilization in adipocytes and skeletal muscle cells. Beyond this, cortisol stimulates hepatic production of enzymes that mediate gluconeogenic, glycogenetic, and related pathways.
This leads to conversion of amino acids and glycerol into glucose and glycogen. In this instance, cortisol acts much like insulin as a non-discriminatory storage hormone. Clearly, the metabolic action of cortisol ultimately leads to adipose-cell accumulation, especially of the visceral-adipose-tissue type.
What can you expect from VAT Attack!?
- Significant and noticeable reduction in elevated cortisol levels via selective 11ß-HSD1 inhibition.
- Dramatic increase in lipolytic action within the deep visceral-adipose-tissues (VAT), leading to a significant trimming of VAT accumulation, inducing noticeable fat loss, and bringing you closer to your desired six-pack.
- Enhanced “burning” of subcutaneous adipose tissue (SCAT), triggering a cascade of events that ultimately deliver noticeable fat loss.
- Preservation of lean mass by reducing the action of the catabolic hormone, cortisol.
- Enhanced cellular insulin sensitivity, leading to the breakdown of another supportive factor in weight gain.
- Elevation of the markers of optimal cardiovascular and endothelial functions.
- Improvement in the testosterone:cortisol ratio, following the strong negative correlation between testosterone (total and free) and cortisol.
But what is abdominal obesity and how is it connected to visceral adipose tissue and cortisol?
Abdominal obesity is a function of the accumulation of visceral adipose tissues (VAT) and subcutaneous adipose tissue (SCAT). Accounting for up to a fifth of total fat in men, VAT is distributed in the deep cavity beneath abdominal muscles. Its location makes it very difficult to target and detonate.
VAT has a very powerful impact on abdominal obesity. On its part, SCAT is located on top of abdominal muscles, right beneath the skin, and is consequently easier to reach and trim than VAT. VAT accumulation is known to not only be positively correlated with, but also sustains the development of, such metabolic abnormalities as hyperlipidemia, cardiovascular disorders (including endothelial dysfunction, insulin disturbances, and so on. VAT accumulation is not just a problem for obese individuals. Even lean individuals with elevated VAT accumulation are equally susceptible to the problems outlined earlier. Consequently, and as VAT adipocyte is more sensitive to lipolysis, even a modest (5-10 percent) body weight loss can preferentially produce a greater reduction in VAT deposits compared to SCAT.
Based on the earlier discussion, this reduced concentration in the VAT depot can trigger dramatic improvements in pro-inflammatory and pro-atherogenic markers, including reductions in insulin insensitivity, improved fat oxidation, and markers of cardiovascular function.
So, what are the key differences between VAT and SCAT, and why is reduction of VAT depots significantly more beneficial?
- VAT adipocytes are more sensitive to lipolysis, and produce more inflammatory cytokines such as IL-6 and plasminogen activator inhibitor-1 (PA-1). VAT supports the increased transport of glycerol and free fatty acids to the liver, leading to a stimulation of hepatic glucose production, and ultimately insulin abnormalities.
- VAT adipocytes have a higher GLUT-4 expression than SCAT adipocytes, leading to a higher level of insulin-triggered glucose uptake, ultimately inducing preferential triglyceride stores in VAT.
- VAT is strongly negatively correlated with plasma levels of total testosterone, free testosterone, and sex-hormone binding globulin levels.
- VAT possesses more glucocorticoid receptors than SCAT, making 11ß-HSD1 especially active in VAT. As 11ß-HSD1 activity is significantly higher in VAT adipocytes than in SCAT ones, a much higher amount of cortisol is produced in VAT, leading to further VAT accumulation, and metabolic abnormalities.
To note, besides inducing fat accumulation, cortisol would also initiate and sustain the systematic breakdown of muscle tissue. But, by inhibiting 11ßHSD1 activity, VAT Attack! down-regulates the conversion of cortisone to metabolically active cortisol, leading to a reduction of skeletal-muscle and adipose-tissue glucocorticoid levels. This supports effective protein synthesis and shunts fat accumulation. Furthermore, considering the existence of a positive relationship between high levels of circulating cortisol and insulin insensitivity, reductions in cortisol levels induce improvements in cellular insulin sensitivity with benefits for blood-glucose optimization, diabetic states, and fat loss.
So, VAT Attack! is a simple-but-potent product that has a myriad of benefits including supporting the reduction in cellular visceral-adipocyte content and body weight via 11ßHSD1 inhibition; inducing favorable changes in lipid levels, thus providing considerable cardiovascular support; improving insulin sensitivity, thus providing diabetic-amelioration support; preservation of muscle mass via its anti-catabolic action induced through cortisol down-regulation; supporting the management of obese states; and so on.
Whether you are dieting, whether you want to preserve muscle mass, or you simply wish to reduce cortisol levels to reap the associated string of benefits, whether you wish to enrich your current fat-loss stack, or whether you are in PCT (there appears to be a significant associative negative relationship between testosterone and cortisol), VAT Attack! is one non-hormonal-but-potent agent that can help you reach your goals smarter.
Expect VAT Attack! Expect fat loss! Expect abdominal fat loss! Finally expect true (abdominal) lean mass exposure! Expect improved cardiovascular function! Expect unparalleled value for money! Get ready for a mind-blowing summer!