Aspiring DemiGods and DemiGoddesses are continuously working to TR1UMPH over mediocrity to achieve the ultimate physique. A part of that process requires periods when you need to shift your focus to fat loss. The dreaded dieting phase where you reduce calories, usually in the form of carbs to get shredded. A lower calorie diet will reduce energy levels so you increase intake of stimulants. Sound familiar? There has to be a better way!
It would be nice if there was a supplement that helped you lose weight without starving yourself to induce weight loss and subsequently depending on stimulants to remain functional. Thankfully, there is a supplement company that has the foresight to attempt such a feat. Olympus Labs is proud to present ASSASS1NATE, a combined stimulant free fat burner and glucose disposal agent (GDA) supplement.
Olympus Labs considers the customer’s needs before profits and utilizes the best minds in the business to formulate supplements. The end result is innovative and effective products that are worth your hard earned money. ASSASS1NATE is no exception as it achieves everything you would expect in a fat burner plus additional benefits you never would think were possible. ASSASS1NATE allows you to CONQU3R dieting with the following two potent matrices.
The Metabolism Stimulation & Extreme Thermogenic Activation with 630mg Dihydromyricetin, 25mg Trans-Tiliroside and 100mg Carnosic acid will IGNIT3 the thermogenic furnace to start melting the pounds away. This matrix will help you lose weight by stimulating energy metabolism and utilizing caloric intake more effectively. In addition, these compounds have GDA properties that will allow you to utilize food, especially carbs, as fuel instead of storing it as fat. It is recommended you dose ASSASS1NATE prior to your largest meals to take advantage of the GDA aspect of the formula. But don’t worry these compounds will not drop your blood sugar and cause a hypoglycemic effect, so you should not feel pressured to have a high carbohydrate meal.
The second matrix, The Potent Fat Inhibition & Cannabinoid (CB1) Receptor Modulation, is the perfect compliment to the previous blend. It consists of our custom 150mg Olive Leaf Extract, 25mg Lutein and 300mg Orthosiphon Stamineus Extract that target several fat burning pathways. It directly burns fat by targeting several different pathways including PPAR-α, PPARγ, CPT1 and increasing leptin. Leptin is a hormone that regulates how your body utilizes stored energy. It directly burns fat by preventing the storage of fat and reducing appetite. In addition, it will inhibit the Cannabinoid 1 (CB1) receptor in adipocytes , a novel pathway that improves lipid metabolism and regulates glucose levels.
Sound too good to be true? Perhaps you need to raise your expectations on the quality of the supplements you purchase. Olympus Labs care about quality, from the selection of the ingredients in our supplements to the sourcing and testing of said ingredients. That is precisely why Olympus Labs supplements deliver Results! We are extremely confident ASSASS1NATE will continue that trend. A potent stimulant free fat burner and GDA in one. The supplement that you never even thought of, but need to have!
Metabolism Stimulation & Extreme Thermogenic Activation :
The most well known function of a fat burner is its ability to induce thermogenesis. Typically this mechanism is targeted with stimulants. However, ASSASS1NATE utilizes novel compounds; 630mg Dihydromyricetin, 50mg Trans-Tiliroside and 100mg Carnosic acid, to elicit a potent thermogenic effect. That is not the only mechanism of action that these ingredients target. They will stimulate your metabolism to help you ASSASS1NATE fat. Furthermore, these compounds have been found to increase glucose uptake tp help you utilize carbohydrates effectively. Hence the recommendation to dose ASSASS1NATE before meals for optimal metabolic function.
Dihydromyricetin is the active component of Ampelopsis grossedentata, a medicinal and edible plant that has been used in China for hundreds of years. It is a natural flavonoid that exerts various bioactivities including anti-oxidative and hepatoprotective effects. More pertinent to ASSASS1NATE, Dihydromyricetin has been found to activate AMP-activated protein kinase (AMPK) which will stimulate fatty acid oxidation and glucose uptake. In fact, several studies have confirmed that Dihydromyricetin regulates glucose metabolism and improves skeletal muscle insulin resistance. In addition, Dihydromyricetin has been found to stimulate irisin via activation of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α). Irisin, derived from FNDC5, is an exercise-induced myokine that can stimulate the ‘browning’ of white adipose tissue, that is regulated by PGC-1α. This conversion of white adipose tissue (WAT), or stored fat, to brown adipose tissue (BAT) is beneficial because BAT burns calories to generate heat.
The effects of irisin in human primary adipocytes and fresh human subcutaneous white adipose tissue (scWAT) were examined in a study with 28 female donors. Individual responses to irisin in scWAT were correlated with basal expression levels of brown/beige genes. Irisin upregulated the expression of browning-associated genes and uncoupling protein 1 (UCP1) protein in both cultured primary mature adipocytes and fresh adipose tissues. It also significantly increased thermogenesis at 5 nmol/l by elevating cellular energy metabolism (OCR and ECAR). Treating human scWAT with irisin increased UCP1 expression by activating the ERK and p38 MAPK signaling. Blocking either pathway with specific inhibitors abolished irisin-induced UCP1 upregulation. However, test results demonstrated that UCP1 in human perirenal adipose tissue was insensitive to irisin. Basal levels of brown/beige and FNDC5 genes correlated positively with the browning response of scWAT to irisin. In addition, irisin significantly inhibited adipogenic differentiation but promoted osteogenic differentiation. These results indicate that irisin promotes “browning” of mature white adipocytes by increasing cellular thermogenesis, while inhibiting adipogenesis and promoting osteogenesis during lineage-specific differentiation. Thus, irisin can be used to stimulate weight loss and bone formation.
Dihydromyricetin (DHM) was studied to determine whether it, could mimic the effects of exercise on irisin secretion. DHM administration increased circulating irisin in rats and humans. Notably, the serum irisin level had a greater correlation to the level of circulating DHM than to the amount of exercise. DHM treatment upregulated PGC-1α and FNDC5 expression, enhanced energy metabolism and partially abolished the suppressive effects of PGC-1α siRNA on FNDC5 expression. These results suggest that DHM can stimulate irisin secretion partially via the PGC-1α pathway. Thus, DHM will stimulate metabolism, even for those who cannot undergo rigorous exercise.
The effect of Dihydromyricetin (DMY) on osteogenesis, the differentiation of bone mesenchymal stem cells (BMSCs) leading to bone metabolic disease was investigated. Human BMSCs were induced with or without DMY. DMY (0.1-50 μm) exhibited no cytotoxic effect on proliferation, but increased alkaline phosphatase activity, osteoblast-specific gene expression, and mineral deposition. It also enhanced active β-catenin expression and reduced dickkopf-1(DKK1) and sclerostin expression. The Wnt/β-catenin signaling pathway inhibitor (DKK1 and β-catenin-specific siRNA) decreased the enhanced bone mineral formation caused by DMY. These results indicate DMY enhances osteogenic differentiation of human BMSCs partly through Wnt/β-catenin in vitro and therefore will prevent bone metabolic function.
An in-vivo study on rats fed a high-fat diet was conducted to investigate the effect of Dihydromyricetin (DHM) on skeletal muscle insulin resistance (SMIR) and the underlying mechanisms. DHM increased the expression of phosphorylated insulin receptor substrate-1, phosphorylated Akt and glucose uptake capacity in palmitate-treated L6 myotubes under insulin-stimulated conditions. Furthermore, DHM increased the levels of phosphorylated AMP-activated protein kinase (AMPK) and Ulk1, and decreased phosphorylated mTOR levels. AMPK inhibitor compound C (CC) and AMPK siRNA abrogated DHM-induced autophagy and subsequently suppressed DHM-induced SMIR improvement. DHM inhibited the activity of F1F0-ATPase thereby activating AMPK. These results were consistent with the findings of an in vitro study on DHM on SMIR. The study concluded that DHM improved SMIR by inducing the degradation of destructive cellular components, via the activation of AMPK signaling pathway.
Dihydromyricetin (DMY) was studied with respect to its effect on oxidative stress and glucose transport activity in a methylglyoxal (MG) induced PC12 cell line and to explore the related mechanisms. DMY suppressed cellular oxidative stress in PC12 cells and balanced glucose metabolism. DMY reduced GLUT4 translocation dysfunction and increased Glo-1 and p-AMPKα expression. Furthermore, DMY protected PC12 cells against MG-induced apoptosis and glycometabolic disorders, at least in part by restraining the hyperactivation of p-AMPK activity and normalizing the translocation of GLUT4 from the intracellular compartment, resulting in a balance in glucose uptake. These results indicate that DMY may serve as a novel and effective agent to treat diabetic encephalopathy by reducing the toxicity of MG.
In a double-blind clinical trial was carried out to investigate the effects of dihydromyricetin on glucose and lipid metabolism, inﬂammatory mediators and several biomarkers in nonalcoholic fatty liver disease. Sixty adult non-alcoholic fatty liver disease patients were randomly assigned to receive either 150mg of dihydromyricetin or placebo twice daily for three months.The serum levels of alanine, aspartate aminotransferase, -glutamyl transpeptidase, glucose, low-density lipoprotein-cholesterol and apolipoprotein B, and the homeostasis model assessment of insulin resistance (HOMA-IR) index were signiﬁcantly decreased in the dihydromyricetin group compared with the placebo group. In the dihydromyricetin group, the serum levels of tumor necrosis factor-alpha, cytokeratin-18 fragment and ﬁbroblast growth factor21 were decreased, whereas the levels of serum adiponectin were increased at the end of the study. The study included that dihydromyricetin supplementation improves glucose and lipid metabolism as well as various biochemical parameters. Furthermore, the therapeutic effects of dihydromyricetin are likely attributable to improved insulin resistance and decreases in the serum levels of tumor necrosis factor-alpha, cytokeratin-18, and ﬁbroblast growth factor 21.
Trans-Tiliroside is a glycosidic flavonoid derived from several plants including Potentilla Chinesis and Rosa Canina L. (Rosaceae). You may be more familiar with the name of the fruit of the plant, Rosehip extract. It is a plant rich in antioxidants such as ascorbic acid, phenolic compounds, and carotenoids It has been used as a diuretic, laxative, anti-gout, and anti-rheumatic remedy in traditional European medicine. Recent research has shown that Rosa Canina L. and Tiliroside exhibit antiobesity and antidiabetic activities via enhancement of fatty acid oxidation in the liver and skeletal muscle. Specifically, it inhibits body weight gain and decreases visceral fat. Furthermore, Trans-Tiliroside also has PPARγ antagonistic properties whereby it can inhibit lipid accumulation in white adipose tissue (WAT). WAT is the largest subset of fat in the human which stores energy so the more you store is more that you need to burn.
A 12-week, single-center, double-blind, randomized, placebo-controlled study was performed with 32 subjects who had a body mass index of ≥25 but <30. The subjects were assigned to two random groups, and they received one tablet of placebo or 100 mg of rosehip extract once each day for 12 weeks with no dietary intervention. Abdominal total fat area, abdominal visceral fat area, body weight, and body mass index decreased significantly in the rosehip group at week 12 compared with their baseline levels (P<0.01) after receiving the rosehip tablet intake, and the decreases in these parameters were significantly higher when compared with those in the placebo group. Additionally, body fat percent tended to decrease compared with the placebo group and their baseline level. Moreover, the abdominal subcutaneous fat area was significantly lower in the rosehip group than in the placebo group at week 12 after the initiation of intake (P<0.05). There were no abnormalities, subjective symptoms, and findings that may indicate clinical problems during the study period. The study concluded that rosehip extract can be a beneficial supplement for preventing obesity.
A study was completed to investigate the effects of rosehip extract (RHE) and Tiliroside on lipid accumulation and protein expression of key transcription factors in both in vitro and in vivo models. RHE and Tiliroside inhibited lipid accumulation in a dose-dependent manner in 3T3-L1 cells. The inhibitory effect of RHE on white adipose tissue (WAT) in high-fat diet (HFD)-induced obesity mice model was also analyzed. Male C57BL/6J mice were fed HFD or HFD supplemented with 1% RHE (HFDRH) for 8 weeks. The HFDRH-fed group gained less body weight and had less visceral fat than the HFD-fed group. Liver weight was significantly lower in the HFDRH-fed group and total hepatic lipid and triglyceride (TG) content was also reduced. A significant reduction in the expression of peroxisome proliferator-activated receptor gamma (PPARγ) was observed in epididymal fat in the HFDRH-fed group, compared to the control group. The study concluded that RHE had a suppressive effect on lipid accumulation in WAT and the downregulation of PPARγ expression was a contributing factor to that finding.
In another study, the hypothesis that Trans-Tiliroside isolated from Potentilla chinensis has anti-hyperglycemic, anti-hyperlipidemic and antioxidant effects was investigated. Biochemical parameters were assayed in blood samples of different groups of alloxan-induced diabetic mice and streptozotocin-induced diabetic rats. The level of fasting serum glucose levels, triglycerides (TG) and total cholesterol (TC) in alloxan-induced diabetic mice were significantly decreased after daily oral administration of Trans-Tiliroside in normal and diabetic mice at doses of 0.4, 0.8 and 1.6 mg/kg/day, for 15 days. Blood glucose level was significant decreased in STZ induced diabetic rats by Trans-Tiliroside (1.2 and 0.3 mg/kg body weight for 10 weeks). The content of TC, low density lipoprotein (LDL–C) and TG levels were decreased while high density lipoprotein (HDL–C) content was increased, so lipid metabolism was improved. Moreover, Trans-Tiliroside revealed antioxidant activity as shown by increased activities of superoxide dismutase (SOD), decreased level of malondialdehyde (MDA) in diabetic rats. Histological morphology examination showed that the Trans-Tiliroside restored the damage of pancreas tissues in rats with diabetes mellitus. In conclusion, the hypothesis was proven that Trans-Tiliroside isolated from Potentilla chinensis does have anti-hyperglycemic, anti-hyperlipidemic and antioxidant effects.
Carnosic acid is an organic chemical compound that is naturally found in rosemary and sage. The carnosic acid component of rosemary extracts are believed to be the cause of body weight, energy metabolism and inflammation regulatory properties in animal models. Carnosic acid also acts as a ppar-γ antagonist, thus inhibiting fat gain. In addition, it can stimulate glucose uptake in skeletal muscle which provides further impetus to supplement with ASSASS1NATE with meals.
A study was performed to test the hypothesis that Carnosic acid (CA) acts to mimic the metabolic actions of insulin by directly stimulating glucose uptake in rat skeletal L6 myotubes, concomitant with increased translocation of the GLUT4 glucose transporter to the plasma membrane. Mechanistically, CA-induced glucose transport was found to be dependent on protein kinase B (PKB/Akt) but not AMPK, despite both kinases being activated by CA. Crucially, in accordance with its ability to activate PKB and stimulate glucose uptake, we show that CA conveys these effects through a pathway involving PME-1 (protein phosphatase methylesterase-1), a key negative regulator of the serine/threonine phosphatase PP2A (protein phosphatase 2A). CA was found to promote PME-1 mediated demethylation of the PP2A catalytic subunit leading to its suppressed activity, and in doing so, alleviates the repressive action of PP2A towards PKB. Collectively, our findings provide new insight into how CA may improve glucose homeostasis through enhancing peripheral glucose clearance in tissues such as skeletal muscle through a PME-1/PP2A/PKB signalling axis, thereby mitigating pathological effects associated with the hyperglycaemic state.
3T3-L1 pre-adipocytes were treated with Carnosic acid (CA) (0.1, 1, and 10 μM per day) for 8 days. Oil Red O staining results, triglyceride (TG) accumulation, and glycerol 3-phosphate dehydrogenase activity suggested that CA significantly inhibited lipid accumulation in 3T3-L1 adipocytes. CA significantly decreased mRNA expression of peroxisome proliferator-activated receptor-γ, sterol regulatory element-binding protein 1, and CCAAT/enhancer binding protein-α in a dose-dependent manner. Moreover, it decreased the ratio of both C16:1/C16:0 and C18:1/C18:0, with reduced expression of stearoyl CoA desaturase 1 mRNA and protein. These results suggest that CA efficiently mitigated fat gain in 3T3-L1 adipocytes and its action, at least in part, is associated with the downregulation of adipogenesis-related genes and the fatty acid composition of TG accumulated in adipocytes.
Potent Fat Inhibition & Cannabinoid (CB1) Receptor Modulation:
The Potent Fat Inhibition & Cannabinoid (CB1) Receptor Modulation blend utilizes a custom 150mg Olive Leaf Extract, 25mg Lutein and 300mg Orthosiphon Stamineus to target several novel fat burning pathways. It works synergistically with the Metabolism Stimulation & Extreme Thermogenic Activation blend to further rev up your metabolism. That goal is met by targeting several different pathways including PPAR-α, PPARγ and CPT1 we will explore in greater detail.
The Orthosiphon Stamineus in the blend has been found to increase leptin. Leptin is a hormone that regulates how your body utilizes stored energy. It directly burns fat by preventing the storage of fat and reducing appetite. There is another pathway as well that we were very excited to include in ASSASS1NATE. The custom Olive Leaf Extract has been shown to inhibit the Cannabinoid 1 (CB1) receptor, a novel pathway that improves lipid metabolism and regulates glucose levels.
Olive leaf extract
Olive leaf has been widely used in in the European and Mediterranean countries in the human diet as an extract in herbal tea and in powder form for medicinal purposes. It has several health benefits validated by research, including the prevention of hypertension, atherosclerosis, cancer, diabetes and cardiovascular diseases. Olive leaves are comprised of multiple compounds known as olive biophenols; with oleuropein at the largest proportion, followed by verbascoside, luteolin, rutin, catechin, and hydroxytyrosol in lower quantities. These biophenols largely influence the aforementioned therapeutic properties and have also been found to have fat loss benefits. However, let’s focus on the two components that are most abundant in ASSASS1NATE, oleuropein and hydroxytyrosol.
Oleuropein has also been found to exert anti-adipogenic effects through direct inhibition of PPARγ. Furthermore, it has been shown to enhance thermogenesis by increasing the uncoupling protein 1 (UCP1) in Inducible Brown Adipose Tissue (IBAT) and urinary noradrenaline and adrenaline secretions.
The antiobesity effect of oleuropein was investigated in mice that were fed with a normal diet, HFD-40% fat of total energy) and HFD-supplemented with 0.03% oleuropein for 10 weeks. Oleuropein significantly reduced HFD-induced body weight gain and visceral adiposity. Oleuropein also significantly reversed the HFD-induced elevations of adipogenic related gene expression involved in WNT10b- and galanin-mediated signalings in adipose tissue of mice. Consistent with the in vivo findings, oleuropein dose-dependently suppressed lipid accumulation in 3T3-L1 cells during preadipocyte differentiation. Additionally, exposure of the 3T3-L1 preadipocytes to oleuropein resulted in a marked attenuation of the secreted frizzled-related protein 2 (WNT inhibitor) or galanin (galanin receptor agonist) induced cellular lipid accumulation. These results suggest that oleuropein has a protective effect against HFD-induced adiposity in mice and can reduce body weight gain and visceral adiposity.
ASSASS1NATE contains an olive leaf extract with a relatively high percentage of Hydroxytyrosol (20%) because recent research has found it can inhibit the Cannabinoid 1 (CB1) receptor. CB1 is a G-protein coupled receptor primarily located in the central and peripheral nervous system. Activation of the CB1 receptor inhibits the production of cyclic adenosine monophosphate (cAMP) which regulates glycogen, glucose and lipid metabolism. Therefore, supplementation with Hydroxytyrosol will stimulate metabolism and prevent adipogenesis.
A research study was conducted to evaluate the effect of n-3-PUFA, α-Linolenic acid (OM-3), n-6-PUFA, Linoleic acid (OM-6), and hydroxytyrosol (HT) in cultured 3T3-L1 pre-adipocytes on the expression of CB1 receptor gene and the adipogenesis-related genes PPAR-γ, Fatty Acid Synthase (FAS) and Lipoprotein Lipase (LPL). The 3T3-L1 preadipocyte cell line was chosen for its ability to synthesize and degrade endocannabinoid anandamide (AEA) and their differentiation into adipocytes which increases the expression of cannabinoid (CB1) and PPAR-γ receptors. HT was able to inhibit 3T3-L1 cell differentiation by down-regulating cell proliferation and CB1 receptor gene expression. HT exhibited anti-adipogenic effects, whereas OM-3 and OM-6 exerted an inhibitory action on cell proliferation associated with an induction of the preadipocytes differentiation and CB1 receptor gene expression. Moreover, the expression of FAS and LPL genes resulted increased after treatment with both HT and OM-3 and OM-6. These findings suggest that the consumption of HT can elicit anti-obesity and anti-neoplastic properties by acting directly on the adipose tissue and modulating CB1 receptor gene transcription.
Orthosiphon Stamineus also known as Java or Cat’s Whiskers is a plant whose leaves make a tea typically used for medicinal purposes. It has been found to reduce appetite and visceral fat mass. In addition, Orthosiphon stamineus contains a significant amount of rosmarinic acid and methylated flavonoids. The flavonoids in Orthosiphon stamineus have been found to increase leptin, a hormone in fat cells that regulates appetite. Sufficient levels of leptin signals to your brain that you have adequate amounts of stored energy in your fat cells that can be utilized for metabolic processes. However, when you reduce your food intake for extended periods, particularly when dieting, leptin levels start to decrease and can reach a resistant state where your brain does not receive a signal you have energy to burn. Therefore, the combined effect of reduced appetite and increased leptin from Orthosiphon stamineus is exactly what you want to ASSASS1NATE fat.
A study was completed to assess whether Orthosiphon stamineus (OS) can reduce appetite and fat deposition, food intake and visceral fat mass in Sprague-Dawley (SD) rats. The supplementation group was treated with OS (oral) for 2 weeks and compared to a control (saline-treated rats). Two weeks of OS treatment reduced food intake and visceral fat mass compared to saline-treated SD rats. In addition, OS treatment elevated the expression of proopiomelanocortin (POMC) in the hypothalamus, whereas neuropeptide Y (NPY) expression was decreased, which may be associated with the elevation of plasma leptin concentration in the OS treated rats. Methanol and butanol extracts of OS increased leptin mRNA expression in 3T3-L1 cells in dose-dependent manner. The study concluded that OS can reduce appetite as a result of the increased expression of POMC and decreased expression of NPY in the hypothalamus in association with the elevation of leptin. This mechanism was specifically targeted by the methanol and butanol extracts of OS, hence the reason why ASSASS1NATE contains a 70% ethanolic extract.
Lutein is a carotenoid pigment that is found in high quantities in spinach and kale and also in the milk of grazing cows. Lutein is best known for its ability to mitigate the risk of macular degeneration, the loss of central vision typically associated with old age. It also possesses strong anti-oxidative properties and has suppressive effects on carcinogenesis and can improve physical activity levels. Most interestingly, lutein has been found to increase carnitine palmitoyltransferase 1 (CPT-1) thus stimulating energy metabolism. CPT-1 is an enzyme responsible for the formation of acylcarnitines by catalyzing the transfer of the acyl group of a long-chain fatty acyl-CoA from coenzyme A to l-carnitine. Since carnitine is known to have lipolytic properties it fits perfectly with the objective of ASSASS1NATE.
In order to validate previous studies that showed a positive relationship between serum lutein concentrations and higher physical activity levels a randomized, placebo-controlled study was performed. Forty-four older adults (BMI, 25.3 ± 2.6 kg/m2; age, 68.8 ± 6.4 year) that did not meet Australian physical activity guidelines (150 min/week of moderate to vigorous activity) were randomized and given 21mg capsules containing lutein or placebo with 250 mL of full-cream milk per day for 4 weeks and encouraged to increase physical activity. Thirty-nine participants completed the study (Lutein = 19, Placebo = 20). Lutein increased plasma lutein concentrations compared with placebo (p < 0.001). Absolute and percentage changes in plasma lutein were inversely associated with absolute (r = −0.36, p = 0.03) and percentage changes (r = −0.39, p = 0.02) in sedentary time. Percentage change in plasma lutein was positively associated with the percentage change in average daily activity counts (r = 0.36, p = 0.03). Exercise self-efficacy did not change (p = 0.16). Lutein increased plasma lutein, which was associated with increased physical activity and reduced sedentary time in older adults.
To evaluate the effects of lutein-fortified milk administration on running exercise, a voluntary wheel-running model was performed in rats. Four-week-old F344 rats were administered test milk (10 mL/kg) daily following a 4-h fasting period, and their running distances were measured each day for a 9-week period. Total weekly running distance significantly increased from the sixth week until the end of the test period in lutein-supplemented rats (lutein-fortified milk administered) compared with control rats (vehicle administered). This increase was not apparent in rats administered lutein alone. In the lutein-fortified-milk exercise group compared with the sedentary control group, carnitine palitroyltransferase 1 (CPT-1), total AMP-activated protein kinase (tAMPK), and phosphorylated AMP-activated protein kinase (pAMPK) contents were significantly increased in the gastrocnemius muscle, with a concomitant decrease in triglyceride and total cholesterol levels in the blood and liver. Furthermore, the lutein level in blood of lutein-administered rats significantly decreased with exercise. These results suggest that lutein-fortified milk may enhance the effect of exercise by effective utilization of lipids when combined with voluntary running.
Oleoylethanolamide (OEA) is a lipid that is naturally occurring in the intestines of the human body that regulates appetite. When you eat, OEA levels increase and ultimately produces a feeling of satiety. However, when your caloric intake is reduced, especially when dieting, your OEA levels may not reach the levels necessary to satisfy your appetite. Olympus Labs has you covered with an additional 200mg of OEA to mitigate excessive eating. In addition, since OEA has been identified as an endogenous agonist of peroxisome proliferator activated receptor alpha (PPAR-α) it will influence the brain to reduce food intake as well as stimulate lipolysis. It also enhances thermogenesis in both white adipose tissue (WAT) and brown adipose tissue (BAT), at the same dose used to suppress appetite.
A study was conducted to determine if there is an association between plasma oleoylethanolamide levels and body mass index (BMI). 21 obese patients, with a BMI above 30, and 24 non-obese individuals utilized as a control participated. The mean age of participants was 40.8 years and BMIs ranged from 18.2 to 47.5. In obese individuals, oleoylethanolamide showed a trend toward a positive correlation with BMI (P = .06, ρ = 0.42), while this relationship was inverse for nonobese control participants (P = .07, ρ = -0.34). Similarly, significant interactions were found between oleoylethanolamide levels and obesity on food-related brain activation in cortical areas associated with reward processing and interoceptive signaling (P = .009). Specifically, nonobese individuals with higher oleoylethanolamide levels had higher insular brain activity (P < .001, ρ = 0.70); again, the relationship trended to be inverse for obese patients (P = .11, ρ = -0.36). These effects were not associated with plasma levels of leptin and anandamide, suggesting an independent role of oleoylethanolamide in hunger-associated interoceptive signaling. Analysis of food craving during the functional magnetic resonance imaging task suggested that the identified brain areas may be involved in suppressing food-liking reactions in nonobese individuals. These findings suggest that oleoylethanolamide-mediated signaling plays an important role for hedonic regulation of food craving and obesity in humans.
The effect of Oleoylethanolamide (OEA) on intestinal fatty acid uptake and FAT/CD36 expression was investigated in vivo and in vitro. OEA was intraperitoneally administered to rats and examined FAT/CD36 mRNA level and fatty acid uptake in enterocytes isolated from the proximal small intestine, as well as in adipocytes. Our results indicate that OEA treatment significantly increased FAT/CD36 mRNA expression in intestinal mucosa and isolated jejunal enterocytes. In addition, we also found that OEA treatment significantly increases fatty acid uptake in isolated enterocytes in vitro. These results suggest that in addition to appetite regulation, OEA may regulate body weight by altered peripheral lipid metabolism, including increased lipolysis in adipocytes and enhanced fatty acid uptake.
Let’s recap the data that was presented above; ASSASS1NATE will reduce appetite, inhibit fat storage, increase glucose uptake and stimulate your metabolism. All those benefits without any stimulants. You may be wondering, if ASSASS1NATE will be so effective why does nearly every fat burner contain high amounts of stimulants? The reason is cost; stimulants are typically inexpensive, especially caffeine and most supplement companies will not spend the time and money to source truly effective fat burning ingredients at proper doses. Fortunately, at Olympus Labs we prioritize R&D over marketing, hence our exceptional formulations.
ASSASS1NATE employs innovation to elicit results befitting a DemiGod or DemiGoddessess. It targets a myriad of different fat burning pathways including AMPK, PPAR-α, PPARγ as well as more novel pathways; irisin, leptin, PGC-1α, PME-1/PP2A/PKB, CPT-1, UCP1 and CB1. All in one product? Yes, that’s correct, Olympus Labs does it B1G or not at all!
We adhere to the following three pillars in every supplement we produce; Innovation, Value and Results. ASSASS1NATE is no exception, in fact it is on the leading edge of sports supplementation which you will hardpressed to observe from the competition.
Most importantly, ASSASS1NATE will deliver the results you have been hoping to achieve. It will recalibrate the way you think about fat burning. An effective stimulant free fat burner and GDA in one. The supplement that was inconceivable but now a reality. In addition, ASSASS1NATE can be stacked with IGNIT3 or BLOODSHR3D for a explosive fat incineration combination.
CONQU3R the dread of dieting and attack fat by stealth with ASSASS1NATE
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