Re-posting the main body of the original write-up for those interested...
ASSASS1NATE
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, 300mg Orthosiphon Stamineus Extract and and 200mg of Oleoylethanolamide (OEA) that targets 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
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.