Peptide
Glycyrrhetinic Acid & Aminophylline Transdermal Fat Loss Cream

 

Glycyrrhetinic Acid & Aminophylline Transdermal Fat Loss Cream

Aminophylline and glycyrrhetinic acid transdermal cream are used for fat loss. Aminophylline and glycyrrhetinic prevent cAMP breakdown. Cyclic AMP (cAMP) functions in several biochemical processes including the regulation of glycogen, sugar, and lipid metabolism. cAMP works by activating protein kinase A (PKA) which assists in glycogen, sugar, and lipid metabolism. Aminophylline has displayed topical fat reduction from the waist. In a study examining aminophylline cream application, the reduction in waist circumference was significant for both men and women. Over a period of 12 weeks, participants in the study lost 11cm in waist circumference. In differentiated adipocytes, 18β-glycyrrhetinic acid increases the level of glycerol release and up-regulates the mRNA of hormone-sensitive lipase, adipose triglyceride lipase, and perilipin, as well as the phosphorylation of hormone-sensitive lipase. 18 β- glycyrrhetinic acid alters fat mass by directly affecting adipogenesis in maturing preadipocytes and lipolysis in mature adipocytes. Therefore, aminophylline and 18β- glycyrrhetinic acid may be useful for treating obesity. Both aminophylline and glycyrrhetinic acid combined effectively combat fat loss. Aminophylline and glycyrrhetinic acid fat loss cream yield the best results through topical application.

CLINICAL RESEARCH:

18β-Glycyrrhetinic acid inhibits adipogenic differentiation and stimulates lipolysis 18β-Glycyrrhetinic acid (18β-GA) obtained from the herb licorice has various pharmacological properties including anti-inflammatory and antibacterial activities. However, potential biological anti-obesity activities are unclear. In this study, novel biological activities of 18β-GA in the adipogenesis of 3T3-L1 preadipocytes and in lipolysis of differentiated adipocytes were identified. Mouse 3T3-L1 cells were used as an in vitro model of adipogenesis and lipolysis, using a mixture of insulin/dexamethsone/3- isobutyl-1-methylxanthine (IBMX) to induce differentiation. The amount of lipid droplet accumulation was determined by an AdipoRed assay. The expression of several adipogenic transcription factors and enzymes was investigated using real-time reverse transcriptase- polymerase chain reaction (RT-PCR) and Western blotting. 18β-GA dose-dependently (1–40 lM) significantly decreased lipid accumulation in maturing preadipocytes. In 3T3-L1 preadipocytes, 10 lM of 18β-GA down-regulated the transcriptional levels of peroxisome proliferator-activated receptor c, CCAAT/enhancer-binding protein and adiponectin, which are markers of adipogenic differentiation via Akt phosphorylation. Also, in differentiated adipocytes, 18β-GA increased the level of glycerol release and up-regulated the mRNA of hormone-sensitive lipase, adipose TG lipase, and perilipin, as well as the phosphorylation of hormone-sensitive lipase at Serine 563. The results indicate that 18β-GA alters fat mass by directly affecting adipogenesis in maturing preadipocytes and lipolysis in matured adipocytes. Thus, 18β-GA may be useful for the treatment of obesity.

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