The lipolytic herbal extract forskolin inhibits fat tissue inflammation, may help fight obesity and overweight complications

Forskolin, lipolysis, fat tissue inflammation and circulation

In a study published last week it was shown that forskolin, one of the most important lipolytic natural chemicals, also inhibits fat tissue inflammation, making it a valuable anti-obesity and anti-cellulite natural agent.

Fat tissue inflammation is the major cause of obesity's adverse health complications, so fighting fat tissue inflammation is an important step in restoring health in obese and overweight individuals.


One of the most important leg wellness actives

Previous studies have also shown that, in addition to its widely recognised slimming properties, and the newly discovered anti-inflammatory action, forskolin also boosts local circulation, thereby  helping maintain leg wellness and fight cellulite in three fronts: fat tissue inflammation, fat reduction  and circulation enhancement.

Forskolin works best topically and in combination with caffeine, raspberry ketone and other natural phytochemicals as actives in a high concentration leg wellness cream formulation.



  • Paper: Forskolin Inhibits Lipopolysaccharide-Induced Modulation of MCP-1 and GPR120 in 3T3-L1 Adipocytes through an Inhibition of NFκB.
  • Abstract: In an obese state, Toll-like receptor-4 (TLR-4) upregulates proinflammatory adipokines secretion including monocyte chemotactic protein-1 (MCP-1) in adipose tissue. In contrast, G-protein coupled receptor 120 (GPR120) mediates antiobesity effects. The aim of this study was to determine the signaling pathway by which Forskolin (FK), a cyclic adenosine monophosphate- (cAMP-) promoting agent causing positive changes in body composition in overweight and obese adult men, affects MCP-1 and GPR120 expression during an inflammatory response induced by lipopolysaccharide (LPS) in adipocytes, such as in an obese state. 3T3-L1 cells differentiated into adipocytes (DC) were stimulated with LPS in the absence or presence of FK and inhibitors of TLR-4 and inhibitor of kappa B (IκBα). In DC, LPS increased MCP-1, TLR-4, and nuclear factor-κB1 (NFκB1) mRNA levels, whereas it decreased GPR120 mRNA levels. In DC, FK inhibited the LPS-induced increase in MCP-1, TLR-4, and NFκB1 mRNA levels and the LPS-induced decrease in GPR120 mRNA. BAY11-7082 and CLI-095 abolished these LPS-induced effects. In conclusion, FK inhibits LPS-induced increase in MCP-1 mRNA levels and decrease in GPR120 mRNA levels in adipocytes and may be a potential treatment for inflammation in obesity. Furthermore, TLR-4-induced activation of NFκB may be involved in the LPS-induced regulation of these genes.
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