Sunday, June 10, 2012

Pungent Ingredient, piperine, in Black Pepper Targets Fat Cells

A preliminary new study suggests that the pungent component in black pepper known as piperine fights fat by blocking the formation of new fat cells.
If further studies confirm these effects, researchers say black pepper may offer a natural alternative for the treatment of fat-related disorders like obesity.

"Our findings suggest that piperine (see above structure), a major component of black pepper, inhibits fat cell differentiation ... thus leading to its potential use in the treatment of obesity-related diseases," writes researcher Ui-Hyun Park of Sejong University in Seoul, Korea 
Black Pepper the Fat Fighter....

Researchers say the benefits of black pepper and the black pepper plant have been known for centuries in traditional Eastern medicine, in which it is used to treat cholera, diarrhea, and other gastrointestinal issues.

In their study, researchers looked at the effects of piperine on gene expression in fat tissue in the lab and in computer models.

The results showed that piperine interfered with the activity of genes responsible for forming new fat cells.

Researchers say this benefit of black pepper sets up a chain reaction that helps keep the formation of fat in check in other ways as well.
"Overall, our results suggest that piperine could be a lead natural compound for the treatment of fat-related disorders," the researchers write.


This study investigated the antiadipogenic activity of black pepper extract and its constituent piperine in 3T3-L1 preadipocytes as well as the underlying molecular mechanisms. Both black pepper extract and piperine, without affecting cytotoxicity, strongly inhibited the adipocyte differentiation of 3T3-L1 cells. The mRNA expression of the master adipogenic transcription factors, PPARγ, SREBP-1c, and C/EBPβ, was markedly decreased. Intriguingly, mRNA levels of PPARγ target genes were also down-regulated. Moreover, a luciferase reporter assay indicated that pipierine significantly represses the rosiglitazone-induced PPARγ transcriptional activity. Finally, GST-pull down assays demonstrated that piperine disrupts the rosiglitazone-dependent interaction between PPARγ and coactivator CBP.  





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