Sea Anemone Venom Offers Promise in Fight against Obesity

Natali Anderson - sci-news.com - 06/04/2013
Weight Loss Theories

If all of these are true, then we can expect to see miracle pill within 10 years.

However, the study did not explain where the energy went. Calorie-burning brown fat? Did it mean the body temperature of the mice was higher than usual?

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The study says that the compound called ShK-186 selectively blocks the activity of a protein that promotes inflammation through the Kv1.3 potassium channel, and presents the first evidence that the drug candidate may also work in an anti-obesity capacity.

Potassium channels regulate cell membrane potential and control a variety of cellular processes. Earlier studies using mice that lack Kv1.3, a potassium channel gene, suggested that Kv1.3 regulated body weight and the basal metabolic rate.

In the new study, Prof George Chandy from the University of California Irvine and his colleagues evaluated ShK-186 because it has high selectivity for the Kv1.3 target, a favorable pharmacokinetic profile, and meets the qualities of an industry-standard drug.

In tests on obese mice that ate a high-fat, high-sugar diet, ShK-186 therapy reduced weight gain, white fat deposits, fatty liver, blood cholesterol and blood sugar by activating calorie-burning brown fat, suppressing inflammation of white fat and augmenting liver function.

The compound had no effect on mice that ate a standard chow diet, suggesting that the obesity-causing diet triggers the expression of the Kv1.3 target.

“This is a new twist in a sustained journey of discovery made over the 30 years that charts the course for expeditious translation to humans who suffer from potentially lethal consequences of metabolic syndrome and autoimmune diseases,” Prof Chandy said.

“We evaluated ShK-186 in an obesity model because it has high selectivity for the Kv1.3 target, a favorable pharmacokinetic profile, and meets the qualities of an industry-standard drug.”

Prof Gary Desir of Yale University, who was not involved in the current study, explained: “these data are quite exciting and strongly support the notion that inhibition of the Kv1.3 channel provides a highly effective method for managing obesity and its associated metabolic abnormalities.”

“The results obtained with ShK-186 are consistent with what one would expect to see with a potent inhibitor of this channel. While additional studies are needed, the potential clinical relevance of this work is enormous, since a significant number of people are afflicted with obesity and its associated complications, and no Kv1.3 inhibitor, as a drug candidate for obesity, has reached the clinic until now.”

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