안 먹어도 먹은 느낌을 주는 '살 빼는 약' 개발 "Imaginary meal" tricks the body into losing weight(VIDEO)
Ronald Evans, director of Salk’s Gene Expression Laboratory, has developed a compound called
fexaramine that acts like an imaginary meal. Fexaramine, which tricks the body into reacting as if
it has consumed calories, could lead to an effective obesity and diabetes treatment in humans. .
Image: Courtesy of the Salk Institute for Biological Studies
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재미 한국 과학자들이 참여한 미국 소크연구소(Salk Institute) 연구진이 복용하면 음식을 먹은 것처럼 느끼도록 몸을 속여 신진대사가 활발해지게 하는 '살 빼는 약'을 개발했다. 펙사라민은 최근 세계 주요 제약사들이 살 빼는 약을 개발하는 데 표적으로 삼고 있는 '파렌소이드 X 수용체'(FXR)에 작용하는 물질이다. FXR은 음식을 먹을 때 활성화돼 담즙산 분비와 지방 연소를 유도하는 등 몸에 저장된 에너지를 소비, 새로 음식을 받아들일 준비를 하게 한다. 즉 음식을 먹지 않은 상태에서 이 물질을 활성화하면 지방연소 등으로 체중을 줄일 수 있게 된다. 그러나 지금까지 FXR을 표적으로 개발된 살 빼는 약들은 복용 후 핏속에 흡수되면서 장뿐만 아니라 간과 신장, 부신 등에 영향을 미치고 부작용을 일으키는 문제가있었다. 연구진이 펙사라민은 혈류에 흡수되지 않고 장에서만 작용한다고 밝혔다. 연구진이 이 약을 실험용 비만 생쥐에 5주간 투여한 결과, 체중 증가가 멈추고 지방이 감소했으며 혈당과 콜레스테롤 수치도 떨어진 것으로 확인됐다. 연구진은 또 펙사라민을 투여한 생쥐는 체온이 상승해 신진대사가 활발해지고 백색 지방이 건강에 좋은 갈색 지방으로 전환됐다고 설명했다. 에번스 박사는 "이 약은 상상 음식과 같다"며 "(음식을 먹지 않은 상태에서도) 사람들이 보통 음식을 많이 먹었을 때와 똑같은 신호를 보내 몸이 새로 섭취할 음식을 받아들일 준비, 즉 몸을 비우는 기능을 한다"고 설명했다. 연구진은 펙사라민이 혈류에 도달하지 않기 때문에 FXR을 표적으로 한 다른 약들보다 안전할 것으로 보고 있다며 비만과 대사질환에 대한 효과를 시험하기 위한 사람 대상의 임상시험을 준비 중이라고 밝혔다. 연합뉴스 |
Salk scientists made a more effective diet pill
LA JOLLA–Salk researchers have developed an entirely new type of pill that tricks the body into thinking it has consumed calories, causing it to burn fat. The compound effectively stopped weight gain, lowered cholesterol, controlled blood sugar and minimized inflammation in mice, making it an excellent candidate for a rapid transition into human clinical trials. Unlike most diet pills on the market, this new pill, called fexaramine, doesn’t dissolve into the blood like appetite suppressants or caffeine-based diet drugs, but remains in the intestines, causing fewer side effects. “This pill is like an imaginary meal,” says Ronald Evans, director of Salk’s Gene Expression Laboratory and senior author of the new paper, published January 5, 2014 in Nature Medicine. “It sends out the same signals that normally happen when you eat a lot of food, so the body starts clearing out space to store it. But there are no calories and no change in appetite.” In the United States, more than a third of adults are obese and 29.1 million people have diabetes, according to the Centers for Disease Control and Prevention. Both obesity and diabetes lead to an increase in health spending, a greater risk of health complications and a shorter lifespan. Pharmaceutical companies aiming to treat obesity, diabetes, liver disease and other metabolic conditions have developed systemic drugs that activate FXR, turning on many pathways that FXR controls. But these drugs affect several organs and come with side effects. Evans wondered whether switching on FXR only in the intestines–rather than the intestines, liver, kidneys and adrenal glands all at once–might have a different outcome “When you eat, you have to quickly activate a series of responses all throughout the body,” says Evans. “And the reality is that the very first responder for all this is the intestine.” Evans and his colleagues developed the fexaramine compound by departing from the drug scaffold that most pharmaceutical companies typically pursue when targeting FXR. “It turns out that when we administer this orally, it only acts in the gut,” explains Michael Downes, a senior staff scientist at Salk and co-corresponding author of the new work. Giving one such drug in a daily pill form that only reaches the intestines–without transporting into the bloodstream that would carry the drug throughout the body–not only curtails side effects but also made the compound better at stopping weight gain. From left: Salk researchers Ruth Yu, Sungsoon Fang, Annette Atkins, Ronald Evans, Michael Downes and Sandra Jacinto Click here for a high-resolution image. Image: Courtesy of the Salk Institute for Biological Studies So, why does fexaramine in the intestines work even better than drugs that simultaneously activate FXR throughout the body? Evans thinks it has to do with the natural order in which the body’s molecular pathways normally responds to a meal. “The body’s response to a meal is like a relay race, and if you tell all the runners to go at the same time, you’ll never pass the baton,” says Evans. “We’ve learned how to trigger the first runner so that the rest of the events happen in a natural order.” http://www.salk.edu/news/pressrelease_details.php?press_id=2068
Evans’ laboratory has spent nearly two decades studying the farensoid X receptor (FXR), a protein that plays a role in how the body releases bile acids from the liver, digests food and stores fats and sugars. The human body turns on FXR at the beginning of a meal, Evans and others have shown, to prepare for an influx of food. FXR not only triggers the release of bile acids for digestion, but also changes blood sugar levels and causes the body to burn some fats in preparation for the incoming meal. 
When the group gave obese mice a daily pill of fexaramine for five weeks, the mice stopped gaining weight, lost fat and had lower blood sugar and cholesterol levels than untreated mice. In addition, the mice had a rise in body temperature–which signals metabolism ramping up–and some deposits of white fat in their bodies converted into a healthier, energy-burning beige form of the tissue. Even the collection of bacteria in the guts of mice shifted when they received the drug, although what those changes mean isn’t clear yet.
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