加拿大渥太華大學科學家使用肌肉干細胞，在實驗室老鼠身上制造出可以燃燒卡路里的棕色脂肪，有助于治療加拿大人日漸普遍的肥胖癥。
據介紹，棕色脂肪是哺乳類動物身體制造的兩種脂肪之一。棕色脂肪與白色脂肪相比，屬于好脂肪，因為它屬于發熱組織，能夠燃燒掉存在白色脂肪中的卡路里。棕色脂肪多在新生嬰兒及冬眠動物體內發現。
渥太華大學附屬機構、渥太華醫院研究所科學家使用成年老鼠的肌肉干細胞制成復合物，然后將復合物注射入實驗室老鼠體內，導致實驗老鼠產生棕色脂肪，體重迅速下降。
渥太華醫院研究所再生醫學計劃暨Sprott干細胞研究中心主任魯德尼基(Michael Rudnicki)表示，令人驚訝的是，在經過4個月觀察后，經注射復合物的實驗老鼠，體重持續減輕。
魯德尼基指出，此一發現使得科學家們未來能夠再進一步利用這種好脂肪，治療所有與肥胖有關的病癥。
根據加拿大公共衛生署的資料，迄至2007年，每4個加拿大人中就有1人屬于肥胖，且有很高比率的人是超重。同一年，加拿大人民的肥胖情形被世界衛生組織列為全球第35，在超過15歲的加拿大人中，61.1%體重超重。
渥太華大學科學家的上述報告刊載于《細胞代謝》(Cell Metabolism)期刊，但使用這種新方法治療肥胖癥，可能還需要相當一段時間。
MicroRNA-133 Controls Brown Adipose Determination in Skeletal Muscle Satellite Cells by Targeting Prdm16
Summary
Brown adipose tissue (BAT) is an energy-dispensing thermogenic tissue
that plays an important role in balancing energy metabolism.
Lineage-tracing experiments indicate that brown adipocytes are derived
from myogenic progenitors during embryonic development. However, adult
skeletal muscle stem cells (satellite cells) have long been considered
uniformly determined toward the myogenic lineage. Here, we report that
adult satellite cells give rise to brown adipocytes and that
microRNA-133 regulates the choice between myogenic and brown adipose
determination by targeting the 3′UTR of Prdm16. Antagonism of
microRNA-133 during muscle regeneration increases uncoupled respiration,
glucose uptake, and thermogenesis in local treated muscle and augments
whole-body energy expenditure, improves glucose tolerance, and impedes
the development of diet-induced obesity. Finally, we demonstrate that
miR-133 levels are downregulated in mice exposed to cold, resulting in
de novo generation of satellite cell-derived brown adipocytes.
Therefore, microRNA-133 represents an important therapeutic target for
the treatment of obesity.