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　　發(fā)表在2014年1月的FASEB Journal雜志上的一項最新研究中，科學(xué)家證實(shí)隨著(zhù)年齡的增長(cháng)，棕色脂肪的產(chǎn)熱活動(dòng)減少。

　　棕色脂肪是“好”脂肪，坐落在我們的脖子的背部，幫助燃燒“壞的”白色脂肪。此外，研究人員還發(fā)現了一個(gè)可能的代謝開(kāi)關(guān)，可以重新激活棕色脂肪。

　　Junko Sugatanii博士表示：研究是關(guān)于PAF / PAFR如何通過(guò)調控動(dòng)物以及人類(lèi)的棕色脂肪中β3 -AR生成信號控制UCP1的水平，研究可發(fā)現新的治療靶點(diǎn)來(lái)治療與肥胖癥相關(guān)的代謝紊亂。

　　為了獲得這一發(fā)現，科學(xué)家分析了兩組小鼠。第一組血小板活化因子受體（PAFR）基因敲除小鼠。第二組是正常小鼠。與野生型同窩小鼠相比，PAFR缺陷的小鼠隨著(zhù)年齡增長(cháng)發(fā)展了更嚴重的肥胖狀態(tài)，具有更高的身體和附睪脂肪量。

　　從PAFR基因敲除小鼠模型結果顯示，PAFR缺乏會(huì )導致褐色脂肪組織（BAT）功能障礙，從而誘發(fā)肥胖的發(fā)展，由于BAT產(chǎn)熱作用受損。該研究闡明了PAF/PAF受體介導抗肥胖相關(guān)的分子機制，將有助發(fā)現肥胖癥和相關(guān)病癥如糖尿病，高血壓，心臟疾病，癌癥，不育和潰瘍等治療的新靶標。

　　原文閱讀：

　　Abstract

　　Platelet-activating factor receptor (PAFR)-deficient mice developed a more severe obese state characterized by higher body mass (?25%) and epididymal fat mass (?55%) with age than that of wild-type (WT) littermates. PAFR-deficient mice did not show changes in the expression of critical genes involved in anabolic and catabolic metabolism in adipose, liver, and muscle tissues between 6 and 36 wk. However, a 38?81% reduction in β3/β1-adrenergic receptor (AR) and uncoupling protein 1 (UCP1) mRNA and protein levels was observed in the interscapular brown adipose tissue (BAT) of PAFR-deficient mice. Whereas a single injection of the β3-adrenergic agonist, CL-316,243 (25 μg/kg) increased temperatures in the brown fat and rectums of WT mice, this increase in temperature was markedly suppressed in PAFR-deficient mice. Acetyl-CoA:lyso-platelet-activating factor (PAF) acetyltransferase, which is involved in PAF biosynthesis, and the PAF receptor were predominantly localized in BAT macrophages, whereas brown adipocytes possessed the enzyme and functional PAF receptors. The stimulation of brown adipocytes by PAF induced the expression of β3-AR mRNA and protein (1.5- and 1.9-fold, respectively), but not that of UCP1. These results indicate that obesity in PAFR-deficient mice resulted from impaired BAT activity and suggest that the antiobese function of PAF occurs through β3-AR/UCP1 expression in BAT.