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氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell

更新時間:2024-09-28   點擊次數(shù):492次

中文摘要:

米色脂肪在調(diào)節(jié)全身能量穩(wěn)態(tài)中起關(guān)鍵作用;然而,其激活的詳細(xì)機制和安全策略仍然難以捉摸。在這項研究中,我們發(fā)現(xiàn)針對米色脂肪的局部熱療療法 (LHT) 促進了其在人類和小鼠中的激活。使用基于水凝膠的光熱療法實現(xiàn) LHT,激活米色脂肪,預(yù)防和治療小鼠肥胖,無不良反應(yīng)。HSF1 是效果所必需的,因為 HSF1 缺陷減弱了 LHT 的代謝益處。HSF1 調(diào)節(jié) Hnrnpa2b1 (A2b1) 轉(zhuǎn)錄,導(dǎo)致關(guān)鍵代謝基因的 mRNA 穩(wěn)定性增加。重要的是,對人類關(guān)聯(lián)研究的分析以及隨后的功能分析表明,HSF1 功能獲得性變體 p.P365T 與人類代謝性能的改善以及小鼠和細(xì)胞中 A2b1 轉(zhuǎn)錄的增加有關(guān)??傮w而言,我們證明 LHT 通過 HSF1-A2B1 轉(zhuǎn)錄軸誘導(dǎo)米色脂肪激活,提供了一種有前途的對抗肥胖的策略。

英文摘要:

Beige fat plays key roles in the regulation of systemic energy homeostasis; however, detailed mechanisms and safe strategy for its activation remain elusive. In this study, we discovered that local hyperthermia therapy (LHT) targeting beige fat promoted its activation in humans and mice. LHT achieved using a hydrogel-based photothermal therapy activated beige fat, preventing and treating obesity in mice without adverse effects. HSF1 is required for the effects since HSF1 deficiency blunted the metabolic benefits of LHT. HSF1 regulates Hnrnpa2b1 (A2b1) transcription, leading to increased mRNA stability of key metabolic genes. Importantly, analysis of human association studies followed by functional analysis revealed that the HSF1 gain-of-function variant p.P365T is associated with improved metabolic performance in humans and increased A2b1 transcription in mice and cells. Overall, we demonstrate that LHT offers a promising strategy against obesity by inducing beige fat activation via HSF1-A2B1 transcriptional axis.

論文信息:

論文題目:Local hyperthermia therapy induces browning of white fat and treats obesity

期刊名稱:Cell

時間期卷: Volume 185, Issue 6

在線時間:2022年3月17日

氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell:

氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell


氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell產(chǎn)品引用截圖

氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell


Liposoma巨噬細(xì)胞清除劑Clodronate Liposomes氯膦酸鹽脂質(zhì)體清除脂肪組織巨噬的給藥方案可以參考該Cell文獻。

Macrophage depletion in adipose tissues

In prior to macrophage depletion, 8-weeks old mice were injected with PDA/PEG hydrogel (PDA) bilaterally in inguinal fat pads. Two days later, these mice were injected with 110mg/kg of clodronate-loaded liposomes (Liposoma, CP-005-005) every two days for three times. Afterwards, skin areas covering beige fat were illuminated unilaterally on one side of iWAT with an 808-nm near-infrared (NIR) laser for 10 min (LHT) while the other side of iWAT remained unilluminated (Sham). Mice were sacrificed to collect iWAT tissues for further analysis after 24 h.

脂肪組織中巨噬細(xì)胞耗竭

在巨噬細(xì)胞耗竭之前,在腹股溝脂肪墊中雙側(cè)注射 PDA/PEG 水凝膠 (PDA) 的 8 周齡小鼠。兩天后,這些小鼠每兩天注射 110 mg/kg 負(fù)載氯膦酸鹽的脂質(zhì)體 (Liposoma, CP-005-005),持續(xù) 3 次。之后,用 808 nm 近紅外 (NIR) 激光單側(cè)照射 iWAT 一側(cè)覆蓋米色脂肪的皮膚區(qū)域 10 分鐘 (LHT),而 iWAT 的另一側(cè)保持未照明 (Sham)。24 小時后處死小鼠以收集 iWAT 組織用于進一步分析。

氯膦酸鹽脂質(zhì)體助力肥胖研究頻登頂刊Cell


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