Abstract：
Obesity is a significant global health concern linked to excessive dietary energy intake. This research focuses on the mammalian hairless protein (HR), known for its role in skin and hair function, and its impact on metabolism. Examining male wild-type (Hr+/+) and Hr null (Hr-/-) mice over a 14-week normal chow diet (NCD) or high-fat diet (HFD) intervention. This study reveals that HR deficiency exhibited a protective effect against HFD-induced obesity and insulin resistance. This protective effect is attributed to increased energy expenditure in Hr-/- mice. Moreover, the brown adipose tissue (BAT) of Hr-/- mice displays elevated levels of the thermogenic protein, uncoupling protein 1 (Ucp1), and its key transcriptional regulators (PPARγ and PGC1α), compared to Hr+/+ mice. In summary, the findings underscore the protective role of HR deficiency in countering HFD-induced adiposity by enhancing insulin sensitivity, raising energy expenditure, and augmenting thermogenic factors in BAT. Further exploration of HR metabolic regulation holds promise for potential therapeutic targets in addressing obesity-related metabolic disorders.
摘要：
肥胖是与过量饮食能量摄入有关的重要全球健康问题。本研究的重点是哺乳动物无毛蛋白（HR），以其在皮肤和头发功能中的作用而闻名，以及它对新陈代谢的影响。在14周正常饮食(NCD)或高脂肪饮食(HFD)干预下检查雄性野生型(Hr+/+)和Hr无效(Hr-/-)小鼠。这项研究表明，HR缺乏对HFD诱导的肥胖和胰岛素抵抗具有保护作用。这种保护作用归因于Hr-/-小鼠中增加的能量消耗。此外，Hr-/-小鼠的棕色脂肪组织（BAT）显示出产热蛋白水平升高，解偶联蛋白1(Ucp1),及其关键转录调节因子(PPARγ和PGC1α)，与Hr+/+小鼠相比。总之,研究结果强调了HR缺乏通过增强胰岛素敏感性来对抗HFD诱导的肥胖的保护作用,提高能源消耗，并增加BAT中的产热因素。对HR代谢调节的进一步探索有望为解决肥胖相关代谢紊乱的潜在治疗靶标提供希望。
