适应性热发生在色脂肪组织中需要糖原合成,并影响饮食诱导的肥胖症
Shixuan Zhuo1, Meijuan Bai1, Zinan Wang1
1CAS Key Laboratory of Nutrition, Metabolism and Food Safety, Shanghai Institute of Nutrition and HealthUniversity of Chinese Academy of Sciences, Chinese Academy of SciencesShanghaiPeople's Republic of China.
概括
糖原合成对于色脂肪组织在暴露在寒冷中产生热量至关重要. 它的缺失会使饮食引起的肥胖和小鼠的胰岛素耐药性恶化.
科学领域:
- 代谢调节 代谢调节 代谢调节
- 脂肪组织生物学 脂肪组织生物学
- 能量的恒常状态 (Energy homeostasis) 是一种能量的恒常状态.
背景情况:
- 糖原作为肝脏和肌肉中的葡萄糖储存形式,但其在脂肪组织中的作用尚未完全理解.
- 暴露于寒冷会增加棕色和白色脂肪组织中的糖原合成酶1 (Gys1) 表达.
研究的目的:
- 研究Gys1在脂肪组织中的体内功能,特别是其在热生成和代谢适应中的作用.
- 确定脂肪组织中Gys1缺失对感冒诱导的发热和饮食诱导的肥胖的影响.
主要方法:
- 生成了一个小鼠模型,具有脂肪组织特异性的Gys1.1删除.
- 在正常和高脂肪饮食条件下评估体重,葡萄糖代谢和基因表达 (UCP1).
- 用于冷暴露和CL-316,243 (一种β-3上腺素受体激动剂) 来评估发热反应.
主要成果:
- 脂肪组织中的Gys1缺失影响了热生成基因 (UCP1) 对感冒或CL-316,243.3的反应的上调调节.
- 减少基底和刺激的糖原积累在脂肪组织的Gys1-删除的小鼠.
- 在Gys1被删除的小鼠中,加剧高脂肪饮食引起的肥胖和胰岛素抵抗,并在CL-316,243治疗后减轻体重.
结论:
- 糖原合成对于色脂肪组织的适应性热生成至关重要.
- 糖原合成受损会加剧饮食引起的肥胖和胰岛素抵抗.
- 这项研究强调了除了葡萄糖平衡之外,糖原的新角色,影响能源消耗和代谢健康.
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