{"status":"success","ccode_error_type":"success","message":"OK","result":{"status":"success","object":{"id":493736635,"is_active":true,"created":"2023-12-25T15:20:14.383454","last_modified":"2023-12-25T15:20:45.111222","company_id":25521,"datasettable_id":350662,"order":0,"uuid":"8e2675e4-290a-4b6c-98e0-14f20b9f5a1b","siteuser_id":null,"data":{"file":"","name":"ob/ob和db/db小鼠","files":[],"image":"u/jnsw/2023/12/25/cVkarbxGGuFQ9nFnzGNbED/DIO小鼠.png","model":"product","order":0,"price":100,"sales":0,"stock":100,"video":"","images":[],"visits":0,"volume":0,"weight":0,"item_id":0,"summary":"","contexts":{},"property":{},"pub_date":"1970-01-01T00:00:00.000000","sku_code":"","attribute":{},"file_info":{},"is_active":true,"tag_uuids":[],"brand_uuid":null,"video_info":{},"description":"

ob/ob小鼠: 即Lepob/ob，是瘦素 (Leptin, Lep) 基因纯合突变的小鼠。

Leptin为肥胖基因 (ob)编码产物，是脂肪细胞分泌的蛋白质类激素，在调节能量平衡、摄食行为起重要作用。若ob基因突变，食欲大增，体重剧增，产生严重的肥胖特征，多用于肥胖症的研究。

db/db小鼠: 即Leprdb/db，代表瘦素受体 (Leptin receptor, Lepr) 基因纯合突变的小鼠Lepr，又名OBR，是由db基因编码产物，为Leptin受体。若Lepr缺失，导致高血糖症和胰岛素抵抗症，有类似ob/ob小鼠症状，现已广泛用于肥胖和2型糖尿病的研究。

模型特征:

2周时，超重和食欲大增，开始出现高胰岛素血症:

4周时，明显高血糖，血糖浓度继续上升，峰值在3-5个月

期间伴随代谢异常包括高脂血症，严重肥胖、多食、易渴、多尿、体温调节紊乱和活动能力下降。

注意:该纯合子小鼠是不育的。

模型判定: 4周龄后检测血糖，空腹血糖>7mmol/L，餐后血糖>11.1~16.7mmol/L.

应用范围

肥胖症: 抑制食欲，能量消耗研究
糖脂代谢: 如高血脂症，2型糖尿病的胰岛素抵抗的治疗
肝肾疾病:肝硬化，脂肪肝，糖尿病肾病
生殖发育：如不孕不育症
免疫炎症：肥胖和糖尿病都伴随着炎症的加剧:
代谢综合征
糖尿病的并发症治疗

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背景与意义

肥胖及其伴随的代谢综合征（如2型糖尿病、非酒精性脂肪肝病、心血管疾病）已成为全球性的重大公共卫生问题。为了深入理解肥胖的发病机制、探索预防和治疗策略，建立能够模拟人类肥胖发生发展过程的动物模型至关重要。

虽然存在一些单基因突变导致肥胖的自发性动物模型（如ob/ob, db/db小鼠），但这些模型通常代表罕见的单基因遗传性肥胖，与绝大多数人类肥胖（主要是多基因遗传背景与环境因素，尤其是高热量饮食，相互作用的结果）存在显著差异。因此，饮食诱导肥胖 (Diet-Induced Obesity, DIO) 小鼠模型应运而生，并因其高度的临床相关性而成为肥胖研究领域＊重要和＊广泛使用的模型之一。

饮食诱导的动物肥胖模型与人类肥胖相似，常用来研究饮食、基因等因素与肥胖/糖尿病等疾病进程之间的关系。集诺生物通过高热量饮食喂养构建的小鼠肥胖模型（DIO），可作为肥胖及相关并发症临床前药效研究的合适动物模型。

小鼠：C57BL/6J，雄鼠，5-6周龄

造模方法：高脂饲料喂养8周，构建肥胖症模型。

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链脲佐菌素(STZ)是一种可破坏胰岛β细胞的抗生素，在实验中广泛用于制造1型糖尿病(T1DM)模型。STZ是一种含亚硝基的化合物，可通过诱导一氧化氮(NO)的合成，特异性破坏胰岛B细胞，增加胰岛B细胞的氧化侵袭。目前普遍认为，小剂量多次注射STZ可诱导实验动物发生1型糖尿病。其机制可能是注射小剂量STZ后，少量胰岛细胞被破坏，死亡的胰岛细胞被巨噬细胞释放致敏蛋白作为抗原。吞噬作用，产生th1刺激因子(IL-12)，诱导IL-2和IFN-γ分泌增加，在局部胰岛形成炎性细胞浸润，释放IL-1β、TNF-α、IFN-γ等细胞因子和氧自由基杀死少量细胞。死亡细胞将自身作为抗原，经APC细胞处理后释放细胞因子，放大细胞损伤效应，＊终导致1型糖尿病。

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