Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice -: Characterization of a susceptibility locus on chromosome 4 and its relation with obesity
Type 2 diabetes-like hyperglycemia in a backcross model of NZO and SJL mice -: Characterization of a susceptibility locus on chromosome 4 and its relation with obesity
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DOI：
10.2337/diabetes.49.9.1590
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发表时间：
2000-09-01
期刊：
影响因子：
7.7
通讯作者：
Joost, HG
中科院分区：
文献类型：
--
作者：
Plum, L;Kluge, R;Joost, HG
建立新西兰肥胖小鼠 (NZO) 与抗动脉粥样硬化 SJL 品系的回交模型，以定位导致肥胖、胰岛素抵抗和 2 型糖尿病样高血糖的基因。在雄性 NZO X F1 回交小鼠中，在 4 号染色体标记 D4Mit278 和D4Mit232，位于先前描述的 Nidd1 基因座远端 10-28 cM，致糖尿病等位基因可能是由 SJL 基因组贡献的，它似乎与高血糖总患病率的 60% 相似，Nidd/SJL 的存在在第 12 周时并未改变体重或体重增加，此后，它与体重增加或体重减轻减少有关，可能是由于失代偿性高血糖，在所有雄性回交小鼠中，第 22 周时高血糖的发生率随着第 12 周体重的增加而增加，表明高血糖的发生取决于肥胖程度。在没有 Nidd/SJL 的情况下，小鼠体重
A backcross model of New Zealand obese mice (NZO) with the lean, atherosclerosis-resistant SJL strain was established to locate genes responsible for obesity, insulin resistance, and type 2 diabetes-like hyperglycemia, In male NZO X F1 backcross mice, a major susceptibility locus for the development of hyperglycemia and hypoinsulinemia (Nidd/SJL) was identified on chromosome 4 between the markers D4Mit278 and D4Mit232, 10-28 cM distal of the previously described Nidd1 locus, The diabetogenic allele has presumably been contributed by the SJL genome, and it appeared to be responsible for similar to 60% of the total prevalence of hyperglycemia, The presence of Nidd/SJL did not alter body weight or weight gain by week 12, Thereafter, it was associated with reduced weight gain or weight loss, presumably as a consequence of decompensated hyperglycemia, In all male backcross mice, the prevalence of hyperglycemia at week 22 increased with the body weight at week 12, suggesting that the development of hyperglycemia was dependent on the degree of obesity, In the absence of Nidd/SJL, mice weighing