Insulin does not rescue cortical and trabecular bone loss in type 2 diabetic Goto-Kakizaki rats

被引:9
作者
Aeimlapa, Ratchaneevan [1 ,2 ]
Charoenphandhu, Narattaphol [1 ,2 ,3 ]
Suntornsaratoon, Panan [1 ,2 ]
Wongdee, Kannikar [2 ,4 ]
Tiyasatkulkovit, Wacharaporn [2 ,5 ]
Kengkoom, Kanchana [6 ]
Krishnamra, Nateetip [1 ,2 ]
机构
[1] Mahidol Univ, Dept Physiol, Fac Sci, Rama 6 Rd, Bangkok 10400, Thailand
[2] Mahidol Univ, Ctr Calcium & Bone Res COCAB, Fac Sci, Bangkok, Thailand
[3] Mahidol Univ, Inst Mol Biosci, Salaya, Nakhon Pathom, Thailand
[4] Burapha Univ, Off Acad Management, Fac Allied Hlth Sci, Chon Buri, Thailand
[5] Chulalongkorn Univ, Dept Biol, Fac Sci, Bangkok, Thailand
[6] Mahidol Univ, Natl Lab Anim Ctr, Salaya, Nakhon Pathom, Thailand
关键词
Blood glucose; Bone mineral density; Diabetes mellitus; Diabetic osteopathy; Goto-Kakizaki rats; GROWTH-PLATE; ANIMAL-MODELS; BASAL INSULIN; EXPRESSION; RECEPTOR; OSTEOCALCIN; METABOLISM; MELLITUS; THERAPY; INFLAMMATION;
D O I
10.1007/s12576-017-0558-4
中图分类号
Q4 [生理学];
学科分类号
071003 [生理学];
摘要
In type 2 diabetes mellitus (T2DM), the decreased bone strength is often associated with hyperglycemia and bone cell insulin resistance. Since T2DM is increasingly reported in young adults, it is not known whether the effect of T2DM on bone would be different in young adolescents and aging adults. Here, we found shorter femoral and tibial lengths in 7-month, but not 13-month, Goto-Kakizaki (GK) T2DM rats as compared to wild-type rats. Bone A mu CT analysis showed long-lasting impairment of both cortical and trabecular bones in GK rats. Although insulin treatment effectively improved hyperglycemia, it was not able to rescue trabecular BMD and cortical thickness in young adult GK rats. In conclusion, insulin treatment and alleviation of hyperglycemia did not increase BMD of osteopenic GK rats. It is likely that early prevention of insulin resistance should prevail over treatment of full-blown T2DM-related osteopathy.
引用
收藏
页码:531 / 540
页数:10
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