Eur J Endocrinol 166:711–716PubMedCrossRef 47. Zhou G, Myers R, Li Y, Chen Y, Shen X, Fenyk-Melody J, Wu M, Ventre J, Doebber T, Fujii N, Musi N, Hirshman MF, Goodyear LJ, Moller DE (2001) Role of AMP-activated protein kinase in mechanism of metformin action. J Clin Invest 108:1167–1174PubMed 48. Zhou
Loder RT (1988) The influence of diabetes mellitus on the healing of closed fractures. Clin Orthop Relat Res 232:210–216 49. Chaudhary SB, Liporace FA, Gandhi A, Donley BG, Pinzur MS, Lin SS (2008) Complications of ankle fracture in patients with diabetes. J Am Acad Orthop Surg 16:159–170PubMed 50. Hamann C, Goettsch C, Mettelsiefen J, Henkenjohann #17DMAG randurls[1|1|,|CHEM1|]# V, Rauner M, Hempel U, Bernhardt R, Fratzl-Zelman N, Roschger P, Rammelt S, Gunther KP, Hofbauer LC (2011) Delayed bone regeneration and low bone mass in a rat model of insulin-resistant type 2 diabetes mellitus is due to impaired osteoblast function. Am J Physiol Endocrinol Metab 301:E1220–E1228PubMedCrossRef 51. Ogasawara A, Nakajima A, learn more Nakajima F, Goto K, Yamazaki M (2008) Molecular basis for affected cartilage formation and bone union in fracture healing of the streptozotocin-induced diabetic rat. Bone 43:832–839PubMedCrossRef 52. Retzepi M, Donos N (2010) The
effect of diabetes mellitus on osseous healing. Clin Oral Implants Res 21:673–681PubMedCrossRef 53. Hamann C, Kirschner S, Gunther KP, Hofbauer LC (2012) Bone, sweet bone—osteoporotic fractures in diabetes mellitus. Nat Rev Endocrinol 8:297–305PubMedCrossRef”
“Dear Editor, Iki and colleagues conducted a cross-sectional study if serum
undercarboxylated osteocalcin levels were inversely associated with fasting plasma glucose (FPG), hemoglobin A1c, and homeostasis model assessment of insulin resistance (HOMA-IR) levels in elderly Japanese male inhabitants [1]. Regarding basic characteristics of variables they used for the analysis, I have two queries as follows. First, in addition to three markers for bone turnover, the levels of glucose metabolism also showed log-normal distribution. In their Table 2, the levels of Uroporphyrinogen III synthase lipid metabolism also showed log-normal distribution. I agree the log-normal distribution of serum insulin, triglyceride, and HOMA-IR in general habitants, but other variables on glucose and lipid metabolism distribute normal form from my experience. On this point, the characteristics of their population should be explored to check validation on the representativeness of the Japanese male inhabitants. Second, HOMA-IR has a limitation as an indicator of insulin resistance. Iki and colleagues quoted the original reference [2], Thereafter, an advanced procedure has been distributed [3], and some problems of HOMA-IR for the reflection of insulin resistance had been reported [4, 5].