Reduction in Endogenous Insulin Secretion is a Risk Factor of Sarcopenia in Men with Type 2 Diabetes Mellitus

Calcified Tissue International and Musculoskeletal Research Volume 97 Issue 4 Page 385-390 published_at 2015-10
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Title
Reduction in Endogenous Insulin Secretion is a Risk Factor of Sarcopenia in Men with Type 2 Diabetes Mellitus
Creator
Tanaka Ken-ichiro
Source Title
Calcified Tissue International and Musculoskeletal Research
Volume 97
Issue 4
Start Page 385
End Page 390
Journal Identifire
ISSN 0171967X
Descriptions
Sarcopenia has recently attracted widespread attention, because it increases risks of fall and bedridden. Although patients with type 2 diabetes mellitus (T2DM) are known to have lower muscle mass of limbs than healthy people, the mechanism is still unclear. We thus examined the association of muscle mass with parameters of endogenous insulin secretion such as fasting immunoreactive insulin, fasting C-peptide immunoreactivity (CPR), and daily urine CPR in 191 men with T2DM. Muscle mass of arms and legs was evaluated by dual-energy X-ray absorptiometry, and we calculated relative skeletal muscle index (RSMI), which is useful for the diagnosis of sarcopenia. Multiple regression analyses adjusted for age, duration of T2DM, serum creatinine, HbA1c, and insulin-like growth factor-I showed that each parameter of endogenous insulin was significantly and positively correlated with muscle mass of arms and legs as well as RSMI (p < 0.05). Moreover, logistic regression analyses adjusted for confounding factors mentioned above showed that each parameter of endogenous insulin was significantly lower in subjects with sarcopenia than those without it (p < 0.05). In conclusion, reduction in endogenous insulin secretion is an independent risk factor of sarcopenia in men with T2DM.
Subjects
Sarcopenia
Insulin secretion
Diabetes mellitus
Skeletal muscle mass
IGF-Ι
Language
eng
Resource Type journal article
Publisher
Springer US
Date of Issued 2015-10
Rights
The final publication is available at Springer via http://dx.doi.org/10.1007/s00223-015-9990-8.
Publish Type Accepted Manuscript
Access Rights open access
Relation
[DOI] 10.1007/s00223-015-9990-8
[PMID] 25850525