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International Journal of Physical Therapy & Rehabilitation Volume 4 (2018), Article ID 4:IJPTR-143, 8 pages
https://doi.org/10.15344/2455-7498/2018/143
Research Article
Streptozotocin-induced Diabetes Causes Crucial Morphological Changes in Abdominal Motoneurons and Muscles of Rats

Naomi Oshiro1, Ken Muramatsu2, Toru Tamaki3, Masatoshi Niwa1*

1Department of Occupational Therapy, Kyorin University, Tokyo, Japan
2Department of Physical Therapy, Kyorin University, Tokyo, Japan
3Department of Physical Therapy, Health Science University, Yamanashi, Japan
Prof. Masatoshi Niwa, Department of Occupational Therapy, Kyorin University, Tokyo, Japan, 5-4-1 Shimorenjaku, Mitaka, Tokyo 181-8612, Japan, Tel: +81-422-47-8000, Fax:+81-422-47-8077; E-mail: mt-niwa@ks.kyorin-u.ac.jp
05 April 2018; 01 June 2018; 04 June 2018
Oshiro N, Muramatsu K, Tamaki T,Niwa M (2018) Streptozotocininduced Diabetes Causes Crucial Morphological Changes in Abdominal Motoneurons and Muscles of Rats. Int J Phys Ther Rehab 4: 143. doi: https://doi.org/10.15344/2455-7498/2018/143
This study was supported by KAKENHI (16K01468), Japan.

Abstract

Background: Diabetic neuropathy (DN) is a major complication of diabetes. Although it is wellestablished that DN targets sensory and autonomic nerves, little is known about its influence on motor disorders.
Methods: This study investigated morphological alterations inabdominal (Abd) motoneurons and muscles of experimental type I diabetic rats. Alterations in the number and size of Abd motoneurons were studied using retrograde labeling techniques in diabetic rats 6 or 14 weeks after injection of streptozotocin (diabetic group). Age-matched control animals were labeled at 6 or 14 weeks after saline injection (control group). Further, the thicknesses of the external oblique, internal oblique, transversus abdominis (TA), and rectus abdominis muscles were similarly examined and the cross-sectional area of the TA myocytes was measured.
Results: The number and mean size of cell bodies significantly decreased in Abd motoneurons in the diabetic group compared with the control group (P < 0.05). As diabetes progressed, there was a clear decrease in the number and mean motoneuron size (P < 0.05). In the diabetic group, the thickness of Abd muscles was reduced, as was the cross-sectional area of the TA myocytes (P < 0.05). Moreover, there was a clear decrease in muscle thickness and in the cross-sectional area of the myocytes (P < 0.05).
Conclusion: We suggest that hyperglycemia induceda reduction in the number and size of Abd motoneurons and atrophy of Abd muscles at 6 and 14 weeks after induction of diabetes by streptozotocin. Therefore, Abd muscular disorders caused by hyperglycemia may relate to a wide range of disorders, such as those involved with expiratory, defecation function, and trunk movement.