| Literature DB >> 28229243 |
Hideaki Nakatsuji1, Amane Araki1,2, Atsushi Hashizume1, Yasuhiro Hijikata1, Shinichiro Yamada1, Tomonori Inagaki1, Keisuke Suzuki1,3, Haruhiko Banno1, Noriaki Suga1,4, Yohei Okada5,6, Manabu Ohyama7, Tohru Nakagawa8, Ken Kishida9,10, Tohru Funahashi9,11, Iichiro Shimomura9, Hideyuki Okano6, Masahisa Katsuno12, Gen Sobue13,14.
Abstract
This study aimed to evaluate various metabolic parameters in patients with spinal and bulbar muscular atrophy (SBMA), to investigate the association between those indices and disease severity, and to explore the underlying molecular pathogenesis. We compared the degree of obesity, metabolic parameters, and blood pressure in 55 genetically confirmed SBMA patients against those in 483 age- and sex-matched healthy control. In SBMA patients, we investigated the correlation between these factors and motor functional indices. SBMA patients had lower body mass index, blood glucose, and Hemoglobin A1c, but higher blood pressure, homeostasis model assessment of insulin resistance (HOMA-IR, a marker of insulin resistance), total cholesterol, and adiponectin levels than the control subjects. There were no differences in visceral fat areas, high-density lipoprotein-cholesterol (HDL-C), or triglyceride levels in two groups. Revised amyotrophic lateral sclerosis functional rating scale (ALSFRS-R) correlated positively with HDL-C, but negatively with HOMA-IR. Through stepwise multiple regression analysis, we identified HOMA-IR as a significant metabolic determinant of ALSFRS-R. In biochemical analysis, we found that decreased expressions of insulin receptors, insulin receptor substrate-1 and insulin receptor-β, in autopsied muscles and fibroblasts of SBMA patients. This study demonstrates that SBMA patients have insulin resistance, which is associated with the disease severity. The expressions of insulin receptors are attenuated in the skeletal muscle of SBMA, providing a possible pathomechanism of metabolic alterations. These findings suggested that insulin resistance is a metabolic index reflecting disease severity and pathogenesis as well as a potential therapeutic target for SBMA.Entities:
Keywords: Insulin receptor; Insulin resistance; SBMA; Spinal and bulbar muscular atrophy
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Year: 2017 PMID: 28229243 DOI: 10.1007/s00415-017-8405-3
Source DB: PubMed Journal: J Neurol ISSN: 0340-5354 Impact factor: 4.849