2007 Fiscal Year Final Research Report Summary
Molecular and pathogenic mechanisms for peripheral neuropathy associated with metabolic syndrome
| Project/Area Number |
18590520
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Hirosaki University |
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Principal Investigator |
SUGIMOTO Kazuhiro Hirosaki University, Hirosaki University Graduate School of Medicine, Associate Professor (70271799)
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| Co-Investigator(Kenkyū-buntansha) |
YASUJIMA Minoru Hirosaki University, Graduate School of Medicine, Professor (90142934)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Insulin signaling / Insulin resistance / Metabolic syndrome / Neuropathy / Diabetes / Impaired glucose tolerance |
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| Research Abstract |
Small sensory fiber dysfunction has recently been recognized as a component of impaired glucose tolerance and metabolic syndrome. However, few studies have investigated whether small sensory fiber dysfunction develops in normoglycemic or prediabetic animal models with metabolic syndrome. Longitudinal trends for thermal and mechanical nociceptive responses were assessed in 8-to 36-week-old male obese Zucker rats, 8-to 36-week-old male Zucker diabetic fatty (ZDF) rats. Data were compared with metabolic disorders in these rats. Both obese Zucker and ZDF rats at 8 weeks of age showed compensatory hyperinsulinemia and developed thermal hyperalgesia prior to the onset of overt hyperglycemia. These animals also exhibited progression from thermal hyperalgesia to hyperalgesia, which occurred more rapidly and coincided with a more rapid decline in pancreatic insulin secretion in ZDF rats than in obese Zucker rats. Based on these findings we conclude that metabolic syndrome with or without compensatory hyperinsulinemia is associated with nociceptive dysfunction having different phenotypes, independently of glycemic levels.
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Research Products
(24 results)
