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DYSLIPIDEMIA AND PERIPHERAL PREDIABETIC NEUROPATHY
Author(s) -
Maksimchyk Yury,
Watcho Pierre,
Lupachyk Sergey,
Obrosova Irina G
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1035.3
Subject(s) - medicine , endocrinology , impaired glucose tolerance , nefa , hypertriglyceridemia , prediabetes , dyslipidemia , hyperinsulinemia , diabetes mellitus , insulin , peripheral neuropathy , impaired fasting glucose , triglyceride , type 2 diabetes , insulin resistance , cholesterol
Evidence for the presence of diabetes‐like neuropathy at prediabetic stage, prior to development of hyperglycemia, is emerging from both experimental and clinical studies. Until now, it has not been sorted out whether prediabetic neuropathy (PN) results from glucose intolerance, or other factors such as impaired insulin signaling, hypertriglyceridemia, hypercholesterolemia, and/or increased NEFA. We evaluated relative roles of the aforementioned factors in prediabetic neuropathy. Experiments were performed in Zucker lean and Zucker fa/fa rats, a model of prediabetes and obesity. 16 wk‐old Zucker fa/fa rats with obesity, glucose intolerance, hyperinsulinemia, hypertriglyceridemia, hypercholesterolemia, and increased serum NEFA levels, displayed sensory nerve conduction velocity (SNCV) deficit, thermal and mechanical hypoalgesia, and tactile allodynia. A 4‐wk treatment with the niacin derivative acipimox reduced serum insulin, NEFA, and triglyceride without affecting impaired glucose tolerance and total and VLDL‐LDL cholesterol levels. It also reversed SNCV deficit and alleviated small sensory fiber neuropathy. These findings suggest that impaired insulin signaling, hypertriglyceridemia, and/or increased fatty acids, rather than impaired glucose tolerance or hypercholesterolemia, are responsible for the development of neuropathic changes associated with prediabetes.