title: High energy diets-induced metabolic and prediabetic painful polyneuropathy in rats.
abstract: To establish the role of the metabolic state in the pathogenesis of polyneuropathy, an age- and sex-matched, longitudinal study in rats fed high-fat and high-sucrose diets (HFSD) or high-fat, high-sucrose and high-salt diets (HFSSD) relative to controls was performed. Time courses of body weight, systolic blood pressure, fasting plasma glucose (FPG), insulin, free fatty acids (FFA), homeostasis model assessment-insulin resistance index (HOMA-IR), thermal and mechanical sensitivity and motor coordination were measured in parallel. Finally, large and small myelinated fibers (LMF, SMF) as well as unmyelinated fibers (UMF) in the sciatic nerves and ascending fibers in the spinal dorsal column were quantitatively assessed under electron microscopy. The results showed that early metabolic syndrome (hyperinsulinemia, dyslipidemia, and hypertension) and prediabetic conditions (impaired fasting glucose) could be induced by high energy diet, and these animals later developed painful polyneuropathy characterized by myelin breakdown and LMF loss in both peripheral and central nervous system. In contrast SMF and UMF in the sciatic nerves were changed little, in the same animals. Therefore the phenomenon that high energy diets induce bilateral mechanical, but not thermal, pain hypersensitivity is reflected by severe damage to LMF, but mild damage to SMF and UMF. Moreover, dietary sodium (high-salt) deteriorates the neuropathic pathological process induced by high energy diets, but paradoxically high salt consumption, may reduce, at least temporarily, chronic pain perception in these animals.
authors: Institute for Biomedical Sciences of Pain and Institute for Functional Brain Disorders, Tangdu Hospital, The Fourth Military Medical University, Xi'an, P. R. China.
authors: Fang
authors: F
authors: Xie
authors: Han
authors: H
authors: Fu
authors: Jun-Feng
authors: JF
authors: Hou
authors: Kai
authors: K
authors: Jiao
authors: Michael
authors: M
authors: Costigan
authors: Jun
authors: J
authors: Chen
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D004032:Diet / Q000009:adverse effects*; D059305:Diet, High-Fat / Q000009:adverse effects; D019422:Dietary Sucrose / Q000008:administration & dosage / Q000009:adverse effects; D005215:Fasting / Q000378:metabolism / Q000502:physiology; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006706:Homeostasis / Q000502:physiology; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology; D008137:Longitudinal Studies; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism / Q000473:pathology*; D009048:Motor Skills / Q000502:physiology; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000502:physiology; D036421:Nerve Fibers, Unmyelinated / Q000378:metabolism / Q000502:physiology; D010146:Pain / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D011115:Polyneuropathies / Q000378:metabolism / Q000473:pathology*; D011236:Prediabetic State / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012584:Sciatic Nerve / Q000378:metabolism / Q000502:physiology; D012982:Sodium, Dietary / Q000009:adverse effects; D013116:Spinal Cord / Q000378:metabolism / Q000502:physiology
chemical_list: D001786:Blood Glucose; D019422:Dietary Sucrose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D012982:Sodium, Dietary