title: Modified high-sucrose diet-induced abdominally obese and normal-weight rats developed high plasma free fatty acid and insulin resistance.
abstract: BACKGROUND
  Metabolically obese but normal-weight (MONW) individuals have metabolic features of overt obesity, and abdominal adiposity is common in them. Animal models of MONW individuals are lacking. We aimed to develop an abdominally obese and normal-weight (AONW) rat model.
  
  
  RESULTS
  Young male Sprague-Dawley rats were fed chow or a modified high-sucrose (HS) diet for 20 weeks. The HS diet induced increased visceral adipose tissue without increased body weight, reduced glucose disposal rates, and increased hepatic glucose output during the hyperinsulinemic-euglycemic clamp, increased plasma glucose during the intraperitoneal glucose tolerance test, and increased plasma free fatty acids. Hepatic lipidosis and hepatocyte mitochondria swelling were found in HS rats through light microscopy and transmission electron microscopy; similar impairments were not observed in muscle. RT-PCR showed that mRNA expression of uncoupling protein 3 and peroxisome proliferator-activated receptor-gamma coactivator 1α increased in muscle of HS rats, while expression of mitochondrial transcription factor A, glucose transporter type 4, and insulin receptor substrate-1 did not change significantly.
  
  
  CONCLUSIONS
  AONW rats developed metabolic disorders seen in MONW individuals. Steatosis, mitochondrial morphologic changes, and insulin resistance were more serious in liver than in muscle. Genes involved in fatty acid metabolism and mitochondrial function changed in less impaired muscle.
authors: Division of Geriatrics, West China Hospital of Sichuan University, Chengdu 610041, China.
authors: Li
authors: L
authors: Cao
authors: Xuehui
authors: X
authors: Liu
authors: Hongyi
authors: H
authors: Cao
authors: Qingguo
authors: Q
authors: Lv
authors: Nanwei
authors: N
authors: Tong
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D002784:Cholesterol / Q000097:blood; D019422:Dietary Sucrose; D005230:Fatty Acids, Nonesterified / Q000097:blood*; D005786:Gene Expression Regulation; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications / Q000235:genetics / Q000473:pathology; D006614:Hindlimb / Q000473:pathology / Q000648:ultrastructure; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000187:drug effects / Q000473:pathology; D050356:Lipid Metabolism / Q000235:genetics; D008064:Lipidoses / Q000097:blood / Q000150:complications / Q000235:genetics / Q000473:pathology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008297:Male; D008928:Mitochondria / Q000378:metabolism; D009132:Muscles / Q000473:pathology / Q000648:ultrastructure; D056128:Obesity, Abdominal / Q000097:blood* / Q000150:complications / Q000235:genetics / Q000473:pathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood
chemical_list: D001786:Blood Glucose; D019422:Dietary Sucrose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol