Role of fatty acid composition in the development of metabolic disorders in sucrose-induced obese rats.
Fatty acids have been shown to be involved in the development of insulin resistance associated with obesity. We used sucrose loading in rats to analyze changes in fatty acid composition in the progression of obesity and the related metabolic disorder. Although rats fed a sucrose diet for 4 weeks had body weights similar to those of control animals, their visceral fat pads were significantly larger, and serum triglyceride levels were higher; however, neither plasma glucose nor insulin levels were significantly higher. After 20 weeks of sucrose loading, body weight and visceral and subcutaneous fat pads had increased significantly compared with those in control rats. Moreover, plasma glucose, insulin, and triglyceride levels were significantly higher. An analysis of individual fatty acid components in the blood and peripheral tissues demonstrated phase- and tissue-dependent changes. After 20 weeks of sucrose loading, palmitoleic acid (16:1 n-7) and oleic acid (18:1 n-9), the major components of monounsaturated fatty acid, showed a ubiquitous increase in plasma and all tissues analyzed. In contrast, linoleic acid (18:2 n-6) and arachidonic acid (20:4 n-6), the major components of polyunsaturated fatty acid in the n-6 family, decreased in plasma and all tissues analyzed. After 4 weeks of sucrose loading, these changes in fatty acid composition were observed only in the liver and plasma and not in fat and muscle. This led us to conclude that elevation of plasma glucose and insulin develop at the late phase of sucrose-induced obesity, when changes in fatty acid composition appear in fat and muscle. Furthermore, changes in fatty acid composition in liver seen after 4 weeks of sucrose loading, when increases in neither plasma glucose nor insulin were detected, suggest that liver may be the initial site of fatty acid imbalance and that aberrations in hepatic fatty acid composition may lead to fatty acid imbalances in other tissues.
Fukuchi
Satoshi
S
Department of Internal Medicine I, Faculty of Medicine, Oita University, Hasama, Oita, 879-5593, Japan.
Hamaguchi
Kazuyuki
K
Seike
Masataka
M
Himeno
Katsuro
K
Sakata
Toshiie
T
Yoshimatsu
Hironobu
H
D000273:Adipose Tissue / Q000378:metabolism; D000821:Animal Feed; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D019422:Dietary Sucrose / Q000008:administration & dosage*; D002149:Energy Intake; D004822:Epididymis / Q000378:metabolism; D005227:Fatty Acids / Q000097:blood / Q000378:metabolism*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000097:blood / Q000139:chemically induced* / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
D001786:Blood Glucose; D019422:Dietary Sucrose; D005227:Fatty Acids; D007328:Insulin; D014280:Triglycerides