on September 21, 2006
Published online before print September 21, 2006, doi: 10.1161/01.ATV.0000245808.12493.40
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Submitted on March 13, 2006
Accepted on July 15, 2006
Hereditary Postprandial Hypertriglyceridemic Rabbit Exhibits Insulin Resistance and Central Obesity. A Novel Model of Metabolic Syndrome
Takashi Kawai *;
From Laboratory Animal Center (T.K., T.I., K.O.), Yamagata University School of Medicine, Yamagata-shi, Yamagata, Japan; Japan Tobacco Inc (Y.M., M.M.), Central Pharmaceutical Research Institute, Biological/Pharmacological Research Laboratories, Murasaki-cho, Takatsuki, Osaka, Japan; National Cardiovascular Center (H.T.), Fujishiro-dai, Suita, Osaka, Japan.
* To whom correspondence should be addressed. E-mail: takashi.kawai{at}ims.jti.co.jp.
Objective--We have established a hereditary postprandial hypertriglyceridemic (PHT) rabbit. The present study was designed to define whether this rabbit model represents both insulin resistance and central obesity.
Methods and Results--Body weight, abdominal circumference, visceral fat weight, and glucose tolerance were compared between PHT and Japanese white (JW) rabbit. Plasma levels of triglycerides (TG), total cholesterol (TC), glucose, and insulin were measured before and after feeding. Abdominal circumference of PHT rabbit was larger than that of JW rabbit, with no difference in body mass index. Visceral fat accumulation was noted as obvious in mesenterium, retroperitoneal space, and epididymal area. Plasma TG and TC levels were high preprandially and markedly increased postprandially in PHT rabbit compared with JW rabbit. Although plasma glucose levels were comparable in both groups, plasma insulin levels were elevated in PHT rabbit. Glucose tolerance tests indicated that plasma insulin levels in PHT rabbit were consistently higher than in JW rabbit. A positive correlation was observed between plasma insulin levels and visceral fat weight in PHT rabbit.
Conclusions--PHT rabbit shows insulin resistance along with central obesity. PHT rabbit will serve as a model for elucidating genetic predisposition and pathophysiology in metabolic syndrome.
Key words: central obesity • heritable model • insulin resistance • metabolic syndrome • postprandial hypertriglyceridemia
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