Effects of fructose and glucose on plasma leptin, insulin, and insulin resistance in lean and VMH-lesioned obese rats
1 First Department of Internal Medicine, Showa University School of Medicine, Shinagawa-ku, Tokyo 142-8666; 2 Division of Geriatric Health and Nutrition, National Institute of Health and Nutrition, Tokyo 162-8636; 3 Mitsubishi Kagaku Bio-Clinical Laboratory, Tokyo 174-8555, Japan To determine the...
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Published in | American journal of physiology: endocrinology and metabolism Vol. 278; no. 4; pp. E677 - E683 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.04.2000
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Subjects | |
Online Access | Get full text |
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Summary: | 1 First Department of Internal Medicine, Showa
University School of Medicine, Shinagawa-ku, Tokyo 142-8666;
2 Division of Geriatric Health and Nutrition,
National Institute of Health and Nutrition, Tokyo 162-8636;
3 Mitsubishi Kagaku Bio-Clinical Laboratory,
Tokyo 174-8555, Japan
To determine the influence of dietary
fructose and glucose on circulating leptin levels in lean and obese
rats, plasma leptin concentrations were measured in ventromedial
hypothalamic (VMH)-lesioned obese and sham-operated lean rats fed
either normal chow or fructose- or glucose-enriched diets (60% by
calories) for 2 wk. Insulin resistance was evaluated by the
steady-state plasma glucose method and intravenous glucose tolerance
test. In lean rats, glucose-enriched diet significantly increased
plasma leptin with enlarged parametrial fat pad, whereas neither leptin
nor fat-pad weight was altered by fructose. Two weeks after the
lesions, the rats fed normal chow had marked greater body weight gain,
enlarged fat pads, and higher insulin and leptin compared with
sham-operated rats. Despite a marked adiposity and hyperinsulinemia,
insulin resistance was not increased in VMH-lesioned rats. Fructose
brought about substantial insulin resistance and hyperinsulinemia in
both lean and obese rats, whereas glucose led to rather enhanced
insulin sensitivity. Leptin, body weight, and fat pad were not
significantly altered by either fructose or glucose in the obese rats.
These results suggest that dietary glucose stimulates leptin production
by increasing adipose tissue or stimulating glucose metabolism in lean
rats. Hyperleptinemia in VMH-lesioned rats is associated with both
increased adiposity and hyperinsulinemia but not with insulin
resistance. Dietary fructose does not alter leptin levels, although
this sugar brings about hyperinsulinemia and insulin resistance,
suggesting that hyperinsulinemia compensated for insulin resistance
does not stimulate leptin production.
ventromedial hypothalamic-lesioned rats; hyperinsulinemia |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0193-1849 1522-1555 |
DOI: | 10.1152/ajpendo.2000.278.4.e677 |