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Departments of 1 Internal Medicine and 2 Pediatrics, Washington University School of Medicine, St. Louis, Missouri 63110 and 3 University College London Medical School, Whittington Hospital, London N2 9QA, United Kingdom
We evaluated abdominal adipose tissue
leptin production during short-term fasting in nine lean [body
mass index (BMI) 21 ± 1 kg/m2] and nine upper body
obese (BMI 36 ± 1 kg/m2) women. Leptin kinetics were
determined by arteriovenous balance across abdominal subcutaneous
adipose tissue at 14 and 22 h of fasting. At 14 h of fasting, net
leptin release from abdominal adipose tissue in obese subjects (10.9 ± 1.9 ng · 100 g
tissue · 
1 · min1)
was not significantly greater than the values observed in the lean
group (7.6 ± 2.1 ng · 100 g1 · min1).
Estimated whole body leptin production was approximately fivefold greater in obese (6.97 ± 1.18 µg/min) than lean subjects (1.25 ± 0.28 µg/min) (P < 0.005). At 22 h of fasting, leptin
production rates decreased in both lean and obese groups (to 3.10 ± 1.31 and 10.5 ± 2.3 ng · 100 g adipose
tissue1 · min1,
respectively). However, the relative declines in both arterial leptin
concentration and local leptin production in obese women (arterial
concentration 13.8 ± 4.4%, local production 10.0 ± 12.3%) were
less (P < 0.05 for both) than the relative decline in lean women (arterial concentration 39.0 ± 5.5%, local production 56.9 ± 13.0%). This study demonstrates that decreased leptin production accounts for the decline in plasma leptin concentration observed after
fasting. However, compared with lean women, the fasting-induced decline
in leptin production is blunted in women with upper body obesity.
Differences in leptin production during fasting may be responsible for
differences in the neuroendocrine response to fasting previously
observed in lean and obese women.
adipose tissue; lipid metabolism; obesity
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