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1 Department of Medicine, University of Adelaide, Royal Adelaide Hospital, Adelaide, South Australia 5000, Australia; and 2 Division of Geriatric Medicine, St. Louis University and Geriatric Research Education and Clinical Center, St. Louis Veterans Affairs Medical Center, St. Louis, Missouri 63104
The aim of this study was to determine in
the marsupial Sminthopsis
crassicaudata
1) the effect of leptin on food
intake, body fat stores, and metabolism and
2) whether leptin can prevent a
diet-induced increase in adiposity. In response to 21 days of feeding
with mealworms (2.99 kcal/g, 30% fat), body weight
(P < 0.0001) and tail width
(P < 0.0001) increased, compared
with control animals fed with laboratory diet (1.01 kcal/g, 20% fat). Subsequently, S. crassicaudata were
randomly allocated to receive either laboratory diet or a choice
between laboratory diet and mealworms. For 13 days, one-half of the
animals in each dietary group received intraperitoneal human leptin
(2.5 mg/kg twice daily), while the other one-half received
phosphate-buffered saline. In animals receiving laboratory diet alone,
leptin induced a decrease in body weight
(P < 0.0001), tail width
(P < 0.0001), and energy intake
(P < 0.01). In animals receiving
both laboratory diet and mealworms, leptin had no effect on body weight
or tail width, although the proportion of laboratory diet eaten was
reduced (P = 0.0001), and there was a
nonsignificant fall in overall energy intake
(P = 0.07). We conclude that
in S. crassicaudata,
1) a high-calorie, higher-fat diet
induces an increase in adiposity and
2) leptin induces weight loss, but
3) an increase in dietary calories
and fat content is associated with resistance to the actions of leptin.
adiposity; calorie; fat; food intake
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