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    iNTERESTING ABSTRACT

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    Changes in environmental temperature influence leptin responsiveness in low- and high-fat-fed mice

    Loss of body fat in leptin-treated animals has been attributed to reduced energy intake, increased thermogenesis, and preferential fatty acid oxidation. Leptin does not decrease food intake or body fat in leptin-resistant high-fat (HF)-fed mice, possibly due to a failure of leptin to activate hypothalamic receptors. We measured energy expenditure of male C57BL/6 mice adapted to low-fat (LF) or HF diet and infused them for 13 days with PBS or 10 g leptin/day from an intraperitoneal miniosmotic pump to test whether leptin resistance prevented leptin-induced increases in energy expenditure and fatty acid oxidation. There was no effect of low-dose leptin infusions on either of these measures in LF-fed or HF-fed mice, even though LF-fed mice lost body fat. Experiment 2 tested leptin responsiveness in LF-fed and HF-fed mice housed at different temperatures (18C, 23C, 27C), assuming that the cold would increase and the hot environment would inhibit food intake and thermogenesis, which could potentially interfere with leptin action. LF-fed mice housed at 23C were the only mice that lost body fat during leptin infusion, suggesting that an ability to modify energy expenditure is essential to the maintenance of leptin responsiveness. HF-fed mice in cold or warm environments did not respond to leptin. HF-fed mice in the hot environment were fatter than other HF-fed mice, and, surprisingly, leptin caused a further increase in body fat, demonstrating that the mice were not totally leptin resistant and that partial leptin resistance in a hot environment favors positive energy balance and fat deposition.

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    Central leptin resistance in HF-fed rats has been attributed to
    a failure of leptin to cross the blood-brain barrier (4) and
    activate hypothalamic leptin signaling pathways (31). Thus, in
    HF-fed mice, peripherally infused leptin would have access to
    peripheral leptin receptors, but may not have activated hypothalamic
    receptors. When the mice also were housed in a hot
    environment, energy expenditure was limited, and under this
    condition the selective activation of leptin receptors located
    outside of the blood-brain barrier resulted in an increase in
    body fat mass. This possibility is supported by observations in
    chronically decerebrate rats, in which the forebrain is surgically
    isolated from the brain stem. A 2-wk infusion of leptin in
    decrebrate rats resulted in a significant increase in body fat
    content, even though their food intake was fixed by tube
    feeding (37). The effect of leptin in HF-fed mice is dependent
    on both the presence of leptin resistance and an environmental
    restraint on energy intake and expenditure (i.e., hot ambient
    temperature). It does not result simply from the mice consuming
    a HF diet, because our laboratory has previously shown
    that there is an overall inhibition of growth in leptin-infused
    young mice housed in a room at 28C and fed HF diet for only
    10 days (22). These mice would have been considered leptin
    responsive, because they decreased food intake and lost weight
    during the leptin infusion, whether they were housed in a hot
    (22) or a warm environment (6). Leptin may also have been
    effective in the young mice, because they were in a phase of
    rapid growth, whereas the mice in this study were gaining
    weight slowly. Therefore, the increase in body fat content of
    the leptin-treated HF-fed mice housed in the hot environment
    in experiment 2 described here was dependent on there being
    some degree of leptin resistance and could not simply be
    explained by an interaction between diet, leptin administration,
    and temperature. We did not define the mechanism of response
    in this study, and the increase in body fat of HF-fed, leptininfused
    mice in the hot environment has to have resulted from
    a decrease in energy expenditure, an increase in energy
    intake, or a change in nutrient partitioning to favor fat
    deposition. We did not find a measurable increase in food
    intake of the mice, but the amount of energy required to
    account for the increase in fat that was observed may have been
    too small to detect with 24-h measures of food intake. Leptin
    has been reported to inhibit activity of leptin-deficient mice
    (35), and restoration of leptin receptors to the arcuate nucleus
    increases locomotor activity of receptor-deficient mice (14).
    Similarly, a decrease in motor activity is a typical thermoregulatory
    response of mice housed in a hot environment (40).
    Therefore, it is possible that the mice deposited more energy as
    body fat due to a decrease in physical activity.
    Overall, the results of the experiments described here suggest
    that physiological doses of leptin administered as continuous
    peripheral infusions do not produce a measurable increase
    in energy expenditure or a dramatic change in RER, which
    would be indicative of increased rates of fatty acid oxidation.
    The results of the second study demonstrate that relatively
    small changes in environmental temperature abolish leptin
    responsiveness in adult LF-fed mice, possibly due to the
    environmental restraint on heat production, leaving open the
    possibility that leptin produces small changes in energy expenditure
    that contribute to the loss of fat in leptin-responsive mice.
    Of most interest is the observation that adult, leptinresistant,
    HF-fed mice housed in a hot environment gained
    body fat when they were treated with leptin; this response is
    similar to that found in leptin-infused chronically decerebrate
    rats (37). These results demonstrate that the HF-fed mice in a
    hot environment are not totally leptin resistant, and it is
    possible that the failure of leptin to activate central leptin
    receptors facilitated a leptin-induced change in nutrient utilization,
    mediated by leptin receptors in the periphery or caudal
    brain stem, to allow an increase in body fat mass. This could
    only occur if forebrain leptin receptors normally inhibited this
    specific peripheral response to leptin.

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