Abstract
The present study was performed to determine the effects of central administration of leptin on food intake and sympathetic nervous system activity in a nonrodent species, the rhesus monkey. Peripheral administration of leptin at doses (1 and 3 μg/kg, sc) that produced increments of circulating leptin concentrations within a physiological range did not inhibit food intake over the subsequent 3 days. In contrast, leptin (1 μg/kg, intracerebroventricularly) had no acute effect on food intake, but caused a significant and sustained suppression (40-50%) of food intake during the entire following day (P < 0.01). In addition, circulating norepinephrine levels increased by 55 ± 16% (P < 0.02) 1 h after intracerebroventricular leptin administration, but did not increase after artificial cerebrospinal fluid administration. These results indicate that leptin can provide a signal to the central nervous system that decreases food intake in primates and in addition acutely activates the sympathetic nervous system. However, the results showing an acute increase in circulating leptin concentrations after peripheral administration of human leptin suggest that in primates, increases in circulating leptin within the physiological range do not acutely regulate food intake. Leptin may be more important in regulating food intake when there are sustained changes in circulating concentrations of leptin (e.g. with obesity, prolonged energy restriction, or diabetes).
| Original language | English (US) |
|---|---|
| Pages (from-to) | 711-717 |
| Number of pages | 7 |
| Journal | Journal of Clinical Endocrinology and Metabolism |
| Volume | 84 |
| Issue number | 2 |
| DOIs | |
| State | Published - 1999 |
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ASJC Scopus subject areas
- Biochemistry
- Endocrinology, Diabetes and Metabolism
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Central administration of leptin inhibits food intake and activates the sympathetic nervous system in rhesus macaques. / Tang-Christensen, Mads; Havel, Peter J; Jacobs, Rebecca R.; Larsen, Philip J.; Cameron, Judy L.
In: Journal of Clinical Endocrinology and Metabolism, Vol. 84, No. 2, 1999, p. 711-717.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Central administration of leptin inhibits food intake and activates the sympathetic nervous system in rhesus macaques
AU - Tang-Christensen, Mads
AU - Havel, Peter J
AU - Jacobs, Rebecca R.
AU - Larsen, Philip J.
AU - Cameron, Judy L.
PY - 1999
Y1 - 1999
N2 - The present study was performed to determine the effects of central administration of leptin on food intake and sympathetic nervous system activity in a nonrodent species, the rhesus monkey. Peripheral administration of leptin at doses (1 and 3 μg/kg, sc) that produced increments of circulating leptin concentrations within a physiological range did not inhibit food intake over the subsequent 3 days. In contrast, leptin (1 μg/kg, intracerebroventricularly) had no acute effect on food intake, but caused a significant and sustained suppression (40-50%) of food intake during the entire following day (P < 0.01). In addition, circulating norepinephrine levels increased by 55 ± 16% (P < 0.02) 1 h after intracerebroventricular leptin administration, but did not increase after artificial cerebrospinal fluid administration. These results indicate that leptin can provide a signal to the central nervous system that decreases food intake in primates and in addition acutely activates the sympathetic nervous system. However, the results showing an acute increase in circulating leptin concentrations after peripheral administration of human leptin suggest that in primates, increases in circulating leptin within the physiological range do not acutely regulate food intake. Leptin may be more important in regulating food intake when there are sustained changes in circulating concentrations of leptin (e.g. with obesity, prolonged energy restriction, or diabetes).
AB - The present study was performed to determine the effects of central administration of leptin on food intake and sympathetic nervous system activity in a nonrodent species, the rhesus monkey. Peripheral administration of leptin at doses (1 and 3 μg/kg, sc) that produced increments of circulating leptin concentrations within a physiological range did not inhibit food intake over the subsequent 3 days. In contrast, leptin (1 μg/kg, intracerebroventricularly) had no acute effect on food intake, but caused a significant and sustained suppression (40-50%) of food intake during the entire following day (P < 0.01). In addition, circulating norepinephrine levels increased by 55 ± 16% (P < 0.02) 1 h after intracerebroventricular leptin administration, but did not increase after artificial cerebrospinal fluid administration. These results indicate that leptin can provide a signal to the central nervous system that decreases food intake in primates and in addition acutely activates the sympathetic nervous system. However, the results showing an acute increase in circulating leptin concentrations after peripheral administration of human leptin suggest that in primates, increases in circulating leptin within the physiological range do not acutely regulate food intake. Leptin may be more important in regulating food intake when there are sustained changes in circulating concentrations of leptin (e.g. with obesity, prolonged energy restriction, or diabetes).
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UR - http://www.scopus.com/inward/citedby.url?scp=0033051923&partnerID=8YFLogxK
U2 - 10.1210/jc.84.2.711
DO - 10.1210/jc.84.2.711
M3 - Article
C2 - 10022442
AN - SCOPUS:0033051923
VL - 84
SP - 711
EP - 717
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 2
ER -