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Central leptin and food restriction reduce the size of certain fat pads without activating the sympathetic nervous system
Author(s) -
Penn Dawn,
Harris Ruth B.S
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a167-a
Subject(s) - leptin , medicine , endocrinology , adipose tissue , lipolysis , white adipose tissue , brown adipose tissue , sympathetic nervous system , chemistry , obesity , blood pressure
Leptin decreases fat mass while preserving lean tissue. Leptin is believed to decrease adipose tissue by either increasing lipolysis and/or inhibiting lipogenesis. The sympathetic nervous system (SNS) is a primary regulator of lipolysis but it is not known if leptin can increase norepinephrine turnover (NETO) in white adipose tissue (WAT). In this study we examined the effect of central leptin administration on NETO and the size of brown and WAT depots in male Sprague‐Dawley rats. Leptin (1.5ug) was injected into the 3rd ventricle, twice daily for 2d. On day 3, rats were killed 1.5 hours after leptin injection and at time 0 or 4 hours after peripheral administration of a NE synthesis inhibitor, alpha‐methyl‐para‐tryrosine. Decline in tissue NE between time 0 and time 4 hours was used to calculate NETO. Food intake, body weight, and fat pad size were significantly decreased in the leptin treated and in PBS injected rats pair‐fed (PF) to leptin rats. Leptin and PF significantly decreased the size of the epididymal (EPI), retroperitoneal (RP), inguinal, and brown adipose pads, but not mesenteric (MES) depots, compared to PBS‐injected controls. NETO did not correspond to changes in pad size. PF caused a significant increase in brown fat NETO and a decrease in RP NETO. Both leptin and PF increased EPI and MES NETO. Thus both leptin and food restriction can reduce the size of some fat depots without activating the SNS. Whether leptin induces loss of fat by acting directly on adipose tissue or indirectly by a cascade of events that ultimately changes adipose metabolism is unclear. This research is supported by NIH R01DK53903.