The effect of chronic immobilization stress on leptin signaling in the ovariectomized (OVX) rat.
Previous studies have shown that both 17β-estradiol (E2) treatment and chronic stress may attenuate post-OVX weight gain in the female rat. However, the interaction between E2 and stress is unclear. This study examined the effect of E2 treatment and chronic immobilization stress on body weight. Adult OVX Sprague-Dawley rats were randomly assigned to one of four treatment groups in a 2X2 factorial design examining hormone treatment [vehicle (VEH) or E2, sc] and stress (no stress vs stress 60 min/day for 22 days). After 22 days, E2 significantly inhibited weight gain and food intake in OVX rats. In contrast, chronic stress reduced body weight only in control OVX animals but did not affect food intake. E2 reduced circulating leptin levels in non-stressed animals, but not in animals subjected to chronic immobilization. Western blot analysis indicated that E2 treatment increased leptin receptor (Ob-Rb) expression in the medial basal hypothalamus (MBH); however, this treatment also increased suppressor of cytokine signaling 3 (SOCS3), which is an inhibitor of leptin signaling. Chronic immobilization stress blunted the E2-induced increase in Ob-Rb and SOCS3 levels. These results suggest that chronic stress counteracts E2 effects on leptin signaling in the MBH without altering body weight.
Program in Molecular and Cellular Biology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road # B2015, Bethesda, MD 20814, USA.
Darwin O
DO
Larco
Danette F
DF
Cruthirds
Michael J
MJ
Weiser
Robert J
RJ
Handa
T John
TJ
Wu
D000818:Animals; D015153:Blotting, Western; D001835:Body Weight / Q000187:drug effects / Q000502:physiology; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D004343:Drug Implants; D004435:Eating / Q000502:physiology; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007033:Hypothalamus, Middle / Q000502:physiology; D020738:Leptin / Q000494:pharmacology / Q000502:physiology*; D010052:Ovariectomy; D010913:Pituitary-Adrenal System / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*; D013315:Stress, Psychological / Q000378:metabolism* / Q000503:physiopathology; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000378:metabolism
D004343:Drug Implants; D020738:Leptin; D050796:STAT3 Transcription Factor; C491410:Socs3 protein, rat; C494088:Stat3 protein, rat; D000071223:Suppressor of Cytokine Signaling 3 Protein; D050826:Suppressor of Cytokine Signaling Proteins; D004958:Estradiol; D003345:Corticosterone