TY - JOUR
T1 - Variation in plasma leptin concentrations after unilateral nephrectomy
AU - Beindorff, Mary Ellen
AU - Larkin, Kevin M.
AU - Coyne, Daniel W.
AU - Sicard, Gregorio A.
AU - Shenoy, Surendra
AU - Lowell, Jeffrey A.
AU - Howard, Todd K.
AU - Landt, Michael
N1 - Funding Information:
From the Nutrition and Laboratory Departments, Barnes-Jewish Hospital, and Departments of Internal Medicine, Surgery, and Pediatrics, Washington University School of Medicine, St Louis, MO. Submitted April 5, 2001; accepted May 31, 2001. Supported by Grant No. RR-00036 to the General Clinical Research Center and the Diabetes Research and Training Center, Grant No. DK-20579 of Washington University. Address reprint requests to Michael Landt, PhD, Department of Pediatrics, Washington University School of Medicine, One Children’s Place, St Louis, MO 63110. Copyright © 2002 by W.B. Saunders Company 0026-0495/02/5102-0036$35.00/0 doi:10.1053/meta.2002.28106
PY - 2002
Y1 - 2002
N2 - The temporal changes in plasma leptin concentrations were studied in healthy adults who underwent unilateral nephrectomy. Another group who underwent abdominal surgery for repair of aneurysm or to relieve arterial stenosis, was also studied. Plasma leptin concentrations increased to 230% ± 74% of prenephrectomy levels at 8 to 16 hours after surgery and then generally declined. Subjects with prenephrectomy leptin concentrations above 14 μg/L maintained elevated postnephrectomy levels, whereas subjects with low prenephrectomy concentrations had final leptin levels below prenephrectomy concentrations. Abdominal surgery subjects did not manifest the increase after surgery, but generally had declining concentrations throughout the convalescent period. Free and bound fractions of plasma leptin and leptin binding capacity were measured in the prenephrectomy and peak specimens (8 to 16 hours postnephrectomy) by high-performance liquid chromatography (HPLC). The increase in total leptin postnephrectomy largely affected the free fraction of leptin, without significant increase in bound leptin or leptin binding capacity. We conclude that (1) plasma leptin concentrations increase acutely after nephrectomy, consistent with the role of the kidneys in eliminating circulating leptin; (2) plasma leptin concentrations decline thereafter, suggesting activation of compensatory elimination capacity; and (3) the postnephrectomy peak in total leptin increases primarily free leptin.
AB - The temporal changes in plasma leptin concentrations were studied in healthy adults who underwent unilateral nephrectomy. Another group who underwent abdominal surgery for repair of aneurysm or to relieve arterial stenosis, was also studied. Plasma leptin concentrations increased to 230% ± 74% of prenephrectomy levels at 8 to 16 hours after surgery and then generally declined. Subjects with prenephrectomy leptin concentrations above 14 μg/L maintained elevated postnephrectomy levels, whereas subjects with low prenephrectomy concentrations had final leptin levels below prenephrectomy concentrations. Abdominal surgery subjects did not manifest the increase after surgery, but generally had declining concentrations throughout the convalescent period. Free and bound fractions of plasma leptin and leptin binding capacity were measured in the prenephrectomy and peak specimens (8 to 16 hours postnephrectomy) by high-performance liquid chromatography (HPLC). The increase in total leptin postnephrectomy largely affected the free fraction of leptin, without significant increase in bound leptin or leptin binding capacity. We conclude that (1) plasma leptin concentrations increase acutely after nephrectomy, consistent with the role of the kidneys in eliminating circulating leptin; (2) plasma leptin concentrations decline thereafter, suggesting activation of compensatory elimination capacity; and (3) the postnephrectomy peak in total leptin increases primarily free leptin.
UR - http://www.scopus.com/inward/record.url?scp=0036177102&partnerID=8YFLogxK
U2 - 10.1053/meta.2002.28106
DO - 10.1053/meta.2002.28106
M3 - Article
C2 - 11833050
AN - SCOPUS:0036177102
SN - 0026-0495
VL - 51
SP - 206
EP - 210
JO - Metabolism: clinical and experimental
JF - Metabolism: clinical and experimental
IS - 2
ER -