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Short‐term β‐adrenergic regulation of leptin, adiponectin and interleukin‐6 secretion in vivo in lean and obese subjects
Author(s) -
Goossens G. H.,
Jocken J. W. E.,
Van Baak M. A.,
Jansen E. H. J. M.,
Saris W. H. M.,
Blaak E. E.
Publication year - 2008
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2008.00856.x
Subject(s) - leptin , endocrinology , medicine , adipose tissue , adiponectin , adipokine , white adipose tissue , chemistry , insulin , obesity , insulin resistance
Aim:  Adipose tissue and skeletal muscle are endocrine organs, secreting substances that have been implicated in obesity‐related disorders. This study examined short‐term β‐adrenergic regulation of circulating leptin, adiponectin and interleukin‐6 (IL‐6) concentrations and secretion from abdominal subcutaneous adipose tissue and muscle (IL‐6) in vivo in lean and obese subjects. Methods:  Systemic concentrations and net fluxes of leptin, adiponectin and IL‐6 across abdominal subcutaneous adipose tissue and forearm skeletal muscle (IL‐6) were assessed before and during β‐adrenergic stimulation (intravenous isoprenaline infusion) in 13 lean and 10 obese men. Results:  Basal circulating leptin concentrations were higher in the obese (p < 0.001), while circulating adiponectin (p = 0.45) and IL‐6 concentrations (p = 0.41) were not different between groups. β‐Adrenergic stimulation decreased leptin concentrations in both groups (p < 0.01), but did not reduce net abdominal subcutaneous adipose tissue leptin release. Increased leptin clearance and/or decreased leptin secretion from other fat depots may explain the reduction in leptin concentrations. Adiponectin concentrations remained unchanged during β‐adrenergic stimulation in both groups. β‐Adrenergic stimulation increased IL‐6 concentration, which was more pronounced in the obese (p = 0.01 vs. lean). This cannot be explained by increased IL‐6 release per unit abdominal subcutaneous adipose tissue and muscle but might be because of the increased fat mass and fat‐free mass at whole‐body level. Conclusions:  Short‐term β‐adrenergic stimulation decreases leptin concentrations, which cannot be explained by reduced net leptin release from abdominal subcutaneous adipose tissue, while it elevates IL‐6 concentration partly by increased release from this fat depot and muscle. Finally, β‐adrenergic stimulation has no short‐term regulatory role in adiponectin secretion.

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