title: Differential sympathetic outflow to adipose depots is required for visceral fat loss in response to calorie restriction.
abstract: The sympathetic nervous system (SNS) regulates energy homeostasis in part by governing fatty acid liberation from adipose tissue. We first examined whether SNS activity toward discrete adipose depots changes in response to a weight loss diet in mice. We found that SNS activity toward each adipose depot is unique in timing, pattern of activation, and habituation with the most dramatic contrast between visceral and subcutaneous adipose depots. Sympathetic drive toward visceral epididymal adipose is more than doubled early in weight loss and then suppressed later in the diet when weight loss plateaued. Coincident with the decline in SNS activity toward visceral adipose is an increase in activity toward subcutaneous depots indicating a switch in lipolytic sources. In response to calorie restriction, SNS activity toward retroperitoneal and brown adipose depots is unaffected. Finally, pharmacological blockage of sympathetic activity on adipose tissue using the β3-adrenergic receptor antagonist, SR59230a, suppressed loss of visceral adipose mass in response to diet. These findings indicate that SNS activity toward discrete adipose depots is dynamic and potentially hierarchical. This pattern of sympathetic activation is required for energy liberation and loss of adipose tissue in response to calorie-restricted diet.
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.
authors.forename: L M
authors.initials: LM
authors.lastname: Sipe
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.
authors.forename: C
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.
authors.forename: J
authors.initials: J
authors.lastname: Ephrem
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.
authors.forename: E
authors.initials: E
authors.lastname: Garren
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.
authors.forename: J
authors.initials: J
authors.lastname: Hirsh
authors.affiliation: Department of Biology, University of Virginia, Charlottesville, VA, USA.|Department of Cell Biology, University of Virginia, Charlottesville, VA, USA.|Department of Biomedical Engineering, University of Virginia, Charlottesville, VA, USA.|Department of Neuroscience, University of Virginia, Charlottesville, VA, USA.
authors.forename: C D
authors.initials: CD
authors.lastname: Deppmann
mesh_terms: D002001:Adipose Tissue, Brown / Q000294:innervation / Q000378:metabolism; D052436:Adipose Tissue, White / Q000294:innervation / Q000378:metabolism; D050154:Adiposity; D058673:Adrenergic beta-3 Receptor Antagonists / Q000494:pharmacology; D000818:Animals; D001835:Body Weight; D031204:Caloric Restriction; D004038:Diet, Reducing; D002149:Energy Intake; D004734:Energy Metabolism; D004822:Epididymis / Q000294:innervation / Q000378:metabolism; D050152:Intra-Abdominal Fat / Q000294:innervation / Q000378:metabolism*; D008066:Lipolysis; D008297:Male; D008810:Mice, Inbred C57BL; D009638:Norepinephrine / Q000378:metabolism*; D009765:Obesity / Q000178:diet therapy / Q000378:metabolism*; D010537:Peritoneum; D011412:Propanolamines / Q000494:pharmacology; D050151:Subcutaneous Fat / Q000294:innervation / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000502:physiology*; D015431:Weight Loss
chemical_list: C097869:3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate; D058673:Adrenergic beta-3 Receptor Antagonists; D011412:Propanolamines; D009638:Norepinephrine