title: Human skeletal muscle lipolysis is more responsive to epinephrine than to norepinephrine stimulation in vivo.
abstract: BACKGROUND
  Triglyceride (TG) deposits in skeletal muscle (SM) are an important energy reservoir, and increased im TG content is associated with muscle insulin resistance.
  
  
  OBJECTIVE
  The objective of the study was to investigate the effect of endogenous catecholamines on TG lipolysis in human SM in vivo. Adipose tissue (AT) was studied for comparison.
  
  
  METHODS
  Glycerol levels (index of lipolysis) were measured using microdialysis in the gastrocnemius muscle and abdominal sc adipose tissue during a hyperinsulinemic, hypoglycemic clamp (n = 13) and in response to in situ perfusion of epinephrine and norepinephrine (10(-10) to 10(-5) m) (n = 12). Local tissue blood flow was monitored with the ethanol perfusion technique.
  
  
  METHODS
  This was an experimental study.
  
  
  METHODS
  The study population consisted of healthy subjects.
  
  
  RESULTS
  Plasma epinephrine increased 10-fold and plasma norepinephrine 2-fold in response to insulin-induced hypoglycemia. In parallel, the fractional glycerol release (difference between tissue and arterial glycerol) increased 2-fold in both tissues (P < 0.0001). No changes in AT and SM blood flow were registered. When the catecholamines were perfused in situ, tissue glycerol increased significantly at 10(-7) m of either epinephrine and norepinephrine (P < 0.0001) in AT. The maximum stimulation was seen at 10(-6) m norepinephrine (2-fold increase) and 10(-5) m epinephrine (3-fold increase). In SM, tissue glycerol increased at 10(-7) m epinephrine and 10(-6) m norepinephrine, respectively (P < 0.0001); the maximum increase of glycerol values (at 10(-6) m) was 2.5 times for epinephrine and 1.6 times for norepinephrine, respectively (P < 0.01).
  
  
  CONCLUSIONS
  The lipolytic activity of SM is increased by endogenous catecholamines in vivo and appears to be more responsive to epinephrine than norepinephrine stimulation.
authors.affiliation: Department of Medicine, M54 Karolinska University Hospital Huddinge, SE-141 86 Stockholm, Sweden.
authors.forename: Veronica
authors.initials: V
authors.lastname: Qvisth
authors.forename: Eva
authors.initials: E
authors.lastname: Hagström-Toft
authors.forename: Staffan
authors.initials: S
authors.lastname: Enoksson
authors.forename: Erik
authors.initials: E
authors.lastname: Moberg
authors.forename: Peter
authors.initials: P
authors.lastname: Arner
authors.forename: Jan
authors.initials: J
authors.lastname: Bolinder
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D004837:Epinephrine / Q000097:blood / Q000378:metabolism*; D005260:Female; D015309:Glucose Clamp Technique; D005990:Glycerol / Q000097:blood / Q000378:metabolism; D006801:Humans; D007003:Hypoglycemia / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D008066:Lipolysis; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D009638:Norepinephrine / Q000097:blood / Q000378:metabolism*; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D014280:Triglycerides; D005990:Glycerol; D009638:Norepinephrine; D004837:Epinephrine