Data from: Sympathetic nervous system activity and anti-lipolytic response to IV-glucose load in subcutaneous adipose tissue of obese and obese type 2 diabetic subjects

The study aim was to investigate the effect of endogenous insulin release
on lipolysis in subcutaneous adipose tissue after adrenergic stimulation
in obese subjects diagnosed with type 2 diabetes (T2D). In 14 obese female
T2D subjects, or 14 obese non-T2D controls, glycerol concentration was
measured in response to the α1,2,ß-agonist norepinephrine, the α1-agonist
norfenefrine and the ß2-agonist terbutaline (each 10-4 M), using the
microdialysis technique. After 60 minutes of stimulation, an intravenous
glucose load (0.5 g/kg lean body mass) was given. Local blood flow was
monitored by means of the ethanol technique. Norepinephrine and
norfenefrine induced a four and three fold rise in glycerol dialysate
concentration (p<0.001, each), with a similar pattern in adipose
tissue. Following agonist stimulation and glucose infusion, endogenous
insulin release inhibited lipolysis in the presence of norepinephrine,
which was more rapid and pronounced in healthy obese controls than in T2D
subjects (p=0.024 obese vs T2D subjects). Insulin-induced inhibition of
lipolysis in the presence of norfenefrine was similar in all study
participants. In the presence of terbutaline the lipolysis rate increased
two fold until the effect of endogenous insulin (p<0.001). A
similar insulin-induced decrease in lipolysis was observed for each of the
norfenefrine groups and the terbutaline groups, respectively. Adipose
tissue blood flow remained unchanged after the iv-glucose load. Both
norepinephrine and norfenefrine diminished blood flow slightly, but
insulin reversed this response (p<0.001 over the entire time).
Terbutaline alone and terbutaline plus increased endogenous insulin
augmented local blood flow (p<0.001 over the entire time). In
conclusion, a difference in insulin-induced inhibition of lipolysis was
observed in obese T2D subjects compared to obese healthy controls
following modulation of sympathetic nervous system activity and is assumed
to be due to ß1-adrenoceptor mediated stimulation by norepinephrine.