PMID- 8770022
OWN - NLM
STAT- MEDLINE
DCOM- 19961205
LR  - 20171213
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 271
IP  - 2 Pt 1
DP  - 1996 Aug
TI  - Increased lipid oxidation but normal muscle glycogen response to epinephrine in 
      humans with IDDM.
PG  - E284-93
AB  - The effects of physiological increments in epinephrine and insulin on glucose 
      production (GP), skeletal muscle glycogen metabolism, and substrate oxidation 
      were studied in eight insulin-dependent diabetes mellitus (IDDM) and nine control 
      subjects. Epinephrine was coinfused for the final 120 min of a 240-min 
      euglycemic, hyperinsulinemic clamp. In both groups, insulin increased glucose 
      uptake, glycogen synthesis, and whole body carbohydrate (CHO) oxidation and 
      inhibited GP (by 70-80%) and lipid oxidation (by approximately 50%), whereas 
      epinephrine antagonized the effect of insulin on glucose uptake and glycogen 
      synthesis. In contrast, GP increased in IDDM subjects (P < 0.02) but remained 
      suppressed by insulin in controls. CHO oxidation fell (1.37 +/- 0.25 vs. 2.08 +/- 
      0.32 mg.kg-1.min-1) and lipid oxidation increased to baseline in IDDM subjects, 
      with increments in plasma free fatty acids (FFA) and glycerol. In contrast, in 
      controls, plasma FFA and glycerol remained suppressed and lipid oxidation 
      decreased further with epinephrine (P < 0.005). Epinephrine completely reversed 
      insulin's activation of muscle glycogen synthase in both groups. Thus, during 
      hyperinsulinemia, the hepatic response to epinephrine in IDDM subjects may be 
      dependent on activation of lipid oxidation. Skeletal muscle glycogen metabolism 
      is exquisitely sensitive to epinephrine despite the presence of hyperinsulinemia.
FAU - Cohen, N
AU  - Cohen N
AD  - Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 
      10461, USA.
FAU - Halberstam, M
AU  - Halberstam M
FAU - Rossetti, L
AU  - Rossetti L
FAU - Shamoon, H
AU  - Shamoon H
LA  - eng
GR  - DK-20541/DK/NIDDK NIH HHS/United States
GR  - DK-45024/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Blood Glucose)
RN  - 0 (C-Peptide)
RN  - 0 (Hormones)
RN  - 0 (Insulin)
RN  - 9005-79-2 (Glycogen)
RN  - EC 2.4.1.- (Phosphorylases)
RN  - EC 2.4.1.11 (Glycogen Synthase)
RN  - YKH834O4BH (Epinephrine)
SB  - IM
MH  - Adult
MH  - Blood Glucose/metabolism
MH  - C-Peptide/blood
MH  - Diabetes Mellitus, Type 1/*metabolism/physiopathology
MH  - Epinephrine/*pharmacology
MH  - Female
MH  - Glycogen/*metabolism
MH  - Glycogen Synthase/metabolism
MH  - Hormones/blood
MH  - Humans
MH  - Insulin/blood
MH  - *Lipid Metabolism
MH  - Male
MH  - Middle Aged
MH  - Muscle, Skeletal/*drug effects/*metabolism
MH  - Oxidation-Reduction/drug effects
MH  - Phosphorylases/metabolism
MH  - Reference Values
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - 10.1152/ajpendo.1996.271.2.E284 [doi]
PST - ppublish
SO  - Am J Physiol. 1996 Aug;271(2 Pt 1):E284-93. doi: 10.1152/ajpendo.1996.271.2.E284.