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1. The actions of the beta-adrenoceptor agonist isoprenaline on glucose and glycogen metabolism, in the presence of various concentrations of insulin, were investigated in isolated soleus muscle preparations taken from eu-, hyper- and hypothyroid rats. 2. Hyperthyroidism, induced by 3,3',5-tri-iodo-D-thyronine (T3) administration for 5 days, increased the rate of lactate formation and suppressed the rate of glycogen synthesis in soleus muscle in response to isoprenaline, even in the presence of physiological or supraphysiological insulin concentrations. 3. Hypothyroidism, induced by administration of 6-n-propyl-2-thiouracil for 4 weeks, decreased the rate of isoprenaline-stimulated lactate formation at all insulin concentrations, but significantly decreased the responsiveness of lactate formation only at low insulin concentrations. In the presence of 100 or 10,000 mu-units of insulin/ml, the ability of isoprenaline to suppress the rate of glycogen synthesis was markedly impaired (inhibition at 100 mu-units of insulin/ml and 1 micro-M-isoprenaline: eu- 72.6 +/- 2.9%; hypo-41.0 +/- 2.1%; P less than 0.001). 4. Hyperthyroidism had no effect on the number or affinity of beta-adrenoceptors, defined by 125I-pindolol binding, or beta-adrenoceptor- or forskolin-stimulated adenylate cyclase activity in membrane preparations of gastrocnemius muscle, whereas hypothyroidism increased the beta-adrenoceptor density and decreased the beta-adrenoceptor-stimulated adenylate cyclase activity, without affecting the receptor affinity or forskolin-stimulated adenylate cyclase activity. 5. It is concluded that there is a complex interplay between insulin, catecholamines and thyroid hormones to regulate skeletal-muscle glucose metabolism. The changes observed in muscles in hypothyroidism may be explained, at least in part, by changes in beta-adrenoceptor-G-protein-adenylate cyclase coupling affecting the generation of cyclic AMP and the regulation of some of the key enzymes of glycogen metabolism; in contrast, the changes observed in muscles in hyperthyroidism do not appear to result from alterations at the level of the receptor-mediated second-messenger generation.
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
March 1996,
British journal of pharmacology,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
October 2007,
American journal of physiology. Endocrinology and metabolism,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
August 1985,
The Journal of biological chemistry,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
November 1985,
The Biochemical journal,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
January 1986,
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G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
April 1998,
Journal of animal science,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
February 1997,
The American journal of physiology,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
December 1985,
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.),
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
December 2003,
American journal of physiology. Endocrinology and metabolism,
G D Dimitriadis, and
S J Richards, and
M Parry-Billings, and
B Leighton, and
E A Newsholme, and
R A Challiss
July 1988,
Metabolism: clinical and experimental,
