Lack of an acute effect of parathyroid hormone within skeletal muscle.
Secondary hyperparathyroidism is commonly present in patients with chronic renal failure. It has been suggested that elevated levels of parathyroid hormone (PTH) may be responsible for the glucose, amino acid and protein turnover abnormalities present in uremia. We utilized an in vitro muscle perfusion system to explore this possibility in more detail. We measured glucose uptake, muscle alanine and glutamine release, protein synthesis and both total and myofibrillar degradation rates, in the presence and absence of exogenous PTH and/or insulin. The addition of PTH either in the presence or absence of insulin had no effect on glucose uptake, protein synthesis or degradation or amino acid release by peripheral muscle tissue. Measurement of PTH revealed that 84% of the initial dose of immunoreactive hormone was still present at the end of the perfusion period. Our results suggest that PTH has no effect on skeletal muscle glucose or protein metabolism.
Wassner
S J
SJ
Li
J B
JB
D000409:Alanine / Q000378:metabolism; D000818:Animals; D005947:Glucose / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006801:Humans; D006962:Hyperparathyroidism, Secondary / Q000209:etiology / Q000378:metabolism*; D007328:Insulin / Q000494:pharmacology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism; D008297:Male; D009124:Muscle Proteins / Q000378:metabolism; D009132:Muscles / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000378:metabolism* / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D009124:Muscle Proteins; D010281:Parathyroid Hormone; D005973:Glutamine; D005947:Glucose; D000409:Alanine