Increase of glucagon receptors in hyperthyroidism

Abstract

THYROID hormones influence the lipolytic response of rat adipocytes to adrenaline, glucagon, ACTH and TSH1,2. Krishna, Hynie and Brodie3 provided evidence that hyperthyroidism is followed by an increase in the nor-adrenaline-sensitive adenylate cyclase without any change in phosphodiesterase activity. Subsequent investigations have shown that adenylate cyclase activity measured as fluoride stimulated activity is unchanged in hyperthyroidism4 and confirmed that phosphodiesterase activity is normal4,5. Since the amount of hormone-sensitive lipase does not appear to be increased in hyperthyroidism3 these studies indicate an action of thyroid hormones either on the hormone receptors for lipolytic hormones or on the transmission of the hormonal message from the receptors to adenylate cyclase. This prompted the present study in which we found that hyperthyroidism was associated with an increased binding of glucagon to fat cells as well as increased glucagon stimulated production of cyclic AMP and glycerol.

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