Hormone-dependent lipolysis in fat-cells from thyroidectomized rats

Decreased secretin and glucagon responsiveness of adenylate cyclase in cardiac membranes from hypothyroid rats

“…adenylate cyclase activity ( fig.2), These effects were observed as early as 10 days after tbyroidectomy in the second experiment. In line with these data, reduced glucagon-stimulated adenylate cyclase activity has been reported in fat cells [ 13] and liver membranes together with a lower density of glucagon receptors in liver membranes [14] in thyroidectomized rats. The latter result was, however, not confirmed in [ 15].…”

Thyroid hormone control of cyclic nucleotide phosphodiesterases and the regulation of the sensitivity of the liver to hormones

“…The changes in CAMP-and cGMP-phosphodiesterases in the liver of thyroidectomized rats reported here, parallel those found in adipose tissue in this condition as reported [6][7][8][9]151. The similarity between these results on different tissues perhaps points to a unifying hypothesis for the action of thyroid hormone on two major insulin-and glucagon-responsive tissues, liver and adipose tissue.…”

“…The remarkable parallelism between changes in hepatic and adipose tissue enzymes related to glucose oxidation and lipid synthesis was also emphasized by Bacquer et al [lo] . Further, there is substantial evidence that both liver and adipose tissue from thyroidectomized rats exhibit changes which can be attributed to a glucagon-insensitive state, namely, in liver, a decreased rate of gluconeogenesis, as shown by studies with perfused liver presented with lactate as substrate [ 191 and by changes in key gluconeogenic enzymes, pyruvate carboxylase and phosphoenolpyruvate carboxykinase [ 161 and, in adipose tissue, by a decreased lipolytic response to glucagon and epinephrine [6][7][8][9]151. Thyroidectomy, and the accompanying rise in the potential rate of hydrolysis of CAMP and cGMP, could effectively counteract the signals received at the plasma cell membrane from insulin (with the associated rise in cGMP) and glucagon (with the associated rise in CAMP) in both liver and adipose tissue and, in this sense, thyroid hormone could exert a 'permissive' role in insulin and glucagon action.…”

Sensitivity of adipocyte lipolysis to stimulatory and inhibitory agonists in hypothyroidism and starvation

“…Receptors for the inhibitory agonists are coupled to adenylate cyclase by a guanine nucleotide-binding protein (N1) distinct from that (N.) which couples receptors for stimulatory agonists to the enzyme (Rodbell, 1980;Murayama & Ui, 1983;Olansky et al, 1983;Moreno et al, 1983;Bokoch et al, 1984;Codina et al, 1984). In hypothyroidism adenylate cyclase, the increase in cyclic AMP, and lipolysis all show diminished responsiveness to the stimulatory agonists (Goodman & Bray, 1966;Armstrong et al, 1974;Correze et al, 1974;Malbon et al, 1978;Ohisalo & Stouffer, 1979;Goswami & Rosenberg, 1980). Conversely, the inhibitory effect of adenosine mediated by the A1 (Van Calker et al, 1979) or Ri (Londos et al, 1980) adenosine receptor is increased in hypothyroidism (Ohisalo & Stouffer, 1979;Malbon & Graziano, 1983;Chohan et al, 1984;Malbon et al, 1985).…”