Dennis A. Popp

TL;DR: It is confirmed that patients with IDDM are, to varying degrees, dependent upon epinephrine-mediated beta-adrenergic mechanisms to promote glucose recovery from hypoglycemia and that the degree of this dependence uponEpinephrine is an inverse function of the residual capacity to secrete glucagon in response to hypoglyCEmia in individual patients.

TL;DR: Oral administration of the relatively selective β1-adrenergic antagonist metoprolol and of the nonselective β-adRenergic antagonist propranolol both impaired recovery from insulin-induced hypoglycemia in patients with IDDM.

TL;DR: In this article, a single active fraction was found to stimulate mitochondrial pyruvate dehydrogenase by activating the phosphatase and not by altering the kinase activity, and the involvement of the kinases in this activation mechanism was eliminated by the fact that, in the presence of ATP, NaF completely blocked the stimu ation of the active fraction, and dichloroacetic acid, akinase inhibitor, was add itive to the stimulation caused by the active fractions.

TL;DR: Insulin treatment of adipocytes increased the amount or activity of a low molecular weight, acid-stable material which, when isolated from intact adipocytes by heat extraction and subsequent Sephadex G25 chromatography, yielded a single active fraction that stimulated mitochondrial pyruvate dehydrogenase by activating the phosphatase and not by altering the kinase activity.

TL;DR: To the extent that the adrenergic receptors and adenylate cyclase activities of circulating cells reflect those of extravascular catecholamine target cells, these data provide no support for a role of physiological variations of testosterone, estradiol, or progesterone in the regulation of catechlamine action in humans.