In the 1981 study, investigators incubated human adipocytes or their cell membranes from fat near the abdominal lining with epinephrine. They combined detection of bound ligands by radioactive decay with biochemical readouts: adenylyl cyclase activity, cAMP and released glycerol. Blocking alpha-2 adrenergic receptors increased the epinephrine response; blocking alpha-1 adrenergic receptors did not. A separate labeled-phosphate incorporation readout in a phospholipid showed the reverse blocker sensitivity. Thus the comparisons separated response branches.[ref]
Pharmacological Characterizations of Adrenergic Receptors in Human Adipocytes by Thomas W. Burns and others. Abstract, first through fourth paragraphs: human properitoneal preparations, radioligand binding, biochemical readouts; yohimbine versus prazosin comparisons
The glycerol readout indicates lipolysis, rather than directly measuring whole-body fuel use. Isolated adipocytes omit circulation and nervous input; blocker selectivity also limits the inference. These comparisons support receptor-specific responses in that preparation, not identical behavior in all biological cells.
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