Abstract
Serum albumin stimulates the uptake of U-glucose-(14)C and the incorporation of (14)C-counts into triglyceride glycerol and inhibits the incorporation of (14)C-counts into triglyceride fatty acids by isolated adipose cells; insulin and epinephrine enhance these effects. In the absence of hormones, these responses to albumin increase with increasing albumin concentration. In the presence of insulin, a qualitatively similar pattern of increasing responses to albumin is observed; the enhancement of each response by insulin is, however, only slightly potentiated by higher albumin concentrations. In contrast, in the presence of epinephrine, these responses to albumin are maximal at the lowest albumin concentration tested, 0.1%; the enhancement of each response by epinephrine is similarly maximal at 0.1% albumin, but decreases rapidly as the albumin concentration is raised. Increasing serum albumin concentrations do, however, stimulate the release of fatty acids and glycerol by epinephrine-treated cells increasingly until a plateau, determined by the epinephrine dose, is reached. These data support the suggestion that intracellular fatty acid levels function in the regulation of adipose cell activity, and further suggest that serum albumin plays a role in determining the metabolic fate of these fatty acids.
MeSH Terms
Adipose Tissue/drug effects,metabolism
Animals
Carbon Dioxide/biosynthesis
Carbon Isotopes
Epinephrine/pharmacology
Fatty Acids, Nonesterified/metabolism
Glucose/metabolism
Glycerol/metabolism
Insulin/pharmacology
Lipids/analysis
Rats
Serum Albumin, Bovine/pharmacology
Chemicals
Carbon Isotopes
Fatty Acids, Nonesterified
Insulin
Lipids
Carbon Dioxide
Serum Albumin, Bovine
Glucose
Glycerol
Epinephrine
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Cushman S W
Rizack M A
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