Endotoxicosis modulates cytosolic free calcium and basal and ACTH-stimulated lipolysis in rat adipocytes.
Lipolytic rates and intracellular Ca2+ concentration ([Ca2+]i) were determined under basal conditions and upon stimulation with adrenocorticotropic hormone (ACTH), norepinephrine (NE) and insulin (I), in adipocytes isolated from control and acutely endotoxin (ET)-treated rats (1 mg/100 g body weight, LD50 at 6 h). [Ca2+]i measurements were done using the fluorescent Ca2(+)-indicator Fura-2. NE and ACTH, but not I, produced a marked increase of [Ca2+]i in cells of both control and ET-treated rats. ET treatment elicited a significant increase in [Ca2+]i of resting cells, and enhanced the ACTH effect on this parameter. The changes in lipolytic activity correlated well with changes of [Ca2+]i induced by ACTH. The results indicate that ET-induced alterations in intracellular calcium homeostasis of adipocytes may contribute to the mediation of effects on fat mobilization during endotoxemia.
Spitzer
J A
JA
Department of Physiology, Louisiana State University Medical Center, New Orleans.
Deaciuc
I V
IV
D000273:Adipose Tissue / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000032:analysis / Q000378:metabolism*; D003600:Cytosol / Q000032:analysis / Q000378:metabolism*; D004731:Endotoxins / Q000494:pharmacology*; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006090:Gram-Negative Bacteria; D006706:Homeostasis / Q000187:drug effects; D007328:Insulin / Q000494:pharmacology; D008066:Lipolysis / Q000187:drug effects*; D008297:Male; D008856:Microscopy, Fluorescence; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats
D004731:Endotoxins; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D000324:Adrenocorticotropic Hormone; D002118:Calcium; D009638:Norepinephrine