RELATIONSHIP BETWEEN LIPOLYSIS AND CALCIUM IN EPIDIDYMAL ADIPOSE-TISSUE OF OBESE-HYPERGLYCEMIC MICE

In the epididymal adipose tissue of lean (+/+) C57BL/6J mice deprived of Ca by ethyleneglycol-bis(.beta.-aminoethylether) N,N''-tetraacetic acid (EGTA) treatment, ACTH-(1-24)-tetracosapeptide (ACTH)-stimulated lipolysis was abolished and peak levels of cyclic[c]AMP were reduced by 80%. Ca omission was less effective on isoproterenol-stimulated lipolysis and was ineffective on theophylline- or dibutyryl cAMP-stimulated lipolysis. All EGTA effects were reversible. Lipolytic agents stimulated the net uptake of 45Ca. This effect was inhibited by 2,4-dinitrophenol. The 45Ca accumulated in response to lipolytic agents was largely La3+-nondisplaceable and was released with a half-life of 13 min under EGTA treatment. The mechanism promoting 45Ca uptake in response to lipolytic agents was apparently beyond cAMP production in the adipose tissue of lean mice, but independent of free fatty acid release. In turn, intracellular as well as extracellular Ca facilitated maximal rates of lipolysis. In the adipose tissue of obese-hyperglycemic (ob/ob) mice, the response to the lipolytic agents of glycerol release and cAMP levels was reduced by 65% and 45Ca uptake was not stimulated. A 1-2 h preincubation of adipose tissue markedly increased the effect upon lipolysis and 45Ca uptake, but not that of peak cAMP levels of isoproterenol. The adipose tissue of ob/ob mice displayed a reversible impairment of 45Ca uptake in response to lipolytic agents.