Ca2+ and glucose uptake in adipocytes: evidence for biological activity of a Ca2+-palmitate complex

A tightly bound form of Ca2+ in serum, thought to be a Ca2+-fatty acid complex, has been reported to cause accelerated Ca2+ uptake in bone cells. The authors therefore studied the effect of palmitic acid on Ca2+ accumulation and its influence on glucose transport in adipocytes. They assessed 45Ca2+ and 14C-D-glucose uptake into rat adipocytes from solutions containing: 4% (w/v) fatty acid-free albumin, 2.5 mM CaCl2 (free [Ca2+]=1.30 mM), 140 mM NaCl, 3 mM Na phosphate, 1.4 mM MgSO4, 5 mM D-glucose, 5 mM HEPES, pH 7.4 at 370C with and without 4 mM palmitate. Ca2+ was taken up by both rapid (< 30 sec), and slow (reaching steady state within 20 min) cellular accumulation phases. Palmitate increased the rapid binding phase of 45Ca2+ uptake from 2.10 +/- 0.13 to 3.03 +/- 0.16 fmol Ca2+/cell and caused a 2 to 3-fold increase in the slow phase. Palmitate also increased glucose uptake by a mean of 225% above control. This increase was eliminated by a 15 min preincubation with the intracellular Ca2+ chelator, quin 2-AM (50 μM), implying that increased Ca2+ uptake was related to increased glucose transport. They conclude that the Ca2+-palmitate complex enhances Ca2+ uptake, which may be related to an increased ability for adipocytes to transport glucose. The Ca2+-palmitate complex may therefore represent a biologically active form of Ca2+