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1 Diabetes and Metabolism Unit, Evans Department of Medicine and Department of Physiology, Boston University Medical Center, Boston, Massachusetts 02118; 2 Garvan Institute of Medical Research, St. Vincent's Hospital, Sydney, New South Wales 2010, Australia; 3 Diabetes and Nutrition Research Group, Institute of Experimental Endocrinology, Slovak Academy of Sciences, 83306 Bratislava, Slovak Republic; and 4 Department of Biochemistry, Hebrew University, Hadassah Medical School, Jerusalem 91120, Israel
In liver, insulin
and glucose acutely increase the concentration of malonyl-CoA by
dephosphorylating and activating acetyl-CoA carboxylase (ACC). In
contrast, in incubated rat skeletal muscle, they appear to act by
increasing the cytosolic concentration of citrate, an allosteric
activator of ACC, as reflected by increases in the whole cell
concentrations of citrate and malate [Saha, A. K., D. Vavvas, T. G. Kurowski, A. Apazidis, L. A. Witters, E. Shafrir, and N. B. Ruderman. Am. J. Physiol. 272 (Endocrinol. Metab. 35):
E641-E648, 1997]. We report here that sustained increases in
plasma insulin and glucose may also increase the concentration of
malonyl-CoA in rat skeletal muscle in vivo by this mechanism. Thus 70 and 125% increases in malonyl-CoA induced in skeletal muscle by
infusions of glucose for 1 and 4 days, respectively, and a twofold
increase in its concentration during a 90-min
euglycemic-hyperinsulinemic clamp were all associated with significant
increases in the sum of whole cell concentrations of citrate and/or
malate. Similar correlations were observed in muscle of the
hyperinsulinemic fa/fa rat, in
denervated muscle, and in muscle of rats infused with insulin for 5 h.
In muscle of 48-h-starved rats 3 and 24 h after refeeding, increases in
malonyl-CoA were not accompanied by consistent increases in the
concentrations of malate or citrate. However, they were associated with
a decrease in the whole cell concentration of long-chain fatty acyl-CoA
(LCFA-CoA), an allosteric inhibitor of ACC. The results suggest that
increases in the concentration of malonyl-CoA, caused in rat muscle in
vivo by sustained increases in plasma insulin and glucose or
denervation, may be due to increases in the cytosolic concentration of
citrate. In contrast, during refeeding after starvation, the increase
in malonyl-CoA in muscle is probably due to another mechanism.
acetyl-coenzyme A carboxylase; malate; insulin resistance; hyperglycemia; hyperinsulinemia; glucose sensing
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