2002
DOI: 10.1152/ajpendo.00485.2001
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Glitazones regulate glutamine metabolism by inducing a cellular acidosis in MDCK cells

Abstract: -We studied the effect of the antihyperglycemic glitazones, ciglitazone, troglitazone, and rosiglitazone, on glutamine metabolism in renal tubule-derived Madin-Darby canine kidney (MDCK) cells. Troglitazone (25 M) enhanced glucose uptake and lactate production by 108 and 92% (both P Ͻ 0.001). Glutamine utilization was not inhibited, but alanine formation decreased and ammonium formation increased (both P Ͻ 0.005). The decrease in net alanine formation occurred with a change in alanine aminotransferase (ALT) re… Show more

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Cited by 18 publications
(39 citation statements)
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“…Therefore, depending on the concentration and physiologic conditions, the antitumorigenic action of TRO appears to involve both PPAR␥ and PPAR␥-independent pathways. Another apparent PPAR␥-independent action that may play an anticancer role is the ability of TRO to induce cellular acidosis, which we have demonstrated previously in normal cells (35)(36)(37). Our previous findings are consistent with glitazones inducing a spontaneous cellular acidosis associated with a shift in glutamine amino nitrogen metabolism from a predominantly anabolic to a catabolic pathway in canine mesangial cells (35).…”
Section: Introductionsupporting
confidence: 89%
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“…Therefore, depending on the concentration and physiologic conditions, the antitumorigenic action of TRO appears to involve both PPAR␥ and PPAR␥-independent pathways. Another apparent PPAR␥-independent action that may play an anticancer role is the ability of TRO to induce cellular acidosis, which we have demonstrated previously in normal cells (35)(36)(37). Our previous findings are consistent with glitazones inducing a spontaneous cellular acidosis associated with a shift in glutamine amino nitrogen metabolism from a predominantly anabolic to a catabolic pathway in canine mesangial cells (35).…”
Section: Introductionsupporting
confidence: 89%
“…We also assess the ability of TRO-induced acidosis to inhibit DNA synthesis in a dosedependent manner and partially independent from PPAR␥ activation. Our results present a novel action of TRO as an antiproliferative compound that broadens the spectrum of various PPAR␥-independent effects described previously (35)(36)(37).…”
Section: Introductionsupporting
confidence: 63%
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