Abstract
To determine whether the oxidation of long-chain fatty acids (LCFA) derived from renal tissue lipids can support renal function, we perfused isolated rat kidneys with a substrate-free Krebs-Ringer bicarbonate solution containing 6 g/100 ml substrate-free (defatted) albumin. We measured GFR, TNa+, and Qo2 at 7-min intervals from 15 to 99 min after cannulation of the renal artery. Two groups (A and B) of 12 perfusions each were done. During substrate-free perfusion mean %TNa+ was low (A = 45 +/- 2%, B = 62 +/- 5%). When 10(-4) M 2-tetradecylglycidic acid (2-TDGA), a specific and irreversible inhibitor of long-chain acylcarnitine transferase-I, was added to the substrate-free perfusate, significant decreases in %TNa+ (A to approximately 25%; B to approximately 35%) and in Qo2 (delta = -25%) occurred. During perfusion with either 5 mM lactate or 5 mM alpha-ketoglutarate (alpha-KG) %TNa+ increased to approximately 80%. When 2-TDGA was added in the presence of lactate or of alpha-KG no decrease in %TNa+ or Qo2 occurred. Thus, 2-TDGA does not inhibit net renal Na+ transport or O2 uptake in the presence of high concentrations of lactate or alpha-KG, substrates not requiring long-chain acylcarnitine transferase for their utilization. We conclude that oxidation of LCFA released from renal tissue lipids can support a significant portion of Na+ reabsorption.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
