AJP - Renal Physiology, Vol 244, Issue 3 235-F246, Copyright © 1983 by American Physiological Society
Support of kidney function by long-chain fatty acids derived from renal tissue
M. C. Fonteles, J. J. Cohen, A. J. Black and S. J. Wertheim
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.
