Me. Christe et Rl. Rodgers, CARDIAC GLUCOSE AND FATTY-ACID OXIDATION IN THE STREPTOZOTOCIN-INDUCED DIABETIC SPONTANEOUSLY HYPERTENSIVE RAT, Hypertension, 25(2), 1995, pp. 235-241
Hypertension intensifies the cardiac dysfunction of diabetes. We inves
tigated the possible role of altered exogenous fuel oxidation in this
phenomenon. Diabetes was induced by streptozotocin in spontaneously hy
pertensive rats and normotensive Sprague-Dawley rats. Two weeks later,
mechanical performance and the oxidation of glucose and palmitate wer
e quantified in working hearts ex vivo at intermediate and high worklo
ads. The results showed that the nondiabetic spontaneously hypertensiv
e rat hearts, compared with those of the normotensive controls, oxidiz
ed glucose at a higher rate but oxidized palmitate at a much lower rat
e, as reported previously. The effects of diabetes in the hypertensive
rats, compared with its effects in the normotensive strain, were char
acterized by (1) a more pronounced decrease in heart performance, (2)
either a similar or a less marked reduction in the rate of glucose oxi
dation, depending on the workload, and (3) a relatively greater increa
se in palmitate oxidation, particularly at the higher workload. These
findings suggest that the exaggerated stimulation of fatty acid oxidat
ion by diabetes in the hypertrophic left ventricle may be a more impor
tant contributor to the premature mechanical dysfunction than the inhi
bition of glucose oxidation. Possible mechanisms include antagonism of
energetically favorable shifts in fuel oxidation or inhibition of acc
elerated membrane lipid biosynthesis in left ventricular hypertrophy.