Diabetes
Back to the scientific study index...

A study describing how carnitine may benefit the heart function of diabetics.

[5-13]

Propionyl-L-carnitine effects on postischemic recovery of heart function and substrate oxidation in the diabetic rat

Broderick TL, Driedzic W, Paulson DJ.

Midwestern University, Department of Physiology, Glendale, Arizona 85308, USA.

Previous studies have shown that propionyl-L-carnitine (PLC) can exert cardiac antiischemic effects in models of diabetes. In the nonischemic diabetic rat heart, PLC improves ventricular function secondary to stimulation in the oxidation of glucose and palmitate. Whether this increase in the oxidation of these substrates can explain the beneficial effects of PLC in the ischemic reperfused diabetic rat heart has yet to be determined. Diabetes was induced in male Sprague-Dawley rats by an intravenous injection of streptozotocin (60 mg/kg). Treatment was initiated by supplementing the drinking water with propionyl-L-carnitine at the concentration of 1 g/L. After a 6-week treatment period, exogenous substrate oxidation and recovery of mechanical function following ischemia were determined in isolated working hearts. In aerobically perfused diabetic hearts, compared with those of controls, rates of glucose oxidation were lower, but those of palmitate oxidation were similar. Diabetes was also characterized by a pronounced decrease in heart function. Following treatment with by propionyl-L-carnitine, however, there was a marked increase in rates at which glucose and palmitate were oxidized by diabetic hearts and a significant improvement in heart performance. Postischemic recovery of function in diabetic hearts was also improved with PLC. This improvement in contractile function was accompanied by an increase in both glucose and palmitate oxidation. Our findings show that postischemic diabetic rat heart function can be improved following chronic PLC treatment. This beneficial effect of propionyl-L-carnitine can be explained, in part, by an improvement in the oxidation of glucose and palmitate.

++++++++++++

This paper describes why everyone who takes a statin drug--no if's, ands or buts--MUST also then take CoQ10.

Frankly, we cannot understand why all doctors who prescribe them do not tell their patients about this.

It's also good to remember the reason WHY the patient was prescribed a statin: heart disease or diabetes. Both these disease processes produce conditions which deplete, and therefore require supplementation of, CoQ10.

[4-17]

Proc. Natl. Acad. Sci. USA

Vol. 87, pp. 8931-8934, November 1990

Medical Sciences

Lovastatin decreases coenzyme Q levels in humans

(hypercholesterolemia/3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors/ubiquinone/drug side effects)

Karl Folkers*1\ Per Langsjoen*, Richard Willis*, Phillip Richardson*, Li-Jun Xia*, Chun-Qu Ye*,

AND HlROO TAMAGAWA*

'University of Texas at Austin, Austin, TX 78712; and *The Health Center at Tyler, The University of Texas at Tyler, Tyler, TX 75710

Contributed by Karl Folkers, June 20, 1990

ABSTRACT       Lovastatin is clinically used to treat patients with hypercholesterolemia and successfully lowers cholesterol levels. The mechanism of action of lovastatin is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. Inhibition of this enzyme could also inhibit the intrinsic bio­synthesis of coenzyme Q_lo (CoQ₁₀), but there have not been definitive data on whether lovastatin reduces levels of CoQ₁₀ as it does cholesterol. The clinical use of lovastatin is to reduce a risk of cardiac disease, and if lovastatin were to reduce levels of CoQio, this reduction would constitute a new risk of cardiac disease, since it is established that CoQio is indispensable for cardiac function. We have conducted three related protocols to determine whether lovastatin does indeed inhibit the biosyn­thesis of CoQ₁₀. One protocol was done on rats, and is reported in the preceding paper [Willis, R. A., Folkers, K., Tucker, J. L., Ye, C.-Q., Xia, L.-J. & Tamagawa, H. (1990) Proc. Natl. Acad. Sci. USA 87, 8928-8930]. The other two protocols are reported here. One involved patients in a hospital, and the other involved a volunteer who permitted extraordinary mon­itoring of CoQio and cholesterol levels and cardiac function. All data from the three protocols revealed that lovastatin does indeed lower levels of CoQ₁₀. The five hospitalized patients, 43-72 years old, revealed increased cardiac disease from lovastatin, which was life-threatening for patients having class IV cardiomyopathy before lovastatin or after taking lovastatin. Oral administration of CoQ₁₀ increased blood levels of CoQ₁₀ and was generally accompanied by an improvement in cardiac function. Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presum­ably can be caused by the lovastatin-induced deficiency of CoQ₁₀.

+++++++++++++

there are osther studies like the above., find them.