Effect of the extract of Ginkgo biloba (EGb 761) on the circulating and cellular profiles of polyunsaturated fatty acids: correlation with the anti-oxidant properties of the extract.

Ginkgo biloba extract (EGb 761) has beneficial effects on cognitive functions in aging patients, and on various pathologies, including cardiovascular diseases. Although the extract is known to have antioxidant properties and improve membrane fluidity, the cellular mechanisms underlying these effects have not been determined. Here, we examined the in vivo effects of EGb 761 on circulating and cellular lipids. EGb 761 treatment induced significant increases in the levels of circulating polyunsaturated fatty acids (PUFAs), and a decrease in the saturation index SI (saturated/polyunsaturated species). Plasma triglycerides and cholesterol were not affected, while phospholipids were slightly increased at the higher dose of EGb 761. EGb 761 treatment also induced a significant increase in the levels of PUFAs in erythrocyte membranes, especially for the eicosapentaenoic acid (EPA omega 3), and a decrease in the saturation index. Moreover, the response of erythrocytes to oxidative stress was improved in EGb 761-treated animals (H(2)O(2)-induced cell lysis decreased by 50%). Considering that PUFAs are known to improve membrane fluidity and response to oxidative damage, and are precursors of signaling molecules such as prostaglandins, the effects of EGb 761 on circulating and cellular PUFAs may explain some of the pharmacological properties of Ginkgo biloba.

Demonstration of defective glucose uptake and storage in erythrocytes from non-insulin dependent diabetic patients and effects of metformin.

1. Red blood cells can store glucose and may thus participate in blood glucose homeostasis. We investigated if a defect in this process exists in non-insulin dependent diabetes (NIDD). 2. Blood was obtained in fasting conditions from 10 normal and 10 newly diagnosed NIDD patients (before and after 4 weeks Metformin therapy). Washed erythrocytes were resuspended in media containing various glucose concentrations (4.4, 6.6, 8.8 and 13.2 mmol/L). Total glucose uptake was calculated as the sum of the measurements of lactate as well as free glucose, the latter being determined before and after addition of amyloglucosidase to the pellet. 3. Cells from diabetics showed a pronounced reduction in glucose uptake, particularly in their capacity to store glucose as glycogen (reactive to amyloglucosidase). Metformin treatment almost normalized glycogen levels, whereas lactate declined concomitantly in the pellet. 4. Our data demonstrate that a defect in glucose uptake exists in erythrocytes from NIDD patients, affecting both free and stored glucose, and that this defect is reversed by Metformin treatment, indicating that this drug can increase glycogen levels even in insulin-insensitive cells. 5. Thus, in view of their total mass, erythrocytes may be important in the impaired glucose homeostasis in NIDD, in particular in marked hyperglycaemia such as after a meal.

Erythrocyte glucose consumption in insulin-dependent diabetes: effect of metformin in vitro.

Erythrocyte glucose consumption in red blood cells from healthy donors or insulin-dependent diabetics with stable glycemia was measured using the 2-deoxyglucose technique. Data showed that the formation of glucose-6P was severely impaired in diabetic red blood cells in both normo- and hyperglycemic incubation conditions. This defect seems to be inherent to the disease. Coincubation with Metformin (6.4 ug/ml) did not modify the G6P levels in RBCs from healthy donors and in RBCs from diabetics when incubated in normoglycemic conditions. However, when diabetics RBCs were incubated in a hyperglycemic medium, addition of Metformin strongly improved the intracellular levels of G6P. The underlying mechanism for the defect and the correction by Metformin remains to be determined. This study shows that also red blood cells may be involved in the failure of glucose homeostasis in diabetes and thus this may represent an additional target for therapy.

[Changes in erythrocyte deformability in Alzheimer's disease]. / Modification de la déformabilité érythrocytaire dans la maladie d'Alzheimer.

In a previous work we showed an alteration of erythrocyte filtration ability in patients with Alzheimer's disease according to their age and illness duration. This study has for aim to find a criteria of deformability that would be constant in all Alzheimer patients and would show a modification of red cell membranes. The erythrocyte filterability was studied in this present paper, in accord to Reid and Dormandy method using two values of depression (5 and 0 cm of water). These depressions correspond to the physiological values of blood pressure at the level of precapillary and capillary systems. The ratio between the result obtained at 5 cm and the result at 0 cm is constant in normal patient without organic disease and it is independent of age. At the opposite, this ratio increase very significantly in all Alzheimer patients, and this is not correlated to the initial value of filtrability. This ratio could be an index of the alteration of red cell membranes.