R-ALA is more potent and supposedly easier for the body to use than regular ALA. I normally use the R-ALA even though it is a lot more expensive than the other.
The polyol pathway is known as the primary cause of cataractogenesis in diabetes. Lipoic acid can exert protective effects in different ways. The reduction of R-lipoic acid by lipoamide re-ductase depends on NADH. Accordingly, intramitochondrial reduction of R-lipoic acid can alleviate NADH surplus in diabetes. In a model of glucose-induced lens opacity in vitro, stereospecific protection by lipoic acid was observed. Although R-lipoic acid completely protected the lens, addition of racemic lipoic acid decreased damage only by about one-half, whereas S-lipoic acid potentiated deterioration of the lens.
Insulin resistance is typical for type II diabetes. Therapeutic intervention to enhance glucose uptake by skeletal muscle is potentially important for the prevention and treatment of non–insulin-dependent diabetes. As early as 1970, lipoic acid was shown to enhance glucose uptake into rat tissues. Subsequently, obese Zucker rats, an animal model of insulin resistance, were used to investigate the effects of acute and chronic intravenous treatments with R,S-lipoic acid on glucose transport in isolated skeletal muscle. Lipoic acid markedly increased net glucose uptake, which was associated with a significant enhancement of glycogen synthesis. This observation was supported by a separate experiment in vitro from the same group showing an increased glucose uptake into muscle from lean (insulin-sensitive) or obese (insulin-resistant) Zucker rats. In the same model, the effect of the individual enantiomers of lipoic acid on glucose disposal, hyperinsulinemia, and dyslipidemia was studied. Obese Zucker rats were treated acutely or chronically by intraperitoneal injection with R- or S-lipoic acid. Acute treatment with R-lipoic acid increased insulin-mediated glucose transport by 64%, whereas the S form showed no significant effect. Chronic R-lipoic acid administration reduced plasma insulin and free fatty acids, whereas S-lipoic acid increased insulin and had no effect on plasma free fatty acids. Further, R-lipoic acid improved insulin-stimulated glycogen synthesis and glucose oxidation. The level of glucose transporter-4 protein was not altered after chronic treatment with R-lipoic acid but was reduced by S-lipoic acid.
The effect of lipoic acid on glucose uptake into heart muscle also has been investigated. Glucose uptake into Langendorff hearts of insulin-resistant Zucker was measured with the [ 14 C] 3-O-methylglucose washout method. Glucose uptake rate increased 1.6-fold with R,S-lipoic acid, 1.8- fold with the R form, and was negatively influenced by the S-enantiomer (-50%).
In the working rat heart during reoxygenation, R-lipoic acid improved aortic flow, reaching 70% of normoxic conditions at nanomolar concentrations, whereas 1 µM of the S form was needed to achieve only 60%. In the same study, R-lipoic acid added to the perfusion medium increased mitochondrial ATP synthesis of the working rat heart, whereas ATP synthesis remained unaltered in response to S-lipoic acid.
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