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Obese Obese Obese Vehicle 10 mg/kg 30 mgfUg Control ALA ALA

Obese Obese Obese Vehicle 10 mg/kg 30 mg/kg Control ALA ALA

Obese Obese Obese Vehicle 10 mg/kg 30 mg/kg Control ALA ALA

Figure 3 Areas under the curve (AUC) for the glucose and insulin responses to an oral glucose tolerance test in control and chronic lipoate-treated obese Zucker rats. The glucose-insulin index represents the product of the glucose AUC and the insulin AUC. Values are means ± SE. *p < 0.05 vs. obese vehicle-treated control.

Figure 4 Effect of chronic treatment of obese Zucker rats with lipoate on in vitro insulin-stimulated glucose transport activity in the isolated epitrochlearis muscle. □, Basal 2-deoxyglucose uptake; ■, increase in 2-deoxyglucose uptake due to insulin (2 mU/mL). This increase is shown in the box for each bar. Values are means ± SE. *p < 0.05 vs. 0 mg/kg lipoate.

a-Lipoic Acid (mg/kg/day)

Figure 4 Effect of chronic treatment of obese Zucker rats with lipoate on in vitro insulin-stimulated glucose transport activity in the isolated epitrochlearis muscle. □, Basal 2-deoxyglucose uptake; ■, increase in 2-deoxyglucose uptake due to insulin (2 mU/mL). This increase is shown in the box for each bar. Values are means ± SE. *p < 0.05 vs. 0 mg/kg lipoate.

ameliorate the oxidant/antioxidant imbalance in this condition will be helpful in improving peripheral insulin action on glucose transport and metabolism in skeletal muscle. Indeed, several animal model and clinical investigations support the beneficial effects of antioxidants, particularly lipoic acid, in the diabetic state.

Ample evidence now exists in the literature indicating that one locus of action of lipoic acid in improving metabolic control in animal models of insulin resistance is at the level of the skeletal muscle itself. Chronic treatment of the streptozotocin-diabetic rat, a model of type 1 diabetes, leads to a reduction in blood glucose that is associated with an increase in muscle GLUT4 protein expression and insulin-stimulated muscle glucose transport. Likewise, chronic treatment of obese Zucker rats, an animal model of the insulin resistance syndrome, with lipoic acid enhances whole body glucose tolerance and is associated with significant improvements in insulin action on skeletal muscle glu

Figure 5 Effect of chronic treatment of obese Zucker rats with lipoate on in vitro insulin-stimulated glucose transport activity in the isolated soleus muscle strips. □, basal 2-deoxyglucose uptake; increase in 2-deoxyglucose uptake due to insulin (2 mU/mL). This increase is shown in the box for each bar. Values are means ± SE. *p< 0.05 vs. 0 mg/kg lipoate.

a-Lipoic Acid (mg/kg/day)

Figure 5 Effect of chronic treatment of obese Zucker rats with lipoate on in vitro insulin-stimulated glucose transport activity in the isolated soleus muscle strips. □, basal 2-deoxyglucose uptake; increase in 2-deoxyglucose uptake due to insulin (2 mU/mL). This increase is shown in the box for each bar. Values are means ± SE. *p< 0.05 vs. 0 mg/kg lipoate.

cose transport and metabolism, and with reductions in plasma insulin and free fatty acids.

There are, however, areas where our knowledge of lipoic acid action on metabolism is incomplete. For example, we still need more information on the underlying molecular mechanism(s) responsible for the lipoic acid-induced improvement in insulin action. Some limited evidence indicates that there may be some interaction between lipoic acid and the insulin signaling cascade in the L6 muscle cell line (46) and in isolated muscle from the Zucker rat (47); however, a more complete characterization of this interaction in skeletal muscle is necessary. In addition, the relationship between lipoic acid action on skeletal muscle metabolism and its effects on cell oxidant/antioxidant status need to be more thoroughly investigated. It is clear that although investigations of the metabolic actions of lipoic acid have yielded much important information over the last few years, there is still much more work to be done

□ Obese Vehicle ■ Obese 10 m g/kg ALA ^ Obese SO rag/kg ALA

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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