*3*.*7*. *Total AA Levels in the Plasma and Cortex*

To determine whether the changes in expression levels of SVCT2 and GLUT1 induced by AA supplementation or by MCAO/Re affect the concentrations of AA in the cortex, we measured total AA (AA + DHA) levels in the plasma and cortex of the experimental groups (Figure 10). It has been indicated that reduction of DHA to AA or decomposition of DHA to 2,3-diketo-1-gulonic acid is rapid in the plasma and brain, and that the concentrations of DHA in these tissues are 0%–2% of AA [19]. Therefore, total AA levels are considered to almost equal to the AA levels. The plasma of the sham-operated diabetic control rats had a significant smaller amount of total AA levels compared with the nondiabetic rats (Figure 10A). AA supplementation restored the decrement of the total AA levels in the diabetic rats to almost the same levels as those in the nondiabetic control rats. MCAO/Re had little effect on the total AA levels in the plasma of all groups. In contrast, neither diabetic state nor AA supplementation affected the total AA levels in the cortex of sham-operated groups. MCAO/Re significantly decreased the total AA levels both in the nondiabetic and diabetic cortex. AA supplementation to the diabetic rats caused a significant increase in the total AA levels in the cortex in response to MCAO/Re.

**Figure 10.** Effects of AA supplementation on levels of total AA (AA + DHA) in the plasma and cortex of nondiabetic and diabetic rats. Total AA (AA + DHA) levels in the plasma (**A**) and cortex (**B**) measured in nondiabetic and diabetic rats after MCAO/Re. The data are presented as mean ± SD (*n* = 3–6). \* *p* < 0.05, \*\* *p* < 0.01.
