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Citrin is a liver-specific mitochondrial aspartate&#8722;glutamate carrier encoded by <i>SLC25A13</i>. Citrin deficiency caused by <i>SLC25A13</i> mutation results in carbohydrate toxicity, citrullinemia type II, and fatty liver diseases, the mechanisms of some of which remain unknown. Citrin shows a functional homolog in yeast aspartate-glutamate carrier (Agc1p) and <i>agc1</i>&#916; yeasts are used as a model organism of citrin deficiency. Here, we found that <i>agc1</i>&#916; yeasts decreased fat utilization, impaired NADH balance in peroxisomes, and decreased chronological lifespan. The activation of <i>GPD1</i>-mediated NAD⁺ regeneration in peroxisomes by <i>GPD1</i> over-expression or activation of the malate&#8722;oxaloacetate NADH peroxisomal shuttle, by increasing flux in this NADH shuttle and over-expression of <i>MDH3</i>, resulted in lifespan extension of <i>agc1</i>&#916; yeasts. In addition, over-expression of <i>PEX34</i> restored longevity of <i>agc1</i>&#916; yeasts as well as wild-type cells. The effect of <i>PEX34</i>-mediated longevity required the presence of the <i>GPD1</i>-mediated NADH peroxisomal shuttle, which was independent of the presence of the peroxisomal malate&#8722;oxaloacetate NADH shuttle and <i>PEX34</i>-induced peroxisome proliferation. These data confirm that impaired NAD⁺ regeneration in peroxisomes is a key defect in the yeast model of citrin deficiency, and enhancing peroxisome function or inducing NAD⁺ regeneration in peroxisomes is suggested for further study in patients&#8217; hepatocytes.