Astrocytes play a key role in brain functioning by providing energy to neurons. Increased astrocytic mitochondrial functions by Korean red ginseng extract (KRGE) have been investigated in previous studies. KRGE administration induces hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in astrocytes in the adult mouse brain cortex. VEGF expression can be controlled by transcription factors, such as the HIF-1α and estrogen-related receptor α (ERRα). However, the expression of ERRα is unchanged by KRGE in astrocytes of the mouse brain cortex. Instead, sirtuin 3 (SIRT3) expression is induced by KRGE in astrocytes. SIRT3 is a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase that resides in the mitochondria and maintains mitochondrial homeostasis. Mitochondrial maintenance requires oxygen, and active mitochondria enhance oxygen consumption, resulting in hypoxia. The effects of SIRT3 on HIF-1α-mediated mitochondria functions induced by KRGE are not well established. We aimed to investigate the relationship between SIRT3 and HIF-1α in KRGE-treated normoxic astrocyte cells. Without changing the expression of the ERRα, small interfering ribonucleic acid targeted for SIRT3 in astrocytes substantially lowers the amount of KRGE-induced HIF-1α proteins. Reduced proline hydroxylase 2 (PHD2) expression restores HIF-1α protein levels in SIRT3-depleted astrocytes in normoxic cells treated with KRGE. The translocation of outer mitochondrial membranes 22 (Tom22) and Tom20 is controlled by the SIRT3-HIF-1α axis, which is activated by KRGE. KRGE-induced Tom22 increased oxygen consumption and mitochondrial membrane potential, as well as HIF-1α stability through PHD2. Taken together, in normoxic astrocytes, KRGE-induced SIRT3 activated the Tom22–HIF-1α circuit by increasing oxygen consumption in an ERRα-independent manner.
Background: Nonalcoholic fatty liver disease dramatically improves after bariatric surgery, primarily due to improvements in hepatic insulin sensitivity. Since the procedure for gastric cancer surgery is very similar to that for bariatric surgery, we investigated changes in fatty liver following gastrectomy for gastric cancer according to the type of surgery.Methods: We evaluated hepatic steatosis in 212 early gastric cancer patients using Hounsfield units (HUs) on non-contrast computed tomography preoperatively and 6, 12, and 24 months after surgery. We compared the preoperative and postoperative liver-to-spleen HU ratio according to the type of surgery: Billroth I, Billroth II, and total gastrectomy with Roux-en-Y reconstruction. Results: The initial results (liver/spleen HUs and the liver-to-spleen HU ratio) did not significantly differ according to surgical group. After surgery, only patients who underwent total gastrectomy with Roux-en-Y exhibited significant changes in the liver-to-spleen HU ratio at 6 months. In 26 patients who had higher initial HU levels of the spleen than the liver, the liver-to-spleen HU ratio significantly increased from 0.836 to 1.115 at 6 months, 1.109 at 12 months, and 1.102 at 24 months (P<0.01). Conclusion: Significant changes in hepatic steatosis were found in even normal patients (with higher liver than spleen HU values) who underwent total gastrectomy with Roux-en-Y. Patients who initially had fatty liver also showed a significant increase in the liver-to-spleen HU ratio. These results suggest that total gastrectomy with Roux-en-Y reconstruction can have a positive effect on the improvement of hepatic steatosis.
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