Determination of the role of insulin in liver regeneration triggered by portal vein ligation

Overview

Portal vein embolization has been applied prior to major hepatectomy for hepatocellular carcinoma, bile duct malignancy, and metastatic liver tumors. This procedure acts to embolize the portal branch of the lobes targeted for resection, and induces compensatory hypertrophy in future remnant lobes, which largely involves the process of liver regeneration. Insulin supplied by the pancreatic islets perfuses hepatocytes continually through the portal vein. If the amount of portal circulation to the liver is decreased, the liver atrophies; in contrast, injection of insulin prevents or reverses this process. Furthermore, given that up to 30% of patients with liver malignancy are associated with diabetes and their livers are potentially less able to regenerate, evaluating the physiological significance of insulin signaling on liver regeneration following portal vein embolization and relevant molecular events is thus intriguing.

Benefits

A way to perform a longitudinal observation of liver regeneration is to perform a 99mTc sulfur colloid liver scan with the NanoSPECT/CT. This type of study allows for the quantification of the volume of the four liver segments (median, right, left and caudate lobe) at different time points.

Images / sample study

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(A) Gross appearance of the liver at d 7 following portal vein ligation in Sprague-Dawley rat. (B) The represented feature of 99mTc sulfur colloid Nano SPECT/CT performed before and d 1 and 7 after portal vein ligation in S-D rats. (C) The comparison of restituted liver mass after portal vein ligation among rats with and without insulin-deficiency. (D) The comparison of redistributed volume ratio of the liver after portal vein ligation among rats with and without insulin-deficiency. (E) The hepatocytes of normal rats became hypertrophic and arrived at their plateau around d 1–3, then restored to the original size at d 7. In contrast, the hepatocytes of insulin-deficient rats following PVL failed to have a compensatory hypertrophic effect. (F) Comparison of serum alanine transferase among rats with and without insulin-deficiency following portal vein ligation. Non-DM = non-diabetes; DM = diabetes.

* represented p<0.05.

References