Changes of insulin and somatostatin and their relationship to liver regeneration in experimental obstructive jaundice

Abstract

The liver is a parenchymal organ that has a substantial capacity to regenerate after damage. Obstructive jaundice is a common surgical disease and potentially risky. A successful outcome of operations depends upon the hepatic regeneration reserve. Insulin is one of factors responsible for hepatotrophic regeneration and somatostatin has a reversal suppressive action. Experimental obstructive jaundice was introduced and relieved. In addition, serum insulin and somatostatin concentrations were measured. We used immuno-histochemical study of pancreatic tissue by immunogold to express the tissue relative insulin and somatostatin concentrations. Nucleolar organizer regions (NORs) were used to predict the nucleolar activity of liver cells. In our studies, we observed the serum concentrations of insulin and somatostatin were similar to the relative tissue concentration in pancreatic tissues. The relative tissue gold-particle score of insulin in group A (rats with common bile duct tied), was CONT: T4: T7: T14 = 100%: 90.5%: 68.3%: 46.2%; of somatostatin was 100%: 120%: 118.2%: 115.5% respectively. In group B (common bile duct tied for 4 days then relieved), the gold-particle score of insulin was T4: T4R4: T4R7: T4R14 = 90.5%: 62.8%: 72.2%: 95.4%; of somatostatin was 120.2%: 114.3%: 108.1%: 106.2% respectively. In group C (common bile duct tied for 7 days then relieved), the gold-particle score of insulin was T7: T7R4: T7R7: T7R14 = 68.3%: 53.3%: 73.5%; of somatostain was 118.2%: 109.4%: 104.6%: 102.1% respectively. The mean numbers of AgNORs in group A revealed CONT: T4: T7: T14 = 2.24 +/- 0.24: 3.02 +/- 0.96: 3.26 +/- 1.02:3.08 +/- 0.84, group B was T4: T4R4: T4R7: T4R14 = 3.02 +/- 0.96: 3.03 +/- 0.73: 3.36 +/- 1.12: 3.72 +/- 1.46, and group C showed T7: T7R4:T7R7: T7R14 = 3.26 +/- 1.02: 3.26 +/- 0.84: 3.31 +/- 1.24: 3.54 +/- 1.24. In conclusion, our studies suggested: (1) liver regeneration appeared promptly after obstructive jaundice developed, but prolonged cholestasis inhibited this process. (2) Insulin levels gradually fell during the process of obstructive jaundice. Those levels elevated when cholestasis was improved. Nevertheless, both insulin and hepatic regeneration power could not reflect the initial improvement of cholestasis simultaneously. It took a longer time for the improvement of cholestasis and the recovery of the liver function. (3) Patho-physiologically, somatostatin had a weak influence on hepatic regeneration during obstructive jaundice. (4) Our studies provided clues that early biliary drainage might improve hepatic regeneration capacity. Supplement of insulin during the obstructive jaundice might be helpful for the improvement of hepatic regeneration power.