肝疾患における血中インスリン動態にかんする研究

抄録

In an attempt to study the mechanism underlying for the impaired glucose tolerance in liver disease, 1) changes in serum IRI levels in response to oral glucose (50g) and 2) the effect of exogenous insulin (0.1U/kg, i.v.) on blood glucose levels were examined in patients with various liver diseases (acute and chronic hepatitis and liver cirrhosis). In some of these patients, IRI response to oral glucose was repeatedly (twice or more times) examined at intervals of 3 to 6 months. In addition, IRI levels following intravenous glucose (25g) and those following intravenous tolbutamide (1g) were also determined in cirrhotics. Subjects with no evidence of either liver disease or diabetes mellitus served as controls.
Results are summarized as follows:
1) Patterns of IRI response to oral glucose were classified into 5 types; namely, a) normal response, b) delayed normal response, c) hyperresponse, d) delayed hyperresponse and e) hyporesponse types, respectively.
2) In a large number of patients with liver disease, IRI response to oral glucose was either normal or hyperresponsive, including delayed response of both types. Mean values for IRI at 30, 60, 90 and 120min. after glucose load in liver diseases were all significantly higher than those in controls.
3) In most of the patients with acute hepatitis, IRI response to oral glucose examined within a month of the onset was hyperresponsive. However, after hepatitis was recovered, the IRI response returned to normal in all of the patients. In cirrhotics, the IRI response was hyperresponsive in a half of them and normal in the remainder. However, the IRI response re-examined 3 to 9 months later was found to be hyperresponsive in all of the patients. In patients with chronic hepatitis, follow-up sutides of IRI response did not show any definite tendency as observed in previous two groups.
4) Sensitivity to the exogenous insulin in liver disease was significantly diminished, suggesting that insulin demand to utilize glucose in the peripheral tissue was augmented in liver disease as compared with that in controls. Thus, insulin output from the Langerhans' islet cell would be compensatorily increased in liver disease.
5) IRI levels following intravenous glucose and those following intravenous tolbutamide, in cirrhotics, were also significantly higher compared to those in controls. These findings indicated that the output of insulin in liver disease could be acceralated after glucose load even without any actions of intestinal hormons such as secretin.