抄録
A 63 year-old-man was admitted for severe hypoglycemia. Insulin levels were constantly low and the anti-insulin antibodies were negative in his serum. Basal levels of counter-regulatory-insulin hormone were within normal ranges.
However the response of counter-insulin hormones to hypoglycemia was inhibited, and administration of glucagon failed to adequately elevate the glucose level. The FDG-PET images showed an immense FDG uptake in the adipose tissues, and a low FDG uptake in the liver. In contrast, the tumor FDG uptake was relatively low. The plasma FDG activity was also low, reflecting accelerated plasma glucose turnover, which was attributed to the massive FDG uptake by the adipose tissues. The patient suffered a myocardial infarction and died. The autopsy confirmed a small gallbladder carcinoma and hypertrophic subcutaneous adipose tissue. The concentrations of IGF-11 did not increase in either the tumor or the serum, suggesting that the tumor did not produce IGF-11.
These findings strongly suggest that the hypoglycemia in this patient was due primarily to massive glucose consumption in the adipose tissues and by the inhibited glucose metabolism in the liver. In addition, the counter regulation activities failed and actually worsened the hypoglycemia. The mechanism of this abnormal glucose metabolism is unclear. However, it is likely that the tumor may have produced an unknown insulin-like material which prominently acts as an adipose tissue.
