{'fraction_non_alphanumeric': 0.02063983488132095, 'fraction_numerical': 0.0, 'mean_word_length': 5.139240506329114, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Glucose release from isolated, perfused liver of alloxan-diabetic rats.

Glucose release from the isolated, perfused rat liver was observed to a greater extent in alloxan-diabetic rats, compared to normal rats. The addition of acetoacetate (an acetone body) to the perfusate increased the glucose release from the normal rat liver, suggesting that the greater glucose release from the alloxan-diabetic rat liver is due to functional disorder(s) of the liver induced by acetoacetate in the diabetic condition. It was observed that lipoic acid suppressed glucose release from the liver of alloxan-diabetic rats, and that the nonprotein thiol level in alloxan-diabetic rat liver was lower than that in normal rat liver. Addition of acetoacetate in the perfusate caused a decrease in nonprotein thiol level in normal rat liver; suggesting that nonprotein thiol loss may mediate the increase in glucose release caused by an increase in acetoacetate in alloxan diabetic rats.