{'fraction_non_alphanumeric': 0.01680672268907563, 'fraction_numerical': 0.0, 'mean_word_length': 5.4391891891891895, '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}}
The ability of pancreatic polypeptides (APP and BPP) to return to normal the hyperglycaemia, hyperinsulinaemia and weight gain of New Zealand obese mice.

Intraperitoneal injections of avian pancreatic polypeptide (APP) and bovine pancreatic polypeptide (BPP) are capable of returning to normal the hyperinsulinaemia, hyperglycaemia and weight gain of New Zealand obese mice. The lag glucose tolerance also becomes indistinguishable from normal. The mechanism whereby these polypeptides cause reversion is not known. Reversion can also be brought about by the intraperitoneal implantation of islets from white mice into New Zealand obese animals. The implanted islets secrete mouse pancreatic polypeptide. We conclude that the New Zealand obese syndrome arises from a genetic lack of mouse pancreatic polypeptide. We suggest that in humans a lack of pancreatic polypeptide might manifest as a syndrome analogous to that found in New Zealand obese mice.