{'fraction_non_alphanumeric': 0.027327070879590094, 'fraction_numerical': 0.013663535439795047, 'mean_word_length': 5.136125654450262, '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}}
Effect of serial test meals on plasma immunoreactive GIP in non-insulin dependent diabetic patients and non-diabetic controls.

Previous reports have shown considerable variation in postprandial gastric inhibitory polypeptide (GIP) response in non-insulin-dependent diabetic (NIDD) patients. One reason for this may be the use of different GIP antisera. Employing antiserum R65, which specifically reacts with the 5000-dalton GIP, we investigated the plasma GIP response to serial test meals in 11 NIDD patients and 11 age- and weight-matched non-diabetic controls. The postprandial GIP response was lower in the NIDD patients than in the non-diabetic controls (p less than 0.05). Although the serum insulin concentrations did not differ between diabetic and non-diabetic subjects, the insulin to glucose ratio was lower in the diabetics than in the non-diabetic subjects (p less than 0.05) indicating some degree of relative insulin deficiency in the diabetic patients. The data suggest that the GIP secretory capacity may be impaired in NIDD patients. Whether the impairment of GIP secretion is associated with impaired insulin secretion requires further investigation.