{'fraction_non_alphanumeric': 0.0424, 'fraction_numerical': 0.0232, 'mean_word_length': 4.985645933014354, 'pattern_counts': {'":': 0, '<': 2, '<?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}}
Insulin Resistance and Insulin Deficiency in Diabetic Retinopathy of Non-insulin-dependent Diabetes

To assess the role of insulin resistance and insulin deficiency in the pathogenesis of diabetic retinopathy in non-insulin-dependent diabetes mellitus, 13 patients with and 12 patients without retinopathy were studied. The glucose clamp technique was used to measure insulin resistance and insulin response to glucose. During the euglycemic clamp, at comparable steady-state levels of glucose and insulin, the mean glucose infusion rate, which indicates the rate of glucose utilization, was lower in the retinopathy group than in the nonretinopathy group (6.1 ± 0.5 versus 8.1 ± 0.7 mg · kg−1 · min−1, P < 0.02). Growth hormone (GH) concentrations were higher in the retinopathy group 8.4 ± 2.5 versus 2.5 ± 0.7 μlU/ml, P < 0.05), but they did not correlate significantly with insulin resistance, expressed as mean glucose turnover. During the hyperglycemic clamp (+7 mmol/L above the fasting plasma glucose), the insulin response in the two groups of diabetics was similar. Increased insulin resistance represents an additional factor, which together with other factors, may be important in the pathogenesis of diabetic microvascular complications.