{'fraction_non_alphanumeric': 0.049606775559588624, 'fraction_numerical': 0.013914095583787053, 'mean_word_length': 5.361538461538461, '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}}
Angiotensin-(1-7) improves Islet Function in a Rat Model of Streptozotocin-induced Diabetes Mellitus by Up-regulating the Expression of Pdx1/Glut2.

OBJECTIVE
To observe the effects of angiotensin-(1-7) (Ang-(1-7)) on glucose metabolism, islet function and insulin resistance in a rat model of streptozotocin-induced diabetes mellitus (DM) and investigate its mechanism.


METHOD
Thirty-four male Wistar rats were randomly divided into 3 groups: control group, which was fed standard diet, DM group, high-fat diet and injected with streptozotocin, and Ang-(1-7) group receiving injection of streptozotocin followed by Ang-(1-7) treatment. Blood glucose level, fasting serum Ang II and insulin levels, and homeostasis model assessment of insulin resistance (HOMA-IR) were measured. The pancreases were collected for histological examination, protein and gene expressions analysis.


RESULTS
Compared with control group, fasting blood glucose, serum angiotensin II level, and HOMA-IR value increased, while serum insulin level decreased in DM group. Moreover, islet structure was damaged, β cells were irregularly arranged, the cytoplasm was loose in DM group. Expressions of Pancreatic duodenal homeobox-1 (Pdx1), glucose transporter-2 (Glut2) and glucokinase (Gk) were significantly decreased in DM group compared with control group. However, the DMassociated changes were dramatically reversed following Ang-(1-7) treatment.


CONCLUSION
Ang-(1-7) protects against streptozotocin-induced DM through the improvement of insulin secretion, insulin resistance and islet fibrosis, which is associated with the upregulation of Pdx1, Glut2 and Gk expressions.