{'fraction_non_alphanumeric': 0.014379868184541641, 'fraction_numerical': 0.015578190533253445, 'mean_word_length': 5.574803149606299, '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}}
Inhibition of Angiotensin Type 1 Receptor Prevents Decline of Glucose Transporter (GLUT4) in Diabetic Rat Heart

There is some evidence that inhibition of angiotensinconverting enzyme (ACE) activity can improve the uptake and conversion of glucose by heart and skeletal muscle in diabetes. To study the underlying mechanisms, we treated streptozotocin-induced diabetic rats with the angiotensin type 1 receptor (AT1) antagonist ICI D8731 and the ACE inhibitor fosinopril for 4 months and determined the expression of the myocardial glucose transporter proteins. In diabetic rats, the expression of the insulin-regulated glucose transporter (GLUT4) was strongly diminished as shown by Western and Northern blots. ICI D8731 prevented the decrease of GLUT4 protein in diabetes but had no influence on the amount of mRNA encoding for GLUT1 and GLUT4. GLUT1 protein was hardly detected in the rat heart and was affected neither by diabetes nor by treatment with the AT1 antagonist. Additionally, ICI D8731 influenced the translocation of GLUT4 from the intracellular pool to the plasma membrane, because treatment increased the amount of GLUT4 protein in the plasma membranes as well as in intracellular membrane fractions compared with membranes of untreated diabetic control rats. In contrast, inhibition of ACE by fosinopril influenced neither the expression nor the translocation of the glucose transporter proteins. These observations indicate that angiotensin II has a distinct influence on the posttranscriptional regulation of the GLUT4 transporter protein, presumably indirectly as a consequence of hemodynamic effects and structural alterations of the vessel wall.