{'fraction_non_alphanumeric': 0.07165109034267912, 'fraction_numerical': 0.03894080996884735, 'mean_word_length': 4.354166666666667, '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 role of GPR91 in the Akita model of diabetic nephropathy (DN)

The importance of local tissue metabolism, succinate accumulation and signaling via its receptor GPR91 in the activation of the intra‐renal renin‐angiotensin system (RAS) in DN has been established by our laboratory using the streptozotocin (STZ) model. However, the genetic Akita (A) mouse model of type I diabetes is an excellent alternative to study DN due to lack of the toxic side effects of STZ. In this study we used wild type A (n=6) and GPR91−/− A (A−/−, n=5) mice at 18‐wks of age. Although both groups develop robust hyperglycemia, we observed noticeable decreases in water intake, food intake and urine volume in A−/− mice. Urinary albumin excretion showed 1.69±0.7 fold increase in A group compared to WT and only 1.04±0.2 increase in in A−/− mice. Immunohistochemical analyses of TGFβ found strong glomerular labeling in A but not A−/− kidneys. Whole kidney Western blots demonstrated higher TGFβ content in A mice (1.27±0.3) than A−/− (0.68±0.1). A mice revealed higher cortical renin content (1.37±0.2) than A−/− (1.0±0.1). A significant difference in medullary renin was observed between A (1.34±0.2) and A−/− mice (0.8±0.1). We concluded that GPR91 plays an important role in the pathogenesis of DN.