{'fraction_non_alphanumeric': 0.031042128603104215, 'fraction_numerical': 0.007760532150776054, 'mean_word_length': 5.688888888888889, '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}}
GLP1R Regualtion of Gap Junction Coupling in the Islet of Langerhans

Pancreatic islets regulate glucose homeostasis through insulin secretion. β‐cells are connected by gap junctions, which regulate depolarization, calcium signaling and insulin secretion. In diabetes, pro‐inflammatory cytokines contribute to β‐cell mass depletion and dysfunction. Low levels decrease Gap Junction Coupling (GJC) in the islet, disrupting calcium signaling and insulin secretion dynamics. Cyclic adenosine monophosphate (cAMP), elevated by a Type 2 Diabetes treatment called Exendin‐4, has been shown to increase GJC. Increased cAMP acts via protein kinase A (PKA) and exchange protein activated by cAMP 2 (Epac2) to regulate GJC in other systems; however, this has not been shown in pancreatic islets. We hypothesized Exendin‐4 can overcome cytokine induced decreases in GJC through PKA and Epac2 dependent mechanisms.