{'fraction_non_alphanumeric': 0.022892238972640984, 'fraction_numerical': 0.014517029592406477, 'mean_word_length': 6.027450980392157, '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}}
Purinergic receptors and metabolic function

Blood glucose concentration is a signal for the endocrine pancreas to release insulin or glucagon. Insulin lowers the level of glucose by inhibiting the hepatic glucose production and stimulating glucose utilization by skeletal muscles and adipocytes. In these latter cells, insulin also inhibits lipolysis and the subsequent release of glycerol (a gluconeogenic precursor) and non esterified fatty acids (energy substrate for hepatic gluconeogenesis). Glucagon opposes the effects of insulin, particularly in the liver, where it stimulates glycogenolysis and neoglucogenesis. A variety of purinoceptor subtypes are expressed in these different tissues, all involved in the regulation of glucose homeostasis: 1) P2Y and A1 receptors in the pancreatic B cell, mediating stimulation or inhibition of insulin secretion respectively, A2 receptors in the pancreatic A cell mediating glucagon secretion; 2) different P2 receptors in liver cells mediating glycogenolysis through multiple transducing systems; 3) A1 receptors in adipocytes mediating antilipolytic action. The thorough characterization of these receptors, together with a better understanding of their metabolic role and position in this integrated physiological regulation may be useful in designing ligands aimed at stimulating insulin secretion or reducing insulin resistance, which are both critical in the pathophysiology of non‐insulin‐dependent diabetes mellitus (NIDDM). Thus, purinoceptors may constitute new targets for pharmacological compounds with potential therapeutic applications in NIDDM, such as P2Y agonists as insulin secretagogues and A1 agonists as antilipolytic agents for improvement of insulin sensitivity. Drug Dev. Res. 39:413–425, 1996. © 1997 Wiley‐Liss, Inc.