{"id":{"repo_id":"aston","oai_identifier":"oai:publications.aston.ac.uk:10481"},"canonical_url":"https://search.dev.ndltd.org/etd/aston/oai:publications.aston.ac.uk:10481","repository":{"repo_id":"aston","name":"Aston University","base_url":"https://publications.aston.ac.uk/cgi/oai2"},"display":{"title":"A Study of Glucose Stimulus Insulin Secretion Coupling using Lean and Obese Mouse Islets of Langerhans","abstract":"Glucose-stimulus insulin secretion coupling has been investigated using isolated islets of Langerhans from lean homozygous (+/+) and genetically obese hyperglycaemic (ob/ob) mice. Streptozotocin inhibition of the insulin response to glucose but not glucagon suggests glucose sensitive sites and adenylate cyclase systems to be separate physiological entities at the level of the B-cell membrane. Perifusion of islets with gradients of mutarotated and the anomeric forms of D-glucose in the presence of phloridzin and the insulin response of islets bound to lectin suggests that lean mouse islets recognise glucose as the stimulus for insulin secretion via a B-cell membrane glucoreceptor that shows a preferential affinity for a-D-glucose. -D-glucose is preferentially transported into the B-cell to maintain the insulin response. The sensitivity of obese mouse islet membrane glucoreceptors to a-D-glucose is reduced and insulin secretion in this case depends upon a greater contribution from that part of the receptor sensitive to B-D-glucose. Studies using 24-hour fasted animals demonstrated that the integrity of glucoreceptor sensitivity depended upon the nutritional status of the animal. Glucoreceptor sensitivity and the characteristic insulin response of lean mouse islets to a-D-glucose develops with age (4-5 weeks). Neonatal mouse islets provide little insulin response to glucose but a prominent response to certain amino acids. A model for glucose-stimulus insulin secretion coupling has been proposed and it is suggested that reduced glucoreceptor sensitivity of obese mouse islets contributes to the manifestation of the obese hyperglycaemic syndrome.","abstract_html":"Glucose-stimulus insulin secretion coupling has been investigated using isolated islets of Langerhans from lean homozygous (+/+) and genetically obese hyperglycaemic (ob/ob) mice. Streptozotocin inhibition of the insulin response to glucose but not glucagon suggests glucose sensitive sites and adenylate cyclase systems to be separate physiological entities at the level of the B-cell membrane. Perifusion of islets with gradients of mutarotated and the anomeric forms of D-glucose in the presence of phloridzin and the insulin response of islets bound to lectin suggests that lean mouse islets recognise glucose as the stimulus for insulin secretion via a B-cell membrane glucoreceptor that shows a preferential affinity for a-D-glucose. -D-glucose is preferentially transported into the B-cell to maintain the insulin response. The sensitivity of obese mouse islet membrane glucoreceptors to a-D-glucose is reduced and insulin secretion in this case depends upon a greater contribution from that part of the receptor sensitive to B-D-glucose. Studies using 24-hour fasted animals demonstrated that the integrity of glucoreceptor sensitivity depended upon the nutritional status of the animal. Glucoreceptor sensitivity and the characteristic insulin response of lean mouse islets to a-D-glucose develops with age (4-5 weeks). Neonatal mouse islets provide little insulin response to glucose but a prominent response to certain amino acids. A model for glucose-stimulus insulin secretion coupling has been proposed and it is suggested that reduced glucoreceptor sensitivity of obese mouse islets contributes to the manifestation of the obese hyperglycaemic syndrome.","abstract_has_math":false,"creators":["Newton, David F."],"institution":"Aston University","degree_name":"Ph.D.","degree_level":"doctoral","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":1979,"date_issued":"1979","date_published":"1979","updated_at":"2026-07-24T01:01:14Z","subjects":[],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://doi.org/10.48780/publications.aston.ac.uk.00010481","outbound_label":"DOI","outbound_source":"dc:identifier.doi"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Newton, David F."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["1979"]},{"key":"dc:date.issued","label":"Date","values":["1979"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["School of Biosciences"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["Aston University"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["https://publications.aston.ac.uk/id/eprint/10481/"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["doctoral"]},{"key":"dc:type.qualificationname","label":"Dc Type Qualificationname","values":["Ph.D."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.doi","label":"DOI","values":["10.48780/publications.aston.ac.uk.00010481"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://publications.aston.ac.uk/id/eprint/10481/1/Newton_D._F_1979_reduced.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Glucose-stimulus insulin secretion coupling has been investigated using isolated islets of Langerhans from lean homozygous (+/+) and genetically obese hyperglycaemic (ob/ob) mice. Streptozotocin inhibition of the insulin response to glucose but not glucagon suggests glucose sensitive sites and adenylate cyclase systems to be separate physiological entities at the level of the B-cell membrane. Perifusion of islets with gradients of mutarotated and the anomeric forms of D-glucose in the presence of phloridzin and the insulin response of islets bound to lectin suggests that lean mouse islets recognise glucose as the stimulus for insulin secretion via a B-cell membrane glucoreceptor that shows a preferential affinity for a-D-glucose. -D-glucose is preferentially transported into the B-cell to maintain the insulin response. The sensitivity of obese mouse islet membrane glucoreceptors to a-D-glucose is reduced and insulin secretion in this case depends upon a greater contribution from that part of the receptor sensitive to B-D-glucose. Studies using 24-hour fasted animals demonstrated that the integrity of glucoreceptor sensitivity depended upon the nutritional status of the animal. Glucoreceptor sensitivity and the characteristic insulin response of lean mouse islets to a-D-glucose develops with age (4-5 weeks). Neonatal mouse islets provide little insulin response to glucose but a prominent response to certain amino acids. A model for glucose-stimulus insulin secretion coupling has been proposed and it is suggested that reduced glucoreceptor sensitivity of obese mouse islets contributes to the manifestation of the obese hyperglycaemic syndrome."]},{"key":"dc:format","label":"Dc Format","values":["text"]},{"key":"dc:title","label":"Title","values":["A Study of Glucose Stimulus Insulin Secretion Coupling using Lean and Obese Mouse Islets of Langerhans"]}]}],"canonical_facts":{"dc:creator":["Newton, David F."],"dc:date":["1979"],"dc:date.issued":["1979"],"dc:description.abstract":["Glucose-stimulus insulin secretion coupling has been investigated using isolated islets of Langerhans from lean homozygous (+/+) and genetically obese hyperglycaemic (ob/ob) mice. Streptozotocin inhibition of the insulin response to glucose but not glucagon suggests glucose sensitive sites and adenylate cyclase systems to be separate physiological entities at the level of the B-cell membrane. Perifusion of islets with gradients of mutarotated and the anomeric forms of D-glucose in the presence of phloridzin and the insulin response of islets bound to lectin suggests that lean mouse islets recognise glucose as the stimulus for insulin secretion via a B-cell membrane glucoreceptor that shows a preferential affinity for a-D-glucose. -D-glucose is preferentially transported into the B-cell to maintain the insulin response. The sensitivity of obese mouse islet membrane glucoreceptors to a-D-glucose is reduced and insulin secretion in this case depends upon a greater contribution from that part of the receptor sensitive to B-D-glucose. Studies using 24-hour fasted animals demonstrated that the integrity of glucoreceptor sensitivity depended upon the nutritional status of the animal. Glucoreceptor sensitivity and the characteristic insulin response of lean mouse islets to a-D-glucose develops with age (4-5 weeks). Neonatal mouse islets provide little insulin response to glucose but a prominent response to certain amino acids. A model for glucose-stimulus insulin secretion coupling has been proposed and it is suggested that reduced glucoreceptor sensitivity of obese mouse islets contributes to the manifestation of the obese hyperglycaemic syndrome."],"dc:format":["text"],"dc:identifier.doi":["10.48780/publications.aston.ac.uk.00010481"],"dc:identifier.uri":["https://publications.aston.ac.uk/id/eprint/10481/1/Newton_D._F_1979_reduced.pdf"],"dc:publisher.department":["School of Biosciences"],"dc:publisher.institution":["Aston University"],"dc:relation.isreferencedby":["https://publications.aston.ac.uk/id/eprint/10481/"],"dc:title":["A Study of Glucose Stimulus Insulin Secretion Coupling using Lean and Obese Mouse Islets of Langerhans"],"dc:type":["Thesis"],"dc:type.qualificationlevel":["doctoral"],"dc:type.qualificationname":["Ph.D."]},"updated_at":"2026-07-24T01:01:14Z"}