{"id":{"repo_id":"aston","oai_identifier":"oai:publications.aston.ac.uk:10561"},"canonical_url":"https://search.dev.ndltd.org/etd/aston/oai:publications.aston.ac.uk:10561","repository":{"repo_id":"aston","name":"Aston University","base_url":"https://publications.aston.ac.uk/cgi/oai2"},"display":{"title":"The effect of oral-hypoglycaemic drugs and obesity on insulin receptor binding","abstract":"This thesis is concerned with the regulation of insulin receptors, with respect to receptor number, affinity and certain postreceptor effects of insulin action. The Aston obese hyperglycaemic (ob/ob) mouse was used as an animal model of obesity and type 2, NID diabetes mellitus. Hepatocyte insulin receptor number and soleus muscle insulin binding were reduced in these mice compared to lean litter mates. The rate of insulin stimulated glycogen synthesis was reduced in the obese mouse between 5 and 40 weeks of age. This defect preceeded the appearance of reduced insulin receptor binding at 10 weeks and a defect beyond the insulin receptor is therefore proposed as a primary aetiological factor in the development of insulin resistance in the obese mouse...","abstract_html":"This thesis is concerned with the regulation of insulin receptors, with respect to receptor number, affinity and certain postreceptor effects of insulin action. The Aston obese hyperglycaemic (ob/ob) mouse was used as an animal model of obesity and type 2, NID diabetes mellitus. Hepatocyte insulin receptor number and soleus muscle insulin binding were reduced in these mice compared to lean litter mates. The rate of insulin stimulated glycogen synthesis was reduced in the obese mouse between 5 and 40 weeks of age. This defect preceeded the appearance of reduced insulin receptor binding at 10 weeks and a defect beyond the insulin receptor is therefore proposed as a primary aetiological factor in the development of insulin resistance in the obese mouse...","abstract_has_math":false,"creators":["Lord, Janet Mary"],"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":1983,"date_issued":"1983","date_published":"1983","updated_at":"2026-07-24T01:01:17Z","subjects":[],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://doi.org/10.48780/publications.aston.ac.uk.00010561","outbound_label":"DOI","outbound_source":"dc:identifier.doi"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Lord, Janet Mary"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["1983"]},{"key":"dc:date.issued","label":"Date","values":["1983"]},{"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/10561/"]},{"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.00010561"]},{"key":"dc:identifier.uri","label":"Identifier URI","values":["https://publications.aston.ac.uk/id/eprint/10561/1/J.M._Lord_1983_reduced.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["This thesis is concerned with the regulation of insulin receptors, with respect to receptor number, affinity and certain postreceptor effects of insulin action. The Aston obese hyperglycaemic (ob/ob) mouse was used as an animal model of obesity and type 2, NID diabetes mellitus. Hepatocyte insulin receptor number and soleus muscle insulin binding were reduced in these mice compared to lean litter mates. The rate of insulin stimulated glycogen synthesis was reduced in the obese mouse between 5 and 40 weeks of age. This defect preceeded the appearance of reduced insulin receptor binding at 10 weeks and a defect beyond the insulin receptor is therefore proposed as a primary aetiological factor in the development of insulin resistance in the obese mouse..."]},{"key":"dc:format","label":"Dc Format","values":["text"]},{"key":"dc:title","label":"Title","values":["The effect of oral-hypoglycaemic drugs and obesity on insulin receptor binding"]}]}],"canonical_facts":{"dc:creator":["Lord, Janet Mary"],"dc:date":["1983"],"dc:date.issued":["1983"],"dc:description.abstract":["This thesis is concerned with the regulation of insulin receptors, with respect to receptor number, affinity and certain postreceptor effects of insulin action. The Aston obese hyperglycaemic (ob/ob) mouse was used as an animal model of obesity and type 2, NID diabetes mellitus. Hepatocyte insulin receptor number and soleus muscle insulin binding were reduced in these mice compared to lean litter mates. The rate of insulin stimulated glycogen synthesis was reduced in the obese mouse between 5 and 40 weeks of age. This defect preceeded the appearance of reduced insulin receptor binding at 10 weeks and a defect beyond the insulin receptor is therefore proposed as a primary aetiological factor in the development of insulin resistance in the obese mouse..."],"dc:format":["text"],"dc:identifier.doi":["10.48780/publications.aston.ac.uk.00010561"],"dc:identifier.uri":["https://publications.aston.ac.uk/id/eprint/10561/1/J.M._Lord_1983_reduced.pdf"],"dc:publisher.department":["School of Biosciences"],"dc:publisher.institution":["Aston University"],"dc:relation.isreferencedby":["https://publications.aston.ac.uk/id/eprint/10561/"],"dc:title":["The effect of oral-hypoglycaemic drugs and obesity on insulin receptor binding"],"dc:type":["Thesis"],"dc:type.qualificationlevel":["doctoral"],"dc:type.qualificationname":["Ph.D."]},"updated_at":"2026-07-24T01:01:17Z"}