| http://purl.uniprot.org/citations/20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20170930 | http://www.w3.org/2000/01/rdf-schema#comment | "Ketosis-prone diabetes (KPD) is heterogeneous. Longitudinal follow-up revealed that patients with "A-β+" KPD (absent autoantibodies and preserved β-cell function) segregated into 2 subgroups with distinct evolution of β-cell function and glycemic control. Generalized linear analysis demonstrated that the variable that most significantly differentiated them was presence of a clinically evident precipitating event for the index diabetic ketoacidosis (DKA). Hence, we performed a comprehensive analysis of A-β+ KPD patients presenting with "provoked" compared with "unprovoked" DKA. Clinical, biochemical, and β-cell functional characteristics were compared between provoked and unprovoked A-β+ KPD patients followed prospectively for 1 to 8 years. Human leukocyte antigen class II allele frequencies were compared between these 2 groups and population controls. Unprovoked A-β+ KPD patients (n = 83) had greater body mass index, male preponderance, higher frequency of women with oligo-/anovulation, more frequent African American ethnicity, and less frequent family history of diabetes than provoked A-β+ KPD patients (n = 64). The provoked group had higher frequencies of the human leukocyte antigen class II type 1 diabetes mellitus susceptibility alleles DQB1*0302 (than the unprovoked group or population controls) and DRB1*04 (than the unprovoked group), whereas the unprovoked group had a higher frequency of the protective allele DQB1*0602. β-Cell secretory reserve and glycemic control improved progressively in the unprovoked group but declined in the provoked group. The differences persisted in comparisons restricted to patients with new-onset diabetes. "Unprovoked" A-β+ KPD is a distinct syndrome characterized by reversible β-cell dysfunction with male predominance and increased frequency of DQB1*0602, whereas "provoked" A-β+ KPD is characterized by progressive loss of β-cell reserve and increased frequency of DQB1*0302 and DRB1*04. Unprovoked DKA predicts long-term β-cell functional reserve, insulin independence, and glycemic control in KPD."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.metabol.2010.01.009"xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Villanueva J."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Hampe C.S."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Patel S.G."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Balasubramanyam A."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Maldonado M."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Gaur L.K."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "O'Brian Smith E."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Ozer K."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Nalini R."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/author | "Guthikonda A."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/name | "Metabolism"xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/pages | "1448-1455"xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/title | "Presence or absence of a known diabetic ketoacidosis precipitant defines distinct syndromes of "A-beta+" ketosis-prone diabetes based on long-term beta-cell function, human leukocyte antigen class II alleles, and sex predilection."xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://purl.uniprot.org/core/volume | "59"xsd:string |
| http://purl.uniprot.org/citations/20170930 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/20170930 |
| http://purl.uniprot.org/citations/20170930 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/20170930 |
| http://purl.uniprot.org/uniprot/#_A0A0A7C3H3-mappedCitation-20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20170930 |
| http://purl.uniprot.org/uniprot/#_A0A0A7C3I1-mappedCitation-20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20170930 |
| http://purl.uniprot.org/uniprot/#_A0A0A7C3I5-mappedCitation-20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20170930 |
| http://purl.uniprot.org/uniprot/#_A0A0E3DC97-mappedCitation-20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20170930 |
| http://purl.uniprot.org/uniprot/#_A0A0E3DC99-mappedCitation-20170930 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/20170930 |