{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,26]],"date-time":"2026-08-26T06:32:42Z","timestamp":1787725962749,"version":"build-2784847793"},"reference-count":42,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"45","license":[{"start":{"date-parts":[[2022,11,11]],"date-time":"2022-11-11T00:00:00Z","timestamp":1668124800000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2022,11,11]]},"abstract":"<jats:p>The study aimed to test the hypothesis that homeostatic microbiome (HM) disorders lead to the increased indirect influence of certain microorganisms (MO) in the gastrointestinal tract, causing a disorder of insulin secretion, insulin resistance, and diabetes. We highlighted <jats:italic toggle=\"yes\">Candida<\/jats:italic> and certain types of bacteria since previous in vitro research showed they significantly affect insulin secretion and can cause insulin resistance in obese patients with metabolic syndrome. After determining the type of MO present in the throat swab and the stool, the oral glucose tolerance test (OGTT) test, and analysis of glucose and insulin secretion were performed in patients (n = 38) who were positive for certain types of MO compared to negative patients. Finally, all patients were divided into two groups: overweight patients (body mass index [BMI] &lt; 30) and obese patients (BMI &gt; 30). These two groups were compared for the percentage of certain types of MO to determine which MO can affect an increase in obesity and BMI. The presence of <jats:italic toggle=\"yes\">Diphtheroids<\/jats:italic> in the throat (60.5%) reduces insulin secretion in patients compared with the negative group (194.5: 332.4) and the difference was statistically significant (<jats:italic toggle=\"yes\">P<\/jats:italic> = .030). The presence of <jats:italic toggle=\"yes\">Candida<\/jats:italic> in the throat (10%) increases insulin secretion, but the difference was statistically insignificant. The presence of <jats:italic toggle=\"yes\">Candida<\/jats:italic> in the stool (28.9%) also increases insulin secretion and the difference was statistically significant (<jats:italic toggle=\"yes\">P<\/jats:italic> = .038). Cumulative results (throat + stool) were similar (180: 332, <jats:italic toggle=\"yes\">P<\/jats:italic> = .022). Analysis of BMI showed that the percentage of <jats:italic toggle=\"yes\">Diphtheroids<\/jats:italic> in the throat decreases with increased body weight (53.8: 75%) while the percentage of <jats:italic toggle=\"yes\">Candida<\/jats:italic> (38.5: 8.3%) and <jats:italic toggle=\"yes\">Enterobacter<\/jats:italic> (61.5: 25%) increases, but these differences were statistically insignificant (<jats:italic toggle=\"yes\">P<\/jats:italic> &gt; .05). <jats:italic toggle=\"yes\">Diphtheroids<\/jats:italic> in the throat can reduce insulin secretion by synthesizing their metabolites. <jats:italic toggle=\"yes\">Candida albicans<\/jats:italic> is a conditional pathogen and as a significant indirect factor induces increased insulin secretion and insulin resistance. There are indications that elevated levels of <jats:italic toggle=\"yes\">Candida<\/jats:italic> in the intestinal system can cause increased body weight of patients. <jats:italic toggle=\"yes\">C albicans<\/jats:italic> should be considered a new factor in the pathogenesis of diabetes.<\/jats:p>","DOI":"10.1097\/md.0000000000031291","type":"journal-article","created":{"date-parts":[[2022,11,17]],"date-time":"2022-11-17T14:04:16Z","timestamp":1668693856000},"page":"e31291","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":14,"title":["Homeostatic microbiome disruption as a cause of insulin secretion disorders. Candida albicans, a new factor in pathogenesis of diabetes: A STROBE compliant cross-sectional study"],"prefix":"10.1097","volume":"101","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5919-1575","authenticated-orcid":false,"given":"Dragan M.","family":"Nikolic","sequence":"first","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vesna","family":"Dimitrijevic-Sreckovic","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lazar T.","family":"Ranin","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Institute of Microbiology and Immunology, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milos M.","family":"Stojanovic","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iva D.","family":"Ilic","sequence":"additional","affiliation":[{"name":"Institute of Public Health of Serbia \u201cDr. Milan Jovanovic Batut\u201d, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Drasko M.","family":"Gostiljac","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, Belgrade, Serbia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ivan A.","family":"Soldatovic","sequence":"additional","affiliation":[{"name":"Faculty of Medicine Belgrade, University of Belgrade, Belgrade, Serbia"},{"name":"Institute of Medical Statistics and Informatics, Belgrade, Serbia."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"R1-20250504","doi-asserted-by":"crossref","first-page":"602","DOI":"10.2337\/diacare.27.2.602","article-title":"Highlights from The First World Congress on the insulin resistance syndrome.","volume":"27","author":"Bloomgarden","year":"2004","journal-title":"Diab Mellit Care"},{"key":"R2-20250504","doi-asserted-by":"crossref","first-page":"17","DOI":"10.1097\/00005082-200201000-00003","article-title":"Risk factors for type 2 diabetes mellitus","volume":"16","author":"Fletcher","year":"2002","journal-title":"J Cardiovasc Nurs"},{"key":"R3-20250504","doi-asserted-by":"crossref","first-page":"799","DOI":"10.1038\/414799a","article-title":"Insulin signalling and the regulation of glucose and lipid metabolism","volume":"414","author":"Saltiel","year":"2001","journal-title":"Nature"},{"key":"R4-20250504","first-page":"11","article-title":"The relation of insulin resistance syndromes to risk of cardiovascular disease","volume":"4","author":"Nesto","year":"2003","journal-title":"Rev Cardiovasc Med"},{"key":"R5-20250504","doi-asserted-by":"crossref","first-page":"335","DOI":"10.1179\/acb.2003.58.6.001","article-title":"Pathophysiology of type 2 diabetes mellitus","volume":"58","author":"Scheen","year":"2003","journal-title":"Acta Clin Belg"},{"key":"R6-20250504","first-page":"1110","article-title":"Diabetes mellitus and obesity as a result of a disrupted homeostatic microbiome. 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