{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T10:46:50Z","timestamp":1770288410225,"version":"3.49.0"},"reference-count":39,"publisher":"Wiley","license":[{"start":{"date-parts":[[2012,1,1]],"date-time":"2012-01-01T00:00:00Z","timestamp":1325376000000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/501100000925","name":"National Health and Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000925","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Victorian Government\u2019s Operational Infrastructure Support Program"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Diabetes Research"],"published-print":{"date-parts":[[2012]]},"abstract":"<jats:p><jats:italic>Aims<\/jats:italic>. Activins A and B, and their binding protein, follistatin, regulate glucose metabolism and inflammation. Consequently, their role in type 2 diabetes (T2D) was examined.<jats:italic>Methods<\/jats:italic>. Blood was taken from fasted participants (34 males; 58 females; 50\u201375 years) with diabetes or during an oral glucose tolerance test (OGTT). Clinical parameters were assessed, and blood assayed for activins, follistatin, and C-reactive protein.<jats:italic>Results<\/jats:italic>. Serum levels of activin A (93.3 \u00b1 27.0\u2009pg\/mL, mean \u00b1 SD), B (81.8 \u00b1 30.8\u2009pg\/mL), or follistatin (6.52 \u00b1 3.15\u2009ng\/mL) were not different (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&gt;<\/mml:mo><mml:mn>0.05<\/mml:mn><\/mml:mrow><\/mml:math>) between subjects with normal OGTT (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M2\"><mml:mrow><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>39<\/mml:mn><\/mml:mrow><\/mml:math>), impaired glucose tolerance and\/or fasting glucose (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:mrow><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>17<\/mml:mn><\/mml:mrow><\/mml:math>), or T2D (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:mrow><mml:mi>n<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>36<\/mml:mn><\/mml:mrow><\/mml:math>). However, activin A and\/or activin B were positively correlated with parameters of insulin resistance and T2D, including fasting glucose (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:mrow><\/mml:math>), fasting insulin (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.02<\/mml:mn><\/mml:mrow><\/mml:math>), glycated hemoglobin (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.003<\/mml:mn><\/mml:mrow><\/mml:math>), and homeostasis model assessment of insulin resistance (HOMA-IR;<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>&lt;<\/mml:mo><mml:mn>0.001<\/mml:mn><\/mml:mrow><\/mml:math>). Follistatin was positively correlated with HOMA-IR alone (<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M9\"><mml:mrow><mml:mi>P<\/mml:mi><mml:mo>=<\/mml:mo><mml:mn>0.01<\/mml:mn><\/mml:mrow><\/mml:math>).<jats:italic>Conclusions<\/jats:italic>. These data indicate that serum measurements of activin A, B, or follistatin cannot discriminate risk for T2D in individual patients, but the activins display a positive relationship with clinical parameters of the disease.<\/jats:p>","DOI":"10.1155\/2012\/410579","type":"journal-article","created":{"date-parts":[[2012,12,16]],"date-time":"2012-12-16T21:00:47Z","timestamp":1355691647000},"page":"1-9","source":"Crossref","is-referenced-by-count":21,"title":["Correlation between Blood Activin Levels and Clinical Parameters of Type 2 Diabetes"],"prefix":"10.1155","volume":"2012","author":[{"given":"Hui","family":"Wu","sequence":"first","affiliation":[{"name":"Monash Institute of Medical Research, Monash University, Clayton, VIC 3168, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael","family":"Wu","sequence":"additional","affiliation":[{"name":"School of Public Health, Monash University, Clayton, VIC 3168, 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