PMID- 18777458 OWN - NLM STAT- MEDLINE DCOM- 20081205 LR - 20131121 IS - 0947-7349 (Print) IS - 0947-7349 (Linking) VI - 116 Suppl 1 DP - 2008 Sep TI - Association of impaired glucose metabolism in morbid obesity with hypoadiponectinaemia. PG - S64-9 LID - 10.1055/s-2008-1081490 [doi] AB - BACKGROUND: Increased circulating levels of cytokines and chemokines and decreased adiponectin levels are associated with impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2DM). As obesity is the major risk factor for T2DM it is not clear why many patients with morbid obesity remain normoglycaemic and if this protection can be attributed to a lower grade of inflammation or higher adiponectin levels. MATERIALS AND METHODS: Glucose tolerance of morbidly obese patients (n=2 754, body mass index > or =40 kg/m2) was assessed by oral glucose tolerance tests. In a case-control design we compared levels of eight immune mediators and adiponectin from patients with IGT/T2DM (n=52) and normal glucose tolerance (NGT; n=59). Gene expression in peripheral blood was determined by quantitative RT-PCR, and serum concentrations of immune mediators and adiponectin were measured by ELISA and bead-based multiplex technology. RESULTS: About 54% of the patients in our morbidly obese cohort were normoglycaemic, while 14% were diagnosed with IGT and 32% with T2DM. There was no statistically significant difference in mRNA expression or serum levels of proinflammatory markers. Interestingly, we could demonstrate an association of NGT with higher adiponectin levels (p=0.039). Adiponectin levels were negatively correlated with interleukin (IL)-6 and macrophage chemoattractant protein (MCP)-1, but independent the other immune mediators. CONCLUSIONS: We found an association of lower adiponectin levels with IGT/T2DM, but no further increase in inflammatory markers in morbid obesity. This suggests that in addition to chronic, low-grade inflammation, adiponectin is an important factor in the development of, or protection against, T2DM in obesity. FAU - Schinner, S AU - Schinner S AD - Department of Endocrinology, Diabetes and Rheumatology, University Hospital Dusseldorf, Germany. sven.schinner@uni-duesseldorf.de FAU - Kempf, K AU - Kempf K FAU - Overmann, H AU - Overmann H FAU - Willenberg, H S AU - Willenberg HS FAU - Schott, M AU - Schott M FAU - Rose, B AU - Rose B FAU - Scherbaum, W A AU - Scherbaum WA FAU - Herder, C AU - Herder C LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20080905 PL - Germany TA - Exp Clin Endocrinol Diabetes JT - Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association JID - 9505926 RN - 0 (Adiponectin) RN - 0 (CCL2 protein, human) RN - 0 (Chemokine CCL2) RN - 0 (Cytokines) RN - 0 (Interleukin-6) RN - 0 (RNA, Messenger) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Adiponectin/*blood/genetics/metabolism MH - Adult MH - Case-Control Studies MH - Chemokine CCL2/genetics/metabolism MH - Cohort Studies MH - Cytokines/genetics/metabolism MH - Diabetes Mellitus, Type 2/blood/complications/genetics/metabolism MH - Female MH - Glucose/metabolism MH - Glucose Intolerance/blood/*complications/genetics/immunology MH - Humans MH - Interleukin-6/genetics/metabolism MH - Male MH - Middle Aged MH - Obesity, Morbid/blood/*complications/genetics/immunology MH - RNA, Messenger/metabolism EDAT- 2008/10/23 09:00 MHDA- 2008/12/17 09:00 CRDT- 2008/10/23 09:00 PHST- 2008/10/23 09:00 [pubmed] PHST- 2008/12/17 09:00 [medline] PHST- 2008/10/23 09:00 [entrez] AID - 10.1055/s-2008-1081490 [doi] PST - ppublish SO - Exp Clin Endocrinol Diabetes. 2008 Sep;116 Suppl 1:S64-9. doi: 10.1055/s-2008-1081490. Epub 2008 Sep 5.