PMID- 20427497 OWN - NLM STAT- MEDLINE DCOM- 20100726 LR - 20151119 IS - 1945-7197 (Electronic) IS - 0021-972X (Linking) VI - 95 IP - 7 DP - 2010 Jul TI - Soluble human leukocyte antigen-g expression and glucose tolerance in subjects with different degrees of adiposity. PG - 3342-6 LID - 10.1210/jc.2009-2747 [doi] AB - CONTEXT: Type 2 diabetes mellitus (T2DM) and obesity are characterized by a low-grade inflammation, which might be related to the development of insulin resistance. Human leukocyte antigen-G (HLA-G) shows antiinflammatory and tolerogenic properties, including the modulation of CD8+ T-cell cytotoxicity and regulation of CD4+ T-lymphocyte function. These functions are partially shared with IL-10, whose levels are reduced in insulin-resistant states. OBJECTIVE: The aim was to explore the relationship between HLA-G and the metabolic and inflammatory pattern of obesity or T2DM. PATIENTS AND MAIN OUTCOME MEASURES: Soluble HLA-G, IL-6, and IL-10 were measured and related with metabolic and biochemical parameters in 230 volunteers with normal glucose tolerance, impaired glucose tolerance, or T2DM by oral glucose tolerance test. RESULTS: sHLA-G, detected in 144 subjects (sHLA-G positive), was more frequent in T2DM or impaired glucose tolerance subjects than in normal glucose tolerance (chi(2) =18.6; P < 0.0001), and its plasma levels increased progressively across the classes of glucose tolerance. sHLA-G-positive individuals had higher body mass index, systolic blood pressure, and cholesterol levels; a reduced degree of insulin sensitivity; and almost 2-fold higher levels of IL-6, a cytokine related to insulin sensitivity, whereas IL-10 was similar. In the sHLA-G-positive subgroup, by a multivariate regression model, sHLA-G was significantly related to 2-h glucose, the area under insulin curve, and IL-6 levels (multiple r(2) = 0.14; P < 0.001), independently of age, gender, and body mass index. CONCLUSIONS: A frequent expression of sHLA-G, linked to a typical biomarker of insulin resistance like IL-6, seems to characterize subjects with an impaired glucose metabolism. FAU - Solini, Anna AU - Solini A AD - Department of Internal Medicine, University of Pisa, Via Roma 67, I-56100 Pisa, Italy. a.solini@med.unipi.it FAU - Muscelli, Elza AU - Muscelli E FAU - Stignani, Marina AU - Stignani M FAU - Melchiorri, Loredana AU - Melchiorri L FAU - Santini, Eleonora AU - Santini E FAU - Rossi, Chiara AU - Rossi C FAU - Astiarraga, Brenno Domingues AU - Astiarraga BD FAU - Rizzo, Roberta AU - Rizzo R FAU - Baricordi, Olavio Roberto AU - Baricordi OR LA - eng PT - Journal Article DEP - 20100428 PL - United States TA - J Clin Endocrinol Metab JT - The Journal of clinical endocrinology and metabolism JID - 0375362 RN - 0 (Biomarkers) RN - 0 (Blood Glucose) RN - 0 (HLA Antigens) RN - 0 (HLA-G Antigens) RN - 0 (Histocompatibility Antigens Class I) RN - 0 (Insulin) RN - 0 (Interleukin-6) RN - 130068-27-8 (Interleukin-10) SB - IM MH - Adiposity/*physiology MH - Adult MH - Analysis of Variance MH - Biomarkers MH - Blood Glucose/*metabolism MH - Diabetes Mellitus, Type 2/*metabolism MH - Enzyme-Linked Immunosorbent Assay MH - Female MH - Glucose Intolerance/*metabolism/physiopathology MH - Glucose Tolerance Test MH - HLA Antigens/*blood MH - HLA-G Antigens MH - Histocompatibility Antigens Class I/*blood MH - Humans MH - Insulin/blood MH - Interleukin-10/blood MH - Interleukin-6/blood MH - Male MH - Middle Aged MH - Obesity/*metabolism/physiopathology MH - Regression Analysis MH - Statistics, Nonparametric EDAT- 2010/04/30 06:00 MHDA- 2010/07/27 06:00 CRDT- 2010/04/30 06:00 PHST- 2010/04/30 06:00 [entrez] PHST- 2010/04/30 06:00 [pubmed] PHST- 2010/07/27 06:00 [medline] AID - jc.2009-2747 [pii] AID - 10.1210/jc.2009-2747 [doi] PST - ppublish SO - J Clin Endocrinol Metab. 2010 Jul;95(7):3342-6. doi: 10.1210/jc.2009-2747. Epub 2010 Apr 28.