PMID- 10751750 OWN - NLM STAT- MEDLINE DCOM- 20000531 LR - 20221207 IS - 1520-7552 (Print) IS - 2005-6648 (Electronic) IS - 1520-7552 (Linking) VI - 16 IP - 2 DP - 2000 Mar-Apr TI - Advanced glycosylation end products (AGEs), insulin-like growth factor-1 (IGF-1) and IGF-binding protein-3 (IGFBP-3) in patients with type 2 diabetes mellitus. PG - 106-13 AB - BACKGROUND: Advanced glycosylation end product (AGE) formation is a major mechanism for the development of complications in diabetes, and the possible roles of insulin-like growth factor 1 (IGF-1) and IGF binding protein 3 (IGFBP-3) are not clearly established. METHODS: We examined the associations of AGEs, free IGF-I and IGFBP-3 in Type 2 diabetes mellitus (DM) patients under diverse conditions. In a cross-sectional design we studied 110 subjects (67 women and 43 men): non-diabetic controls in group 1, (n = 15) and diabetes patients as follows: group 2, without complications (n = 25); group 3, with chronic complications (n = 25); group 4, with acute or chronic infections (n = 24); group 5, hospitalized for reasons unrelated to diabetes (n = 9); group 6, with end-stage renal disease (ESRD) (n = 12). AGEs were determined by a spectrofluorometric method (HPLC). Insulin and IGFBP-3 were measured by RIA and free IGF-1 with an IRMA method. RESULTS: AGEs were 13-fold higher in patients with ESRD (p<0.001), and lower in healthy individuals. Free IGF-1 was lower in the patients with complications (p = 0.017), with infections (p = 0.006) and hospitalized (p = 0.04). IGFBP-3 was higher in hospitalized patients (p=0.017). AGEs were associated with free IGF-1 (r = 0.41, p = 0.04) in the group with complications, and with HbA(1c) (r = -0.90, p = 0.002) in hospitalized patients. In the total group, free IGF-1 (r = -0.25, p = 0.008), and IGFBP-3 (r = -0.22, p = 0.021) were associated with HbA(1c). CONCLUSION: We concluded that AGEs were markedly increased in diabetic patients with ESRD, IGF-1 was decreased in patients with infections and hospitalized, and was negatively associated with HbA(1c). IGFBP-3 was increased in hospitalized patients, with higher levels in patients with long bone fractures. A complex interaction of humoral factors may participate in the acceleration of complications of diabetes. FAU - Garay-Sevilla, M E AU - Garay-Sevilla ME AD - Instituto de Investigaciones Medicas, Universidad de Guanajuato, 20 de Enero 929, 37320 Leon Gto, Mexico. FAU - Nava, L E AU - Nava LE FAU - Malacara, J M AU - Malacara JM FAU - Wrobel, K AU - Wrobel K FAU - Wrobel, K AU - Wrobel K FAU - Perez, U AU - Perez U LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Diabetes Metab Res Rev JT - Diabetes/metabolism research and reviews JID - 100883450 RN - 0 (Biomarkers) RN - 0 (Blood Glucose) RN - 0 (Glycated Hemoglobin A) RN - 0 (Glycation End Products, Advanced) RN - 0 (Insulin-Like Growth Factor Binding Protein 3) RN - 67763-96-6 (Insulin-Like Growth Factor I) RN - 97C5T2UQ7J (Cholesterol) SB - IM MH - Biomarkers/blood MH - Blood Glucose/metabolism MH - Blood Pressure MH - Cholesterol/blood MH - Communicable Diseases/blood MH - Cross-Sectional Studies MH - Diabetes Mellitus, Type 2/*blood/*complications MH - Diabetic Nephropathies/blood MH - Female MH - Glycated Hemoglobin/analysis MH - Glycation End Products, Advanced/*blood MH - Humans MH - Inpatients MH - Insulin-Like Growth Factor Binding Protein 3/*blood MH - Insulin-Like Growth Factor I/analysis/*metabolism MH - Kidney Failure, Chronic/blood MH - Male MH - Middle Aged MH - Reference Values MH - Regression Analysis PMC - PMC2687688 EDAT- 2000/04/07 09:00 MHDA- 2000/06/03 09:00 PMCR- 2007/09/01 CRDT- 2000/04/07 09:00 PHST- 2000/04/07 09:00 [pubmed] PHST- 2000/06/03 09:00 [medline] PHST- 2000/04/07 09:00 [entrez] PHST- 2007/09/01 00:00 [pmc-release] AID - 10.1002/(SICI)1520-7560(200003/04)16:2<106::AID-DMRR88>3.0.CO;2-H [pii] AID - 10.1002/(sici)1520-7560(200003/04)16:2<106::aid-dmrr88>3.0.co;2-h [doi] PST - ppublish SO - Diabetes Metab Res Rev. 2000 Mar-Apr;16(2):106-13. doi: 10.1002/(sici)1520-7560(200003/04)16:2<106::aid-dmrr88>3.0.co;2-h.