File Download
There are no files associated with this item.
Supplementary
-
Citations:
- Appears in Collections:
Conference Paper: Association between Serum Galectin-3 and Advanced Glycation End Products in Type 2 Diabetes
Title | Association between Serum Galectin-3 and Advanced Glycation End Products in Type 2 Diabetes |
---|---|
Authors | |
Issue Date | 2017 |
Publisher | American Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/ |
Citation | The 77th American Diabetes Association (ADA) Scientific Sessions, San Diego, California, USA, 9-13 June 2017. In Diabetes, 2017, v. 66 n. Suppl. 1, p. A-138, abstract no. 526-P How to Cite? |
Abstract | Galectin-3, a member of the multifunctional galectin family, acts a broad-spectrum biological response modifier and is involved in tissue fibrosis, immunity, and inflammatory response. The role of galectin-3 in diabetic complications is unclear and animal studies have provided evidence for protective and detrimental functions of galectin-3. Although galectin-3 is a mediator of inflammation and fibrosis, it is also a scavenger receptor for advanced glycation end products (AGEs) and stimulates their degradation. We have investigated whether serum galectin-3 level is related to circulating AGEs and/or inflammation in type 2 diabetic patients with and without chronic kidney disease (CKD). 270 type 2 diabetic patients (30% with CKD and eGFR <60 ml/min/1.73m2) and 230 controls were recruited. Serum galectin-3 and AGEs were assayed by ELISA and plasma high sensitivity C-reactive protein (CRP) was measured by immunoturbidimetric assay. Diabetic patients had higher HbA1c, AGEs (4.46 ± 1.06 unit/ml (CKD+); 4.10 ± 0.98 (CKD-); 3.56 ± 0.99 (control); ANOVA p<0.01) and CRP levels than controls. Serum galectin-3 was highest in those with CKD (9.07 ± 2.64 ng/ml (CKD+); 7.48 ± 2.36
(CKD-); 5.36 ± 1.65 (control); ANOVA p<0.01). Serum glaectin-3 correlated with AGEs (r=0.34, p<0.01), eGFR (r=-0.35, p<0.01) and age (r=0.25, p<0.01) but there were no associations with duration of diabetes, HbA1c or CRP. The association with AGEs remained significant even after excluding subjects with CKD (r=0.30, p<0.01). On linear regression analysis, serum AGEs and eGFR were independent determinants of serum galectin-3 after adjusting for age, gender, body mass index, and smoking, accounting for 10% and 12% of the variability respectively (p<0.01).
In conclusion, serum galectin-3 was increased in type 2 diabetic patients with and without CKD, and serum level was associated with AGEs and renal function but not with inflammation. The role of galectin-3 in diabetic complications in humans remains to be determined. |
Description | Poster Presentation |
Persistent Identifier | http://hdl.handle.net/10722/248649 |
ISSN | 2023 Impact Factor: 6.2 2023 SCImago Journal Rankings: 2.541 |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tan, KCB | - |
dc.contributor.author | Shiu, SWM | - |
dc.contributor.author | Wong, Y | - |
dc.date.accessioned | 2017-10-18T08:46:27Z | - |
dc.date.available | 2017-10-18T08:46:27Z | - |
dc.date.issued | 2017 | - |
dc.identifier.citation | The 77th American Diabetes Association (ADA) Scientific Sessions, San Diego, California, USA, 9-13 June 2017. In Diabetes, 2017, v. 66 n. Suppl. 1, p. A-138, abstract no. 526-P | - |
dc.identifier.issn | 0012-1797 | - |
dc.identifier.uri | http://hdl.handle.net/10722/248649 | - |
dc.description | Poster Presentation | - |
dc.description.abstract | Galectin-3, a member of the multifunctional galectin family, acts a broad-spectrum biological response modifier and is involved in tissue fibrosis, immunity, and inflammatory response. The role of galectin-3 in diabetic complications is unclear and animal studies have provided evidence for protective and detrimental functions of galectin-3. Although galectin-3 is a mediator of inflammation and fibrosis, it is also a scavenger receptor for advanced glycation end products (AGEs) and stimulates their degradation. We have investigated whether serum galectin-3 level is related to circulating AGEs and/or inflammation in type 2 diabetic patients with and without chronic kidney disease (CKD). 270 type 2 diabetic patients (30% with CKD and eGFR <60 ml/min/1.73m2) and 230 controls were recruited. Serum galectin-3 and AGEs were assayed by ELISA and plasma high sensitivity C-reactive protein (CRP) was measured by immunoturbidimetric assay. Diabetic patients had higher HbA1c, AGEs (4.46 ± 1.06 unit/ml (CKD+); 4.10 ± 0.98 (CKD-); 3.56 ± 0.99 (control); ANOVA p<0.01) and CRP levels than controls. Serum galectin-3 was highest in those with CKD (9.07 ± 2.64 ng/ml (CKD+); 7.48 ± 2.36 (CKD-); 5.36 ± 1.65 (control); ANOVA p<0.01). Serum glaectin-3 correlated with AGEs (r=0.34, p<0.01), eGFR (r=-0.35, p<0.01) and age (r=0.25, p<0.01) but there were no associations with duration of diabetes, HbA1c or CRP. The association with AGEs remained significant even after excluding subjects with CKD (r=0.30, p<0.01). On linear regression analysis, serum AGEs and eGFR were independent determinants of serum galectin-3 after adjusting for age, gender, body mass index, and smoking, accounting for 10% and 12% of the variability respectively (p<0.01). In conclusion, serum galectin-3 was increased in type 2 diabetic patients with and without CKD, and serum level was associated with AGEs and renal function but not with inflammation. The role of galectin-3 in diabetic complications in humans remains to be determined. | - |
dc.language | eng | - |
dc.publisher | American Diabetes Association. The Journal's web site is located at http://diabetes.diabetesjournals.org/ | - |
dc.relation.ispartof | Diabetes | - |
dc.title | Association between Serum Galectin-3 and Advanced Glycation End Products in Type 2 Diabetes | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Tan, KCB: kcbtan@hkucc.hku.hk | - |
dc.identifier.email | Shiu, SWM: swmshiu@hku.hk | - |
dc.identifier.email | Wong, Y: ywong@hku.hk | - |
dc.identifier.authority | Tan, KCB=rp00402 | - |
dc.identifier.hkuros | 282051 | - |
dc.identifier.volume | 66 | - |
dc.identifier.issue | Suppl. 1 | - |
dc.identifier.spage | A-138 | - |
dc.identifier.epage | A-138 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0012-1797 | - |