Adiponectin, Insulin Sensitivity and Diabetic Retinopathy in Latinos With Type 2 Diabetes.

Kleins Lab // Publications // Sep 01 2015

PubMed ID: 26020763

Author(s): Kuo JZ, Guo X, Klein R, Klein BE, Genter P, Roll K, Hai Y, Goodarzi MO, Rotter JI, Chen YD, Ipp E. Adiponectin, insulin sensitivity and diabetic retinopathy in latinos with type 2 diabetes. J Clin Endocrinol Metab. 2015 Sep;100(9):3348-55. doi: 10.1210/jc.2015-1221. Epub 2015 May 28. PMID 26020763

Journal: The Journal Of Clinical Endocrinology And Metabolism, Volume 100, Issue 9, Sep 2015

CONTEXT AND OBJECTIVE Insulin resistance and chronic inflammation are key elements in the pathogenesis of type 2 diabetes. We hypothesized that similar mechanisms could have a role in the development of diabetic retinopathy (DR), an important microvascular complication in Latinos with type 2 diabetes.

DESIGN AND SETTING A cross-sectional, family-based, observational cohort study.

PATIENTS Latino subjects with type 2 diabetes (n = 507), ascertained in families via a proband with known diabetes duration of 10 years or more and/or with DR, were included.

MAIN OUTCOME MEASURES Serum adiponectin was measured and insulin sensitivity was estimated using homeostasis model assessment of insulin resistance (HOMA-IR). DR was assessed by seven-field digital fundus photography and graded using the modified Airlie House classification and the Early Treatment Diabetic Retinopathy Scale (range of severity levels, 10-85).

RESULTS Fasting adiponectin concentrations were elevated in patients with DR compared to those without (12.9 ± 0.5 vs 10.5 ± 0.5 μg/mL; P = .0004) and remained significant after adjusting for multiple covariates (age, gender, body mass index, glycosylated hemoglobin, diabetes duration, statin use, blood pressure, and renal function; P = .013 to .018). Adiponectin was also positively correlated with severity of DR in patients with nonproliferative DR (P < .0003), significant also after all covariate adjustments (P = .018). When the proliferative DR group was included, this relationship was attenuated by adjustments, possibly an influence of estimated glomerular filtration rate reduction in the proliferative DR group. HOMA-IR was not different in the DR and non-DR groups. Although elevated, adiponectin retained a typical inverse relationship with HOMA-IR in DR, similar to that seen in the non-DR group.

CONCLUSIONS Serum adiponectin is elevated in DR, is positively correlated with DR severity in Latinos with type 2 diabetes, and maintains a relationship to insulin sensitivity. Adiponectin, whether as a marker or biological mediator, may play an important role in DR, which appears to be independent of its relationship to insulin sensitivity.