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Published on: January 24, 2025
Adiponectin, Insulin Sensitivity and Diabetic Retinopathy in Latinos With Type 2 Diabetes
Jane Z Kuo1, Xiuqing Guo1, Ronald Klein1
1Department of Ophthalmology (J.Z.K.), Shiley Eye Center, UC San Diego, La Jolla, California 92093; Pathway Genomics Corporation (J.Z.K.), San Diego, California 92121; Institute for Translational Genomics and Population Sciences (X.G., K.R., Y.H., J.I.R., Y.-D.I.C.), Los Angeles BioMedical Research Institute, Harbor-UCLA Medical Center, Torrance, California 90502; Department of Ophthalmology and Visual Sciences (R.K., B.E.K.), University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53726; Section of Diabetes and Metabolism (P.G., E.I.), Los Angeles BioMedical Research Institute, Harbor-UCLA Medical Center, Torrance, California 90502; Division of Endocrinology, Diabetes, and Metabolism (M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048.
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.
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