Depression in Type 2 diabetes is associated with obesity, cardiovascular disease, and mortality. Leptin is a plausible mediating factor because it has been related to obesity, depression, and cardiovascular disease in nondiabetic populations. We sought to assess whether leptin is related to depressive symptoms in people with Type 2 diabetes.
One thousand fifty-seven subjects (48.5% women, mean [standard deviation] age = 67.9 [4.2] years) with Type 2 diabetes were assessed for depressive symptoms using the Hospital Anxiety and Depression Scale and other clinical variables by interview and physical examination. Plasma leptin was determined by radioimmunoassay. Multiple linear regression was performed to assess the relationship between depressive symptoms and ln leptin while adjusting for other covariates. A mediation analysis was performed to test whether depressive symptoms mediated the relationship between obesity and leptin.
In univariate analyses, symptoms of depression were related to leptin in men (r = 0.214, p < .001) and women (r = 0.146, p = .007). When adjusting for other covariates including body mass index, ischemic heart disease, glycated hemoglobin, duration of diabetes, and treatment with antidepressants, insulin, or glucocorticoids, using a hierarchical multiple linear regression, depressive symptoms (ln Hospital Anxiety and Depression Scale—depression score) were significant only in men (B = 0.083, standard error = 0.037, p = .03). In the mediation analysis, depressive symptoms partially mediated the effect of obesity (body mass index) on leptin in men but not in women.
There is a sex difference in the relationship between depressive symptoms and leptin in people with Type 2 diabetes, with a positive association in men but not in women. Adipocyte-derived factors are associated with depressive symptoms in Type 2 diabetes.
HADS-D = Hospital Anxiety Depression Scale—depression subscale; ET2DS = Edinburgh Type 2 Diabetes Study; IHD = ischemic heart disease; MI = myocardial infarction
From the Endocrinology Unit (J.L., J.R.S., B.R.W., R.M.R.), Centre for Cardiovascular Sciences, Queen’s Medical Research Institute, and Division of Community Health Sciences and Centre for Population Health Sciences (J.F.P., F.G.R.F.), School of Clinical Sciences and Community Health, College of Medicine and Veterinary Medicine; and Centre for Cognitive Ageing and Cognitive Epidemiology, Department of Psychology (I.J.D.), School of Philosophy, Psychology, and Language Sciences, University of Edinburgh; Metabolic Unit (M.W.J.S.), Western General Hospital, Edinburgh; British Heart Foundation Glasgow Cardiovascular Research Centre (N.S.), University of Glasgow, Glasgow, Scotland, United Kingdom; and Hospital Psiquiatric Universitari Institut Pere Mata (J.L.), Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Reus, Spain.
Address correspondence and reprint requests to Rebecca M. Reynolds, PhD, Endocrinology Unit, Centre for Cardiovascular Sciences, Queen’s Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, Scotland, United Kingdom. E-mail: R.Reynolds@ed.ac.uk
This study was supported by a grant from the Medical Research Council.
All authors declare no conflicts of interest.
Received for publication February 23, 2011; revision received August 29, 2011.