BACKGROUND: Previous studies have demonstrated that leptin is an angiogenic factor, and an increase in intravitreous leptin concentrations in diabetic patients with proliferative diabetic retinopathy (PDR) has also been described. The aim of the present study was to investigate the source of intravitreal leptin and to determine whether it is related to PDR activity. METHODS: Serum and vitreous fluid samples were obtained simultaneously at the time of vitreoretinal surgery from 25 patients with PDR and 32 nondiabetic patients with nonproliferative ocular diseases (controls). Both groups were matched by age, sex, and body mass index. Leptin levels were determined by ELISA. RESULTS: We did not observe any significant differences in vitreal levels of leptin between diabetic patients with PDR and controls (4.22 [2.6-9.7] versus 3.49 [1.9-9.7] ng/mL; P = not significant). Leptin concentrations were lower in vitreous fluid than in serum samples from diabetic patients with PDR (P < 0.001) and controls (P < 0.001). A direct correlation between serum and vitreous leptin concentrations was detected in diabetic patients with PDR (r = 0.60; P = 0.01) and controls (r = 0.51; P = 0.01). Finally, we did not observe any relationship between intravitreous leptin levels and PDR activity. CONCLUSIONS: The intraocular production of leptin is not critically involved in the etiopathogenesis of PDR. In addition, our results suggest that serum diffusion is a relevant source of leptin in vitreous fluid.
BACKGROUND: Previous studies have demonstrated that leptin is an angiogenic factor, and an increase in intravitreous leptin concentrations in diabeticpatients with proliferative diabetic retinopathy (PDR) has also been described. The aim of the present study was to investigate the source of intravitreal leptin and to determine whether it is related to PDR activity. METHODS: Serum and vitreous fluid samples were obtained simultaneously at the time of vitreoretinal surgery from 25 patients with PDR and 32 nondiabeticpatients with nonproliferative ocular diseases (controls). Both groups were matched by age, sex, and body mass index. Leptin levels were determined by ELISA. RESULTS: We did not observe any significant differences in vitreal levels of leptin between diabeticpatients with PDR and controls (4.22 [2.6-9.7] versus 3.49 [1.9-9.7] ng/mL; P = not significant). Leptin concentrations were lower in vitreous fluid than in serum samples from diabeticpatients with PDR (P < 0.001) and controls (P < 0.001). A direct correlation between serum and vitreous leptin concentrations was detected in diabeticpatients with PDR (r = 0.60; P = 0.01) and controls (r = 0.51; P = 0.01). Finally, we did not observe any relationship between intravitreous leptin levels and PDR activity. CONCLUSIONS: The intraocular production of leptin is not critically involved in the etiopathogenesis of PDR. In addition, our results suggest that serum diffusion is a relevant source of leptin in vitreous fluid.