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Clin Biochem. 2016 Jan;49(1-2):70-8. doi: 10.1016/j.clinbiochem.2015.10.004. Epub 2015 Oct 21.

Erectile dysfunction and diabetes: Association with the impairment of lipid metabolism and oxidative stress.

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Urological and Andrological Unit, Department of Medicine, Surgery and Neuroscience, University Hospital, Siena, Italy.
Department of Medical Biotechnologies, University of Siena, Siena, Italy. Electronic address:
Diabetes Unit, Department of Medicine, Surgery and Neurosciences, University of Siena, Siena, Italy.
Department of Ecological and Biological Sciences, University of Tuscia, Viterbo, Italy.
Department of Medical Biotechnologies, University of Siena, Siena, Italy.



To test the hypothesis that exists an association of non-diabetic and diabetic patients suffering from erectile dysfunction (ED) with lipid metabolism and oxidative stress.


Clinical and laboratory characteristics in non-diabetic (n = 30, middle age range: 41–55.5 years; n = 25, old age range: 55.5–73), diabetic ED patients (n = 30, age range: 55.5–75 years) and diabetic patients (n = 25, age range: 56–73.25), were investigated. Proteomic analysis was performed to identify differentially expressed plasma proteins and to evaluate their oxidative posttranslational modifications.


A decreased level of high-density lipoproteins in all ED patients (P < 0.001, C.I. 0.046–0.10), was detected by routine laboratory tests. Proteomic analysis showed a significant decreased expression (P < 0.05) of 5 apolipoproteins (i.e. apolipoprotein H, apolipoprotein A4, apolipoprotein J, apolipoprotein E and apolipoprotein A1) and zinc-alpha-2-glycoprotein, 50% of which are more oxidized proteins. Exclusively for diabetic ED patients, oxidative posttranslational modifications for prealbumin, serum albumin, serum transferrin and haptoglobin markedly increased.


Showing evidence for decreased expression of apolipoproteins in ED and the remarkable enhancement of oxidative posttranslational modifications in diabetes-associated ED, considering type 2 diabetes mellitus and age as independent risk factors involved in the ED pathogenesis, lipid metabolism and oxidative stress appear to exert a complex interplay in the disease.


Diabetes; Erectile dysfunction; Lipid metabolism; Oxidative posttranslational modifications; Plasma proteome

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