Role of disturbed fatty acids metabolism in the pathophysiology of diabetic erectile dysfunction

Abstract

Background: Vasculogenic erectile dysfunction (VED) is considered as a common complication among people with type 2 diabetes (T2D). We tested whether changes in fatty acid (FAs) classes measured in erythrocytes are associated with increased risk of diabetic VED along with related risk factors.

Methods: We assessed erythrocyte FAs composition, lipid peroxidation parameters and inflammatory cytokines among 72 T2D men with VED, 78 T2D men without VED and 88 healthy volunteers with similar age. Biochemical, hepatic, lipid and hormonal profiles were measured.

Results: T2D people with VED had significant decrease in the indexes of Δ6-desaturase and elongase activities compared to the other studied groups. The same group of participants displayed lower erythrocytes levels of dihomo-γ-linolenic acid (C20:3n-6) (P < .001), precursor of the messenger molecule PGE1 mainly involved in promoting erection. Moreover, absolute SFAs concentration and HOMA IR levels were higher in T2D people with VED when compared to controls and associated with impaired NO concentration (1.43 vs 3.30 ng/L, P < .001). Our results showed that IL-6 and TNF-α were significantly increased and positively correlated with MDA levels only in T2D people with VED (r = 0.884, P = .016 and r = 0.753, P = .035; respectively) suggesting a decrease in the relative availability of vasodilator mediators and an activation of vasoconstrictors release.

Conclusion: Our findings show that the deranged FAs metabolism represents a potential marker of VED in progress, or at least an indicator of increased risk within men with T2D.

Keywords: Diabetic erectile dysfunction; Fatty acids; Inflammation; Insulin resistance; Type 2 diabetes.

Fig. 1

Hypothetical interaction between disturbed FAs metabolism and IR leading to impaired penile erection. SFAs, Saturated Fatty Acids; IR, Insulin Resistance; PI3-kinase, Phosphatidylinositol 3-Kinase; SREBP, Sterol Regulatory Element Binding Protein; Akt, Protein kinase B; eNOS, Endothelial Nitric Oxide Synthase; PGE1, Prostaglandin E1; NO, Nitric Oxide; GPCR, G-Protein-Coupled Receptor; ATP, Adenosine Triphosphate; cAMP, cyclic Adenosine Monophosphate; GTP, Guanosine Triphosphate; cGMP, cyclic Guanosine Monophosphate; Ca²⁺, Calcium; VSMCs, Vascular Smooth Muscle Cells; (), Increase; (), Decrease