Erectile dysfunction may be the first clinical sign of insulin resistance and endothelial dysfunction in young men

Background: Erectile dysfunction (ED) is an evolving health problem in the aging male population. Chronic low-grade inflammation is a critical component of ED pathogenesis and a probable intermediate stage of endothelial dysfunction, especially in metabolic diseases, with the inclusion of obesity, metabolic syndrome, and diabetes. Objective: This review will present an overview of preclinical and clinical data regarding common inflammatory mechanisms involved in the pathogenesis of ED associated with metabolic diseases and the effect of antiinflammatory drugs on ED. Methods: A literature search of existing pre-clinical and clinical studies was performed on databases [Pubmed (MEDLINE), Scopus, and Embase] from January 2000 to October 2019. Results: Low-grade inflammation is a possible pathological role in endothelial dysfunction as a consequence of ED and other related metabolic diseases. Increased inflammation and endothelial/prothrombotic markers can be associated with the presence and degree of ED. Pharmacological therapy and modification of lifestyle and risk factors may have a significant role in the recovery of erectile response through reduction of inflammatory marker levels. Conclusion: Inflammation is the least common denominator in the pathology of ED and metabolic disorders. The inflammatory process of ED includes a shift in the complex interactions of cytokines, chemokines, and adhesion molecules. These data have established that anti-inflammatory agents could be used as a therapeutic opportunity in the prevention and treatment of ED. Further research on inflammation-related mechanisms underlying ED and the effect of therapeutic strategies aimed at reducing inflammation is required for a better understanding of the pathogenesis and successful management of ED.

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Endothelial Dysfunction, Obesity and Insulin Resistance

Current Vascular Pharmacology ◽

10.2174/1570161112666140423221008 ◽

2014 ◽

Vol 12 (3) ◽

pp. 412-426 ◽

Cited By ~ 85

Author(s):

Dolores Prieto ◽

Cristina Contreras ◽

Ana Sanchez

Keyword(s):

Insulin Resistance ◽

Endothelial Dysfunction

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Increased Endothelial Dysfunction and Insulin Resistance in Patients with Klinefelter Syndrome

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530318666180220114322 ◽

2018 ◽

Vol 18 (4) ◽

pp. 401-406 ◽

Cited By ~ 1

Author(s):

Cem Haymana ◽

Aydogan Aydogdu ◽

Ibrahim Demirci ◽

Mustafa Dinc ◽

Orhan Demir ◽

...

Keyword(s):

Insulin Resistance ◽

Endothelial Dysfunction ◽

Klinefelter Syndrome

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Magnesium intake, insulin resistance and markers of endothelial function among women

Public Health Nutrition ◽

10.1017/s1368980021001063 ◽

2021 ◽

pp. 1-9

Author(s):

Narges Ghorbani Bavani ◽

Parvane Saneei ◽

Ammar Hassanzadeh Keshteli ◽

Ahmadreza Yazdannik ◽

Ebrahim Falahi ◽

...

Keyword(s):

Insulin Resistance ◽

Insulin Sensitivity ◽

Endothelial Dysfunction ◽

Endothelial Function ◽

Adhesion Molecule ◽

Cell Function ◽

Intercellular Adhesion Molecule ◽

Model Assessment ◽

Serum Concentrations ◽

Homeostasis Model Assessment

Abstract Objective: We investigated the association of dietary Mg intake with insulin resistance and markers of endothelial function among Iranian women. Design: A cross-sectional study. Setting: Usual dietary intakes were assessed using a validated FFQ. Dietary Mg intake was calculated by summing up the amount of Mg in all foods. A fasting blood sample was taken to measure serum concentrations of glycemic indices (fasting plasma glucose and insulin) and endothelial function markers (E-selectin, soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1). Insulin resistance and sensitivity were estimated using the Homeostasis Model Assessment-Insulin Resistance (HOMA-IR), Homeostasis Model Assessment β-cell function (HOMA-β) and quantitative insulin sensitivity check index (QUICKI). Participants: Iranian female nurses (n 345) selected by a multistage cluster random sampling method. Results: The Mg intake across energy-adjusted quartiles was 205 (se 7), 221·4 (se 8), 254·3 (se 7) and 355·2 (se 9) mg/d, respectively. After adjustments for potential confounders, QUICKI level was significantly different across quartiles of Mg intake (Q1: 0·34 (se 0·02), Q2: 0·36 (se 0·01), Q3: 0·40 (se 0·01), and Q4: 0·39 (se 0·02), P = 0·02); however, this association disappeared after considering markers of endothelial function, indicating that this relation might be mediated through endothelial dysfunction. After controlling for all potential confounders, Mg intake was inversely, but not significantly, associated with serum concentrations of sICAM (Q1: 239 (se 17), Q2: 214 (se 12), Q3: 196 (se 12), and Q4: 195 (se 17), P = 0·29). There was no other significant association between dietary Mg intake and other indicators of glucose homoeostasis or endothelial markers. Conclusions: Higher dietary Mg intake was associated with better insulin sensitivity in Iranian females. This linkage was mediated through reduced endothelial dysfunction.

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