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Journal of the Endocrine Society 2018-Aug

Estradiol Does Not Influence Lipid Measures and Inflammatory Markers in Testosterone-Clamped Healthy Men.

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Ferdinand Roelfsema
Rebecca J Yang
Johannes D Veldhuis

Keywords

Abstract

UNASSIGNED

Experimentally controlled studies of estrogenic regulation of lipid measures and inflammatory cytokines in men are rare.

UNASSIGNED

To delineate the effect of estradiol (E2) on lipids and inflammatory markers.

UNASSIGNED

This was a placebo-controlled, single-masked, prospectively randomized study comprising experimentally degarelix-downregulated healthy men [n = 74; age 65 years (range, 57 to 77)] assigned to four treatment groups: (1) IM saline and oral placebo; (2) IM testosterone and oral placebo; (3) IM testosterone and oral anastrozole (aromatase inhibitor); and (4) IM testosterone, oral anastrozole, and transdermal E2 for 22 (±1) days.

UNASSIGNED

Mean mass spectrometry-quantified serum E2 concentrations ranged from 1.2 to 82 pg/mL in the four treatment groups. E2 extremes did not alter total cholesterol, triglyceride, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein cholesterol (HDL-C) , non-HDL-C, apolipoprotein B, lipoprotein (a), IL-6, or high-sensitivity C-reactive protein (hsCRP) concentrations. Higher E2 concentrations elevated both sex hormone-binding globulin and prolactin as positive controls. LDL cholesterol, adiponectin, and leptin were higher in hypogonadal subjects without testosterone or E2 addback (P = 0.018, 0.039, and 0.023, respectively). Abdominal visceral fat area by CT (independent variable) correlated negatively with HDL-C (P = 0.017), and positively with triglycerides (P = 0.004), hsCRP (P = 0.005), and leptin (P < 0.0001).

UNASSIGNED

In this placebo-controlled prospectively randomized study, wide variations in circulating E2 did not influence lipid measures and inflammatory markers when testosterone concentrations were controlled experimentally. However, medically induced central hypogonadism in older men was accompanied by increased LDL cholesterol and metabolic cytokines, adiponectin and leptin. Abdominal visceral fat correlated strongly and positively with triglycerides, hsCRP, and leptin, but negatively with HDL.

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