Testosterone

About: Testosterone is a research topic. Over the lifetime, 23258 publications have been published within this topic receiving 808079 citations. The topic is also known as: 4-androsten-17beta-ol-3-one & 4-Androsten-3-one-17b-ol.

Angiotensin Converting Enzyme 2 Contributes to Sex Differences in the Development of Obesity Hypertension in C57bl/6 Mice

Abstract: Objectives— Obesity promotes hypertension, but it is unclear if sex differences exist in obesity-related hypertension. Angiotensin converting enzyme 2 (ACE2) converts angiotensin II (AngII) to angiotensin-(1–7) (Ang-[1–7]), controlling peptide balance. We hypothesized that tissue-specific regulation of ACE2 by high-fat (HF) feeding and sex hormones contributes to sex differences in obesity-hypertension. Methods and Results— HF-fed females gained more body weight and fat mass than males. HF-fed males exhibiting reduced kidney ACE2 activity had increased plasma angiotensin II levels and decreased plasma Ang-(1–7) levels. In contrast, HF-fed females exhibiting elevated adipose ACE2 activity had increased plasma Ang-(1–7) levels. HF-fed males had elevated systolic and diastolic blood pressure that were abolished by losartan. In contrast, HF-fed females did not exhibit increased systolic blood pressure until females were administered the Ang-(1–7) receptor antagonist, D-Ala-Ang-(1–7). Deficiency of ACE2 increased systolic blood pressure in HF-fed males and females, which was abolished by losartan. Ovariectomy of HF-fed female mice reduced adipose ACE2 activity and plasma Ang-(1–7) levels, and promoted obesity-hypertension. Finally, estrogen, but not other sex hormones, increased adipocyte ACE2 mRNA abundance. Conclusions— These results demonstrate that tissue-specific regulation of ACE2 by diet and sex hormones contributes to sex differences in obesity-hypertension.

Effects of acute alcohol intake on pituitary-gonadal hormones in normal human males.

Abstract: Plasma luteinizing hormone and testosterone levels were determined in 16 normal adult males during a period of acute alcohol intoxication. Plasma testosterone levels were in the normal range for adult males prior to alcohol administration. Plasma testosterone levels began to fall during the ascending phase of the blood alcohol curve but plasma luteinizing hormone levels did not change significantly. At peak blood alcohol levels [109 +/- 4.6 (S.D.) mg/100 ml], plasma testosterone was significantly depressed and a significant increase in plasma luteinizing hormone values occurred. During the descending phase of the blood alcohol curve, plasma testosterone levels remained depressed and plasma luteinizing hormone levels decreased toward base-line values. These data indicate that acute alcohol intake produces a suppression of plasma testosterone via peripheral mechanisms which regulate the biosynthesis and/or biotransformation of the steroid. The surge in luteinizing hormone values at peak levels of intoxication are most likely due to stimulation of gonadotropin secretion via "long loop" mechanisms associated with low levels of plasma testosterone.