Evaluation of sex hormone levels and some metabolic factors in men with coronary atherosclerosis

Dunajska, Katarzyna; Milewicz, Andrzej; Szymczak, J; Jędrzejuk, Diana; Kuliczkowski, Wiktor; Salomon, P; Nowicki, Przemysław

doi:10.1080/13685530400004181

Cited by 47 publications

(33 citation statements)

References 34 publications

(28 reference statements)

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“…Excess glucocorticoids have also been shown to decrease the number of insulin receptors and affinity in rat liver and adipocytes (Kahn et al, 1978;Buren et al, 2002). Likewise, low levels of estradiol were shown to be associated with insulin resistance in men (Dunajska et al, 2004). In view of these findings, it is proposed that castration-induced changes in corticosterone and estradiol could have contributed for the changes recorded in the present study.…”

Section: Discussionsupporting

confidence: 41%

Testosterone deficiency impairs glucose oxidation through defective insulin and its receptor gene expression in target tissues of adult male rats

et al. 2007

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Section: Discussionsupporting

confidence: 41%

Testosterone deficiency impairs glucose oxidation through defective insulin and its receptor gene expression in target tissues of adult male rats

et al. 2007

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“…27 It has been reported that the lack of male sex hormone is an independent risk factor that contributes to hypercholesterolemia and hyperlipidemia and increases the risk for developing CHD. [28][29][30] Testosterone replacement therapy in hypogonadal men delays CVD by lowering total cholesterol. However, testosterone replacement therapy increases the incidence of prostate cancer.…”

Section: Introductionmentioning

confidence: 99%

Cranberry Juice Increases Antioxidant Status Without Affecting Cholesterol Homeostasis in Orchidectomized Rats

Deyhim

Patil

Villarreal

et al. 2007

Journal of Medicinal Food

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Oxidative stress and hypogonadism are linked to the increased incidence of cardiovascular disease in males. The objective of this research was to delineate whether drinking cranberry juice for 4 months affects antioxidant capacity and lipid profile in orchidectomized rats. Thirty-two 1-year-old male rats were randomized to two groups: a sham-control group (n = 8) and an orchidectomized group (n = 24). The orchidectomized group was divided into three groups of eight and assigned to one of the following treatments: orchidectomy, orchidectomy plus 27% cranberry juice, and orchidectomy plus 45% cranberry juice. At 120 days after initiation of the study, all rats were killed, blood was collected, and plasma was harvested for total antioxidant status, malondialdehyde, nitrate + nitrite, and superoxide dismutase (SOD) activity in liver, and concentrations of cholesterol and triglyceride in liver and in plasma. Orchidectomy depressed (P < .05) plasma antioxidant capacity and SOD activity, elevated (P < .05) nitrate + nitrite and malondialdehyde in plasma, and increased (P < .05) triglyceride and cholesterol values in liver and in plasma. Cranberry juice increased (P < .05) plasma antioxidant capacity and SOD activity and reduced (P < .05) nitrate + nitrite and malondialdehyde concentrations. Drinking cranberry juice did not affect cholesterol concentrations in liver and in plasma. Triglyceride concentration in plasma of orchidectomized rats that were drinking cranberry juice increased (P < .05), but its concentration in liver decreased (P < .05) to the level of shams. The protective effect of cranberry juice from oxidative damage may be mediated by a decrease in nitrate + nitrite and dose-dependent decrease in peroxidation.

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“…Men with low testosterone levels are often more obese, hypertensive, and have increased blood glucose and serum cholesterol levels and increased carotid artery atherosclerosis with diabetes (5, 7). Additionally, Dunajaska et al (6) have shown that low levels of total testosterone, testosterone/estradiol ratio, and free androgen index are associated with coronary artery disease in men. These findings underscore the need to fully understand the effects of testosterone on coronary vascular wall biology.…”

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confidence: 99%

PKCδ Mediates Testosterone-induced Increases in Coronary Smooth Muscle Cav1.2

Maddali

Korzick

Tharp

et al. 2005

Journal of Biological Chemistry

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Sex hormones have emerged as important modulators of cardiovascular physiology and pathophysiology. Our previous studies demonstrated that testosterone increases expression and activity of L-type, voltage-gated calcium channels (Ca v 1.2) in coronary arteries of males. The purpose of the present study was to determine whether testosterone (T) alters coronary protein kinase C ␦ (PKC␦) expression and whether PKC␦ plays a role in coronary Ca v 1.2 expression. For in vitro studies, porcine right coronary arteries (RCA) and post-confluent (passages 3-6) 5-day, serum-restricted coronary smooth muscle cell cultures (CSMC) were incubated in the presence and absence of T or dihydrotestosterone (10 and 100 nM) for 18 h at 37°C in a humidified chamber. For sex and endogenous testosterone-dependent effects, RCA were obtained from intact males, castrated males, castrated males with T replacement, and intact females. In vitro T and dihydrotestosterone caused an ϳ2-3-fold increase in PKC␦ protein levels, ϳ1.5-2-fold increase in PKC␦ kinase activity, and localization of PKC␦ toward the plasma membrane and nuclear envelope. PKC␦ protein levels were higher in coronary arteries of intact males compared with intact females. Elimination of endogenous testosterone by castration reduced RCA PKC␦ protein levels, an effect partially (ϳ45%) reversed by exogenous T (castrated males with T replacement). In CSMC, PKC inhibition with either the general PKC inhibitor, cheylerythrine, or the putative PKC␦ inhibitor, rottlerin, completely inhibited the T-mediated increase in coronary Ca v 1.2 protein levels. Conversely, Go6976, a conventional PKC isoform inhibitor, failed to inhibit T-induced increases in coronary Ca v 1.2 protein levels. PKC␦ short interference RNA completely blocked T-induced increases in Ca v 1.2 protein levels in CSMC. These results demonstrate for the first time that 1) endogenous T is a primary modulator of coronary PKC␦ protein and activity in males and 2) T increases Ca v 1.2 protein expression in a PKC␦-dependent manner.Coronary heart disease is a major cause of global mortality and represents an underlying cause for most heart attacks and sudden death (1). Men 30 -50 years of age have an increased incidence of coronary heart disease compared with women of similar age (2-4), a sex difference that led many to the conclusion that testosterone increases the risk of coronary heart disease in men. However, recent clinical studies have failed to support a detrimental effect of testosterone on coronary heart disease (5-7). On the contrary, low testosterone concentrations in men are associated with a higher risk of atherosclerosis (7). Men with low testosterone levels are often more obese, hypertensive, and have increased blood glucose and serum cholesterol levels and increased carotid artery atherosclerosis with diabetes (5, 7). Additionally, Dunajaska et al. (6) have shown that low levels of total testosterone, testosterone/estradiol ratio, and free androgen index are associated with coronary artery disease in men. These f...

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Evaluation of sex hormone levels and some metabolic factors in men with coronary atherosclerosis

Abstract: Low levels of total testosterone, testosterone/estradiol ratio and free androgen index and higher levels of estrone in men with coronary artery disease appear together with many features of metabolic syndrome and may be involved in the pathogenesis of coronary atherosclerosis.

Cited by 47 publications

References 34 publications

Testosterone deficiency impairs glucose oxidation through defective insulin and its receptor gene expression in target tissues of adult male rats

Testosterone deficiency impairs glucose oxidation through defective insulin and its receptor gene expression in target tissues of adult male rats

Cranberry Juice Increases Antioxidant Status Without Affecting Cholesterol Homeostasis in Orchidectomized Rats

PKCδ Mediates Testosterone-induced Increases in Coronary Smooth Muscle Cav1.2

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