Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Bastida, C.M.; Cremades, Adolfo Díaz-Bautista; Castells, María Teresa; López-Contreras, Andrés J.; López‐García, Carlos; Sánchez-Más, Jesús; Peñafiel, Rafael

doi:10.1152/ajpendo.00316.2006

Cited by 34 publications

(20 citation statements)

References 57 publications

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“…The opposite effect of testosterone on DDC gene expression found in kidney and intestine could be related, in principle, with differences in the set of nuclear receptor co-repressors or co-activators or in other tissue-specific factors, as well as in epigenetic changes that may affect androgen action. In this regard, it must be noted that opposite effects of testosterone on other amino acid decarboxylases, such as ODC, have been also observed in different mouse tissues, where androgens dramatically increased this enzyme in the kidney but down-regulated ODC in the mouse adrenals (Bastida et al 2007). Furthermore, our results on the effect of androgens on renal DDC are in agreement with recent studies that concluded that human neoplastic prostate epithelium DDC is down-regulated by androgens (Nelson et al 2002).…”

Section: Discussionsupporting

confidence: 92%

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

López-Contreras

Galindo²,

López‐García³

et al. 2007

Journal of Endocrinology

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3,4-Dihydroxyphenylalanine decarboxylase (DDC; also known as L-amino acid decarboxylase) is involved in the synthesis of dopamine, norepinephrine, and serotonin, and also acts as an androgen receptor co-regulator protein. In contrast to other amino acid decarboxylases that are modulated by sex hormones, little is known about the influence of these hormones on DDC regulation. In the present work, we studied the influence of gender in the expression of DDC in different mouse tissues. Among the different organs studied, including brain, liver, kidney, intestine, heart, adrenal gland, and skeletal muscle, only kidney and small intestine showed a sex-dependent dimorphism in DDC expression. In the kidney, levels of DDC activity, DDC mRNA, and protein were remarkably higher in females than in males. On the contrary, in the small intestine, male mice displayed higher levels of DDC activity than females but they did not correlate precisely with mRNA levels. This dimorphism was dependent on androgens, since male castration and treatment of female mice with testosterone propionate, oppositely affected DDC levels in kidney and small intestine. However, estrogen ablation or treatment with estradiol did not significantly affect DDC activity in these tissues. Immunocytochemical analysis revealed that DDC was mainly located in the proximal straight tubular cells of the kidney and in the cytoplasm of enterocytes. These data and the fact that renal DDC inversely correlated with renal sodium reabsorption suggest that renal and intestinal gender dimorphism in DDC could be related to sexrelated differences in sodium balance observed between males and females.

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Section: Discussionsupporting

confidence: 92%

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

López-Contreras

Galindo²,

López‐García³

et al. 2007

Journal of Endocrinology

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“…To ascertain this, a separate restraint stress experiment was carried out to evaluate the hypothalamus-pituitary-corticoadrenal axis (HPA). Female mice showed higher adrenal gland and stress circulating corticosterone levels than male mice, as expected [45,46]. Muscle IL-6 KO female mice responded less to restraint stress, in principle ruling out sensitivity to stress as the main reason underlying the differences in body weight during the acclimatization periods of the fasting/refeeding-leptin experiments.…”

Section: Discussionsupporting

confidence: 72%

Role of muscle IL-6 in gender-specific metabolism in mice

et al. 2017

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The aim of the present work was to further explore the physiological roles of muscle-derived IL-6. Adult-floxed and conditional skeletal muscle IL-6 knock out male and female mice were used to study energy expenditure (indirect calorimetry at rest and during treadmill exercise, and body temperature cycle during the light phase) and energy intake (response to fast/refeeding). We also evaluated the responses to leptin and the activity of the insulin signalling pathway in skeletal muscle and liver by phosphorylation of Akt at Ser 473. The stress response was also studied. Results indicate a relevant role of muscle IL-6 in maintaining energy homeostasis, especially in males. Absence of muscle IL-6 in male mice results in lower core body temperature in the light phase, increased respiratory exchange ratio (RER) both at rest and during exercise, increased expression of TCA cycle marked gene, citrate synthase in muscle, reduced fat storage and decreased body weight and food consumption in response to leptin. In females, muscle IL-6 deficiency increases VO2 and CO2 levels similarly. Also in contrast to males, energy expenditure (EE) measured over 48h reveals a significant elevation in female mice with muscle IL-6 deficiency; moreover, they show a modified response to fasting-refeeding and to restraint stress. The present results contribute to the understanding of the role of muscle IL-6 in male and female mouse metabolism, not only during exercise but also in the basal state and in situations where energy balance is altered.

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“…The major rate-limiting enzymes of this pathway are ornithine decarboxylase (ODC), spermidine/spermine N 1 -acetyl transferase (SAT1), and S-adenosylmethionine decarboxylase (AMD1), whose activities are influenced by numerous regulatory proteins as well as the polyamine levels [9]. In addition, not only are polyamines known to influence neurotransmitter systems, such as catecholamines [10,11], gamma-aminobutyric acid (GABA) [12], glutamate [13], and nitric oxide [14], but agmatine is also believed to act as a neurotransmitter [15]. Finally, polyamines are also able to influence the properties of several transmembrane channels, thereby affecting cell excitability [16].…”

Section: -Biosynthesismentioning

confidence: 99%

Suicide and the Polyamine System

Gross¹,

Turecki

2013

CNSNDDT

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Suicide is a significant worldwide public health problem. Understanding the neurobiology is important as it can help us to better elucidate underlying etiological factors and provide opportunities for intervention. In recent years, many lines of research have suggested that the polyamine system may be dysregulated in suicidal behaviors. Initial research in animals provided evidence of a dysfunctional polyamine stress response system, while later work using post-mortem human brain tissue has suggested that molecular mechanisms may be at play in the suicide brain. In this review, we will describe the research that suggests the presence of alterations in the polyamine system in mental disorders and behavioral phenotypes, with particular attention to work on suicide. In addition, we will also describe potential avenues for future work. KeywordsEpigenetics; Major Depressive Disorder; Neurobiology; Polyamines; Polyamine Stress Response; Spermidine/Spermine-N 1 -Acetyltransferase; Suicide -IntroductionSuicide, most often associated with major depressive disorder (MDD) [1], is an important cause of premature death around the world [2]. According to the World Health Organization (www.who.int, 2012), approximately one million people die by suicide annually, and the rate of suicide attempts is 20 times greater than that of suicide completion (www.who.int, 2012). As such, suicidal behaviors (SB) are an important source of public health concern. The etiology of suicide is complex [3], and commonly understood as resulting from the interaction of predisposing (distal) and precipitant (proximal) factors [4]. Biological alterations resulting from a combination of genetic and environmental risk factors underlie predisposition to suicide, but the exact molecular mechanisms at play remain largely unclear. As such, it is important that we gain a better understanding of the molecular processes associated with suicide in order to identify new avenues for prevention and intervention.Over the past several decades, molecular studies of suicide and MDD have focused on the monoamine system. Beginning in the late 1960s, research into the neurobiology of suicide

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Sexual dimorphism of ornithine decarboxylase in the mouse adrenal: influence of polyamine deprivation on catecholamine and corticoid levels

Cited by 34 publications

References 57 publications

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

Opposite sexual dimorphism of 3,4-dihydroxyphenylalanine decarboxylase in the kidney and small intestine of mice

Role of muscle IL-6 in gender-specific metabolism in mice

Suicide and the Polyamine System

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