Regulation of hepatic copper in the rat by the adrenal gland

1970 ◽  
Vol 48 (2) ◽  
pp. 160-163 ◽  
Author(s):  
G. Gregoriadis ◽  
T. L. Sourkes

The concentration of hepatic copper in the adult rat is increased above control values (17%, P < 0.05) 6 weeks following adrenalectomy. At the same time, renal copper is decreased (23%, P < 0.01) and ceruloplasmin (serum oxidase activity) is increased. Administration of deoxycorticosterone or hydrocortisone for 1–2 weeks does not affect the concentration of hepatic copper or serum ceruloplasmin in the intact rat. A role of the adrenals in the metabolism of copper is observed in animals in positive copper balance, achieved by administering Cu2+ intraperitoneally; greater amounts of copper accumulate in the liver of adrenalectomized rats than sham-operated animals. Furthermore, the rate of elimination of the excess copper from the liver of copper-injected rats is reduced following adrenalectomy. 11-Hydroxycorticosteroids have a limited but favorable effect on this process; deoxycorticosterone treatment results in higher concentrations of hepatic copper in such animals.

2004 ◽  
Vol 30 (4) ◽  
pp. 609-610
Author(s):  
Shirley Campbell ◽  
Mélissa Otis ◽  
Nicole Gallo‐Payet ◽  
Marcel Daniel Payet

1992 ◽  
Vol 70 (8) ◽  
pp. 1090-1095 ◽  
Author(s):  
Michael J. Katovich ◽  
David Pitman ◽  
Orit Schechtman

Administration of naloxone to morphine-dependent rats results in an elevation of tail skin temperature and a fall in core temperature. Previous studies have demonstrated a role of the adrenal gland in the thermal responses that accompany morphine withdrawal in the rat. In the present study, experiments were designed to determine if the duration of adrenalectomy significantly influenced the thermal response observed in morphine withdrawal. In addition we evaluated the influence of the adrenal medulla and glucocorticoid replacement in adrenalectomized rats in mediating the thermal responses of the morphine-dependent rat. Ovariectomized rats were addicted to morphine and subsequently withdrawn by administration of naloxone. This treatment results in a significant rise in tail skin temperature and subsequent fall in colonic temperature. These thermal responses were not observed in morphine-naive rats. Adrenalectomy resulted in a significant attenuation of the rise in tail skin temperature associated with withdrawal. This reduced tail skin temperature response was not different among animals adrenalectomized for 1, 7, 14, 21, or 28 days. Likewise, the moderate increase in core temperature associated with morphine treatment was not observed in the adrenalectomized rats. Serum corticosteroid determinations confirmed the loss of the adrenal steroids in the adrenalectomized rats. In a subsequent experiment it was determined that adrenal demedullation did not reduce the tail skin temperature response during morphine withdrawal, and corticosteroids restored the naloxone-induced surge in tail skin temperature in morphine-dependent, adrenalectomized rats. Collectively, these data suggest a role for the adrenal gland, especially the cortical region, in allowing for full expression of the skin temperature changes associated with withdrawal in morphine-dependent animals.Key words: corticosterone, tail skin temperature, morphine withdrawal, adrenal gland, thermal response, naloxone.


Author(s):  
U. Bielenberg

Copper deficiency can cause cardiovascular lesions in experimental animals. Previous experiments have shown that the biochemical and itDrphologic lesions induced by deprivation of dietary copper can be suppressed by feeding diets containing starch or can be magnified by a high sucrose diet. In a recent study it was found that the more severe signs of copper deficiency in rats fed sucrose as compared to starch were due to the fructose moiety of sucrose. Although fructose as compared to starch markedly enhanced the symptoms of copper deficiency, the possibility that an effect of dietary carbohydrates due to the nature of the simple carbohydrate (fructose vs glucose) cannot be excluded. The present study was designed to determine if the severity of copper deficiency in rats fed sucrose as compared to starch is due to the glucose as well as the fructose moiety of sucrose. This portion of the study assessed the morphologic changes in aortas of seventy weanling male rats who were fed, for 9 weeks, copper deficient or copper supplemented diets containing either 62% starch, fructose or glucose. The starch-fed copper supplemented group served as the most normal controls. Rats were sacrificed after 9 weeks of dietary treatments. Copper deficiency was verified by reduced serum ceruloplasmin activity and serum and hepatic copper concentration.


1998 ◽  
Vol 275 (5) ◽  
pp. R1461-R1467 ◽  
Author(s):  
Tetsuya Ando ◽  
Jean Rivier ◽  
Hitoshi Yanaihara ◽  
Akira Arimura

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [d-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12—41(1.5 mg/kg) or cyclo(30—33)[d-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12—41(Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.


2015 ◽  
Vol 1 ◽  
pp. 199-209 ◽  
Author(s):  
Nabila Yousef Abdel Haleem ◽  
Hoda Mahmoud El-Aasar ◽  
Sherif Mohamed Zaki ◽  
Sherif Mohamed Sabry ◽  
Ahmed Wafiq El-Zainy

Endocrinology ◽  
1992 ◽  
Vol 131 (2) ◽  
pp. 807-814 ◽  
Author(s):  
M Sander ◽  
M Bader ◽  
B Djavidani ◽  
C Maser-Gluth ◽  
P Vecsei ◽  
...  
Keyword(s):  

Sexual Health ◽  
2014 ◽  
Vol 11 (2) ◽  
pp. 200 ◽  
Author(s):  
Ian Down ◽  
Garrett Prestage ◽  
Kathy Triffitt ◽  
Graham Brown ◽  
Jack Bradley ◽  
...  

Background In recent years, there has been increasing evidence that early initiation of antiretroviral therapy (ART) may provide health benefits for those infected with HIV. There has also been significant discussion about the role of HIV treatment in preventing onward transmission of the virus. Early provision and uptake of ART to people recently diagnosed with HIV could achieve both individual and public health outcomes. The success of such an initiative relies, in part, on the preparedness of those recently diagnosed with HIV to engage with the therapy. Methods: The HIV Seroconversion Study collects both quantitative and qualitative data from people in Australia who have recently been diagnosed with HIV. During 2011–2012, 53 gay or bisexual men recruited across Australia took part in semistructured interviews as part of the study. The men were asked about their knowledge and experience of, and their decisions about whether or not to commence, HIV treatment. Results: The interviews identified differing levels of knowledge about HIV treatments and divergent views about the health and prevention benefits of ART. For some, treatments provided a sense of control over the virus; others were apprehensive and distrustful, and preferred to resist commencing treatments for as long as possible. Conclusions: If early initiation of treatment is to be encouraged, appropriate measures must be in place to ensure recently diagnosed individuals have access to the appropriate information and the support they need to enable them to make informed choices and, if necessary, to address their fears.


2002 ◽  
Vol 282 (6) ◽  
pp. C1339-C1347 ◽  
Author(s):  
Aïssata Amadou ◽  
Artur Nawrocki ◽  
Martin Best-Belpomme ◽  
Catherine Pavoine ◽  
Françoise Pecker

Tumor necrosis factor (TNF)-α has a biphasic effect on heart contractility and stimulates phospholipase A2 (PLA2) in cardiomyocytes. Because arachidonic acid (AA) exerts a dual effect on intracellular Ca2+ concentration ([Ca2+]i) transients, we investigated the possible role of AA as a mediator of TNF-α on [Ca2+]i transients and contraction with electrically stimulated adult rat cardiac myocytes. At a low concentration (10 ng/ml) TNF-α produced a 40% increase in the amplitude of both [Ca2+]i transients and contraction within 40 min. At a high concentration (50 ng/ml) TNF-α evoked a biphasic effect comprising an initial positive effect peaking at 5 min, followed by a sustained negative effect leading to 50–40% decreases in [Ca2+]i transients and contraction after 30 min. Both the positive and negative effects of TNF-α were reproduced by AA and blocked by arachidonyltrifluoromethyl ketone (AACOCF3), an inhibitor of cytosolic PLA2. Lipoxygenase and cyclooxygenase inhibitors reproduced the high-dose effects of TNF-α and AA. The negative effects of TNF-α and AA were also reproduced by sphingosine and were abrogated by the ceramidase inhibitor n-oleoylethanolamine. These results point out the key role of the cytosolic PLA2/AA pathway in mediating the contractile effects of TNF-α.


1996 ◽  
Vol 17 (12) ◽  
pp. 448-448
Author(s):  
Philip O. Ozuah

Wilson disease (hepatolenticular degeneration) is an autosomal recessive, inherited disorder of copper metabolism resulting in excessive accumulation of copper in the liver, brain, and other organs of the body. The manifestations of the disease are related directly to this accumulation of copper. Copper homeostasis normally is a product of the balance between intestinal absorption of dietary copper and hepatic biliary excretion of excess copper. In Wilson disease, incorporation of hepatic copper into ceruloplasmin is defective and excretion of copper in the bile is reduced. A low level of ceruloplasmin, which until a few years ago was erroneously considered to be the basis for the disease, is a consequence of the underlying metabolic defect.


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