Function of the hypothalamo-hypophyseal-adrenal system in mice with ectopic hyperproduction of the agouti protein

2005 ◽  
Vol 35 (2) ◽  
pp. 187-191 ◽  
Author(s):  
N. R. Karkaeva ◽  
N. M. Bazhan ◽  
T. V. Yakovleva ◽  
E. N. Makarova
1972 ◽  
Vol 68 (3_Suppl) ◽  
pp. S10
Author(s):  
F. W. Lohmann ◽  
H. Schleusener ◽  
F. Adlkofer
Keyword(s):  

Pharmacology ◽  
1973 ◽  
Vol 9 (6) ◽  
pp. 348-356 ◽  
Author(s):  
A. Daniels-Severs ◽  
A. Goodwin ◽  
L.C. Keiland ◽  
J. Vernikos-Danellis

2015 ◽  
Vol 46 (1) ◽  
pp. 100-105
Author(s):  
V. V. Khlebnikov ◽  
S. L. Kuznetsov ◽  
D. A. Chernov ◽  
A. M. Agrytskov ◽  
A. Ahmad ◽  
...  

1980 ◽  
Vol 90 (6) ◽  
pp. 1633-1635
Author(s):  
E. M. Stabrovskii ◽  
M. S. Konstantinova ◽  
K. F. Korovin ◽  
L. S. Shpanskaya
Keyword(s):  

Author(s):  
Irodakhon Makhkambaevna Tashtemirova ◽  

The aim of the given work was study interactions of impairments sympa-thetic – adrenal systems functional condition and processes of peroxidal oxida-tion of lipids in woman with metabolic syndrome. 107women at the age of 25-49 were observation. They were randomized into 3 groups: I (control) – 15 healthy persons, II – 43 patients with arterial hypertension, III – 49 women with arterial hypertension in combination with metabolic syndrome. The results of carried investigations showed that activation of sympathetic adrenal system and processes of peroxidal oxidation of lipids took place in metabolic syn-drome. Marked lowering of sympathetic – adrenal system key ferment catechol-amins (MAO monoaminooxidaze) desamidization activity and considerable ac-tivation of peroxidal oxidation of lipid products which have great significance in revealing the mechanism of metabolic syndrome development were observed in metabolic syndrome. This results in the prolonged toxic influence of catechola-mins on myocardium.


1999 ◽  
Vol 1 (1) ◽  
pp. 11-19 ◽  
Author(s):  
B. Z. XUE ◽  
W. O. WILKISON ◽  
R. L. MYNATT ◽  
N. MOUSTAID ◽  
M. GOLDMAN ◽  
...  

Xue, B. Z., W. O. Wilkison, R. L. Mynatt, N. Moustaid, M. Goldman, and M. B. Zemel. The agouti gene product stimulates pancreatic β-cell Ca2+ signaling and insulin release. Physiol. Genomics 1: 11-19, 1999.—Ubiquitous expression of the mouse agouti gene results in obesity and hyperinsulinemia. Human agouti is expressed in adipose tissue, and we found recombinant agouti protein to stimulate lipogenesis in adipocytes in a Ca2+-dependent fashion. However, adipocyte-specific agouti transgenic mice only became obese in the presence of hyperinsulinemia. Because intracellular Ca2+ concentration ([Ca2+]i) is a primary signal for insulin release, and we have shown agouti protein to increase [Ca2+]i in several cell types, we examined the effects of agouti on [Ca2+]i and insulin release. We demonstrated the expression of agouti in human pancreas and generated recombinant agouti to study its effects on Ca2+ signaling and insulin release. Agouti (100 nM) stimulated Ca2+ influx, [Ca2+]i increase, and a marked stimulation of insulin release in two β-cell lines (RIN-5F and HIT-T15; P < 0.05). Agouti exerted comparable effects in isolated human pancreatic islets and β-cells, with a 5-fold increase in Ca2+ influx ( P < 0.001) and a 2.2-fold increase in insulin release ( P < 0.01). These data suggest a potential role for agouti in the development of hyperinsulinemia in humans.


1917 ◽  
Vol 25 (6) ◽  
pp. 807-817 ◽  
Author(s):  
Tomosaburo Ogata ◽  
Akira Ogata

We have established the fact that the chrome reaction as well as the silver and osmium reactions are merely reductions by adrenalin. In our opinion the naming of the cells giving a positive reaction should not be based upon the reaction i.e., chromaffin cells), but on the presence of adrenalin itself. Biedl's terms, adrenal cell, adrenal organ, adrenal body, adrenal system, and also Bonnamour's term, adrenalin-producing cells, are appropriate in this respect. We propose the names adrenalin cell, adrenalin tissue, adrenalin system, thereby indicating the presence of adrenalin.


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