Dynamic Hormone Control of Stress and Fertility

To assess the possible role of the Na+ pump in mediating physiological responses to thyroid hormone in the rat myocardium, we examined the effects of L-3,5,3'-triiodothyronine (T3) on the activities of the closely associated enzymes, Na+-K+-dependent adenosine triphosphatase (Na-K-ATPase) and K+-dependent p-nitrophenyl phosphatase (K-dep-pNPPase). In hypothyroid rats, administration of T3 (50 microng/100 g body wt) resulted in significant increases (greater than 50%) in Na-K-ATPase and K-dep-pNPPase activities in both crude homogenates and microsomal fractions of the rat ventricle. Significant effects on Na-K-ATPase activity were also attained with low doses (1 microng/100 g body wt) of T3. A method was developed for assaying K-dep-pNPPase activity in cardiac slices. With this technique, enhancement in K-dep-pNPPase activity of 89.2% was found in ventricle slices after treatment of hypothyroid rats with T3 (50 microng/100 g body wt), implying that augmentation of the capacity of the Na+ pump is achieved in vivo. The potent analogue, L-3,5-diiodo-3' isopropyl thyronine (isopropyl T2) had the same effects on cardiac growth and Na-K-ATPase as T3, in hypothyroid rats. In contrast, the relatively inactive isomer, L-3,3',5'-triiodothyronine (reverse T3) had no significant effect on the heart weight-to-body weight ratio or on ventricular Na-K-ATPase activity.

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Hormone-control regions mediate steroid receptor–dependent genome organization

Genome Research ◽

10.1101/gr.243824.118 ◽

2018 ◽

Vol 29 (1) ◽

pp. 29-39 ◽

Cited By ~ 16

Author(s):

François Le Dily ◽

Enrique Vidal ◽

Yasmina Cuartero ◽

Javier Quilez ◽

A. Silvina Nacht ◽

...

Keyword(s):

Genome Organization ◽

Steroid Receptor ◽

Hormone Control ◽

Control Regions

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Direct effect of hypothalamic neuropeptides on the release of catecholamines by adrenal medulla in sheep – study ex vivo

Polish Journal of Veterinary Sciences ◽

10.1515/pjvs-2017-0041 ◽

2017 ◽

Vol 20 (2) ◽

pp. 339-346 ◽

Cited By ~ 1

Author(s):

D. Wrońska ◽

B.F. Kania ◽

M. Błachuta

Keyword(s):

Adrenal Gland ◽

Adrenal Medulla ◽

Noradrenaline Release ◽

Adrenocorticotropic Hormone ◽

Ex Vivo ◽

Adrenal System ◽

Adrenaline Release ◽

Hormone Control

Abstract Stress causes the activation of both the hypothalamic-pituitary-adrenocortical axis and sympatho-adrenal system, thus leading to the release from the adrenal medulla of catecholamines: adrenaline and, to a lesser degree, noradrenaline. It has been established that in addition to catecholamines, the adrenomedullary cells produce a variety of neuropeptides, including corticoliberine (CRH), vasopressin (AVP), oxytocin (OXY) and proopiomelanocortine (POMC) – a precursor of the adrenocorticotropic hormone (ACTH). The aim of this study was to investigate adrenal medulla activity in vitro depending, on a dose of CRH, AVP and OXY on adrenaline and noradrenaline release. Pieces of sheep adrenal medulla tissue (about 50 mg) were put on 24-well plates and were incubated in 1 mL of Eagle medium without hormone (control) or supplemented only once with CRH, AVP and OXY in three doses (10−7, 10−8 and 10−9 M) in a volume of 10 μL. The results showed that CRH stimulates adrenaline and noradrenaline release from the adrenal medulla tissue. The stimulating influence of AVP on adrenaline release was visible after the application of the two lower doses of this neuropeptide; however, AVP reduced noradrenaline release from the adrenal medulla tissue. A strong, inhibitory OXY effect on catecholamine release was observed, regardless of the dose of this hormone. Our results indicate the important role of OXY in the inhibition of adrenal gland activity and thus a better adaptation to stress on the adrenal gland level.

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Hormone control in regeneration: effects of somatostatin on appendage regeneration, blood glucose and liver glycogen in Diemictylus viridescens

Development ◽

10.1242/dev.40.1.115 ◽

1977 ◽

Vol 40 (1) ◽

pp. 115-124

Author(s):

S. Vethamany-Globus ◽

M. Globus ◽

J. A. Hartford ◽

I. Fraser ◽

D. Weber

Keyword(s):

Blood Glucose ◽

Liver Glycogen ◽

Inhibitory Effect ◽

Thyroid Stimulating Hormone ◽

Present Communication ◽

Tail Regeneration ◽

Experimental Animals ◽

Total Inhibition ◽

Daily Dose ◽

Hormone Control

In the present communication, synthetic somatostatin, a hypothalamic factor which has a known inhibitory effect on the release of growth hormone, thyroid-stimulating hormone, prolactin, insulin and glucagon in man and other mammals, was found to have an inhibitory effect on limb and tail regeneration in adult Diemictylus viridescens, when the newts were treated with a daily dose of 3·5 or 15 µg/animal for a period of 34 days post-amputation. At the higher dose, the animals exhibited total inhibition of appendage regeneration in a few cases and the remainder showed a considerable delay compared to the controls; none of the experimental animals reached the advanced four-digit stage achieved by the controls. Furthermore, the blood glucose and liver glycogen values in the somatostatin-treated animals were significantly lower than the control values. Mechanisms in the storage, mobilization and utilization of glucose (involving hormones) are discussed in relation to appendage regeneration in the newt and possible controls of regeneration at the level of the hypothalamus are suggested.

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New Aspects of Steroid Hormone Control: Role of Adrenal Renin

Salt and Hypertension ◽

10.1007/978-3-642-73917-0_10 ◽

1989 ◽

pp. 107-118

Author(s):

P. J. Mulrow ◽

E. Kusano ◽

K. Baba ◽

Y. Doi ◽

D. Shier ◽

...

Keyword(s):

Steroid Hormone ◽

Hormone Control

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Insulin and Growth Hormone Control of Protein Biosynthesis

Novartis Foundation Symposia - Ciba Foundation Symposium - Control Processes in Multicellular Organisms ◽

10.1002/9780470719725.ch6 ◽

2008 ◽

pp. 86-107

Author(s):

A. Korner

Keyword(s):

Growth Hormone ◽

Protein Biosynthesis ◽

Hormone Control

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The Somatomedins: A Family of Insulinlike Hormones under Growth Hormone Control

Proceedings of the 1973 Laurentian Hormone Conference ◽

10.1016/b978-0-12-571130-2.50011-0 ◽

1974 ◽

pp. 259-318 ◽

Cited By ~ 1

Author(s):

J. VAN WYK JUDSON ◽

E. UNDERWOOD LOUIS ◽

L. HINTZ RAYMOND ◽

R. CLEMMONS DAVID ◽

J. VOINA SANDRA ◽

...

Keyword(s):

Growth Hormone ◽

Hormone Control

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Glucagon sensitivity and clearance in type 1 diabetes: insights from in vivo and in silico experiments

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00236.2015 ◽

2015 ◽

Vol 309 (5) ◽

pp. E474-E486 ◽

Cited By ~ 11

Author(s):

Ling Hinshaw ◽

Ashwini Mallad ◽

Chiara Dalla Man ◽

Rita Basu ◽

Claudio Cobelli ◽

...

Keyword(s):

Type 1 Diabetes ◽

In Silico ◽

Artificial Pancreas ◽

Glucose Production ◽

Endogenous Glucose Production ◽

Action Model ◽

The Difference ◽

Hormone Control

Glucagon use in artificial pancreas for type 1 diabetes (T1D) is being explored for prevention and rescue from hypoglycemia. However, the relationship between glucagon stimulation of endogenous glucose production (EGP) viz., hepatic glucagon sensitivity, and prevailing glucose concentrations has not been examined. To test the hypothesis that glucagon sensitivity is increased at hypoglycemia vs. euglycemia, we studied 29 subjects with T1D randomized to a hypoglycemia or euglycemia clamp. Each subject was studied at three glucagon doses at euglycemia or hypoglycemia, with EGP measured by isotope dilution technique. The peak EGP increments and the integrated EGP response increased with increasing glucagon dose during euglycemia and hypoglycemia. However, the difference in dose response based on glycemia was not significant despite higher catecholamine concentrations in the hypoglycemia group. Knowledge of glucagon's effects on EGP was used to develop an in silico glucagon action model. The model-derived output fitted the obtained data at both euglycemia and hypoglycemia for all glucagon doses tested. Glucagon clearance did not differ between glucagon doses studied in both groups. Therefore, the glucagon controller of a dual hormone control system may not need to adjust glucagon sensitivity, and hence glucagon dosing, based on glucose concentrations during euglycemia and hypoglycemia.

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