Anterior Pituitary Responsiveness to Hypothalamic Hormones in Anorexia Nervosa

1981 ◽  
Vol 7 (5) ◽  
pp. 225-237 ◽  
Author(s):  
F. Brambilla ◽  
D. Cocchi ◽  
P. Nobile ◽  
Eugenio E. Müller
1979 ◽  
Vol 4 (7) ◽  
pp. 158-160 ◽  
Author(s):  
Fernand Labrie ◽  
Martin Godbout ◽  
Michèle Beaulieu ◽  
Pierre Borgeat ◽  
Nicholas Barden

1963 ◽  
Vol 109 (461) ◽  
pp. 480-484 ◽  
Author(s):  
V. Marks ◽  
R. G. Bannister

Urinary excretion of adrenal metabolites, especially neutral 17-ketosteroids, is often low in patients with anorexia nervosa (Escamilla, 1949; Bliss and Branch, 1960). This has been taken (Emanuel, 1956; Greenblatt et al., 1951) to provide evidence of adreno-cortical insufficiency secondary to defective pituitary function (Sheldon, 1939; Perloff et al., 1954). According to Perloff et al. (1954) “prolonged starvation may result in functional hypopituitarism, whose differentiation from the syndrome of hypopituitary cachexia due to structural impairment of the anterior pituitary gland is at times extremely difficult, even when the accepted tests for endocrine adequacy are performed”.


1990 ◽  
Vol 157 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Neil L. Holden

Although anorexia nervosa may vary widely in its severity and outcome, it is usually regarded as an illness in its own right, as patients do not display major changes in the form of the illness over time (Russell, 1970). It readily lends itself to being accorded clear-cut diagnostic criteria (Russell, 1977) and this is reflected in ICD–10 (World Health Organization, 1987). However, the nosological independence of anorexia nervosa has undergone vigorous assault since its classic description by William Gull (1874). For example, the psychological nature of anorexia nervosa was obscured for 30 years by Simmond's (1914) description of anterior pituitary lesions and cachexia, and Kay & Leigh's (1954) influential study of anorexia nervosa concluded with their doubts about its status as a ‘psychiatric entity’.


Physiology ◽  
1999 ◽  
Vol 14 (2) ◽  
pp. 54-58
Author(s):  
W. R. Crowley

The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.


Author(s):  
Sergio R. Ojeda

The hypothalamic-pituitary complex represents the core of the neuroendocrine system. The hypothalamus is composed of a diversity of neurosecretory cells arranged in groups, which secrete their products either into the portal blood system that connects the hypothalamus to the adenohypophysis (see later) or directly into the general circulation after storage in the neurohypophysis (see Chapter 6). Because of the nature of their actions, the hypothalamic hormones are classified as releasing or inhibiting hormones. The hypothalamic hormones delivered to the portal blood system are transported to the adenohypophysis, where they stimulate or inhibit the synthesis and secretion of different trophic hormones. In turn, these hormones regulate gonadal, thyroid, and adrenal function, in addition to lactation, bodily growth, and somatic development. No attempt will be made in this chapter to cover the actions of the different pituitary trophic hormones on their target glands, because they are discussed in detail in other chapters. An exception to this is growth hormone (GH). Although Chapter 11 considers several aspects of the control and actions of GH, a broader discussion of its physiological actions will be presented here because GH is the only anterior pituitary hormone that does not have a clear-cut target gland. The pituitary gland has two parts: the neurohypophysis, of neural origin (see Chapter 6), and the adenohypophysis, of ectodermal origin. In embryonic development, an evagination from the roof of the pharynx pushes dorsally to reach a ventrally directed evagination from the base of the diencephalon. The dorsally projecting evagination, known as Rathke’s pouch , forms the adenohypophysis, whereas the ventrally directed evagination of neural tissue forms the neurohypophysis. The neurohypophysis has three parts: the median eminence, the infundibular stem, and the neural lobe itself. The median eminence represents the intrahypothalamic portion and lies just ventral to the floor of the third ventricle protruding slightly in the midline. The main part of the neurohypophysis, the neural lobe, is connected to the median eminence by the infundibular stem.


Sign in / Sign up

Export Citation Format

Share Document