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PubMed2002

The natriuretic peptide system in eels: a key endocrine system for euryhalinity?

The natriuretic peptide system of a euryhaline teleost, the Japanese eel (Anguilla japonica), consists of three types of hormones [atrial natriuretic peptide (ANP), ventricular natriuretic peptide (VNP), and C-type natriuretic peptide (CNP)] and four types of receptors [natriuretic peptide receptors (NPR)-A, -B, -C, and -D]. Although ANP is recognized as a volume-regulating hormone that extrudes both Na(+) and water in mammals, ANP more specifically extrudes Na(+) in eels. Accumulating evidence shows that ANP is secreted in response to hypernatremia and acts to inhibit the uptake and to stimulate the excretion of Na(+) but not water, thereby promoting seawater (SW) adaptation. In fact, ANP is secreted immediately after transfer of eels to SW and ameliorates sudden increases in plasma Na(+) concentration through inhibition of drinking and intestinal absorption of NaCl. ANP also stimulates the secretion of cortisol, a long-acting hormone for SW adaptation, whereas ANP itself disappears quickly from the circulation. Thus ANP is a primary hormone responsible for the initial phase of SW adaptation. By contrast, CNP appears to be a hormone involved in freshwater (FW) adaptation. Recent data show that the gene expression of CNP and its specific receptor, NPR-B, is much enhanced in FW eels. In fact, CNP infusion increases (22)Na uptake from the environment in FW eels. These results show that ANP and CNP, despite high sequence identity, have opposite effects on salinity adaptation in eels. This difference apparently originates from the difference in their specific receptors, ANP for NPR-A and CNP for NPR-B. VNP may compensate the effects of ANP and CNP for adaptation to respective media, because it has high affinity to both receptors. On the basis of these data, the authors suggest that the natriuretic peptide system is a key endocrine system that allows this euryhaline fish to adapt to diverse osmotic environments, particularly in the initial phase of adaptation.

Animals↗
PubMed1993

The pathology of the gastrointestinal endocrine system.

Among endocrine tumors occurring in the gastrointestinal tract, midgut argentaffin EC cell carcinoids, gastric argyrophil ECL cell carcinoids, duodenal gastrin cell tumors, and rectal trabecular L cell carcinoids (in order of decreasing frequency) are those occurring more frequently. Together, they account for more than 80% of such tumors. Duodenal somatostatin cell tumors, gangliocytic paragangliomas, and differentiated neuroendocrine carcinomas are also well-defined tumor entities. The carcinoid syndrome, either classical, with intermittent flushing, hypotension, and diarrhea, or atypical, with persistent histamine-type red flushing, bronchospasm, and no diarrhea, and Zollinger-Ellison syndrome, with severe peptide ulcer disease, are the only hyperfunctional syndromes consistently found in association with these tumors. The carcinoid syndrome occurs in about 10% of gastrointestinal carcinoids, usually in their advanced, metastatic stage. The Zollinger-Ellison syndrome occurs in association with about 40% of intestinal gastrin cell tumors, including small intramural growths. Tumor prognosis depends on the mode and site of presentation, histology, cell type(s), size, level of invasion, metastases (especially distant metastases), and associated clinical syndrome or background disease. Hormones, trophic factors, inherited genetic traits, somatic mutations, and some chronic inflammatory processes are pathogenetically important in a large proportion of cases.

Animals↗
PubMed1984

Obesity and the endocrine system.

The entire endocrine system including the hypothalamus, pituitary gland, thyroid, adrenal cortex, and gonads, has been examined for the cause of obesity. This article discusses the relationship between obesity and the endocrine glandular system. Guidelines for treating obesity caused by specific endocrine dysfunction are presented in detail.

Adrenal Cortex Diseases↗
PubMed1989

Mechanisms that lead to disease of the endocrine system in animals.

Endocrine glands are collections of specialized cells that synthesize, store, and release their secretions directly into the blood stream. They are sensing and signalling devices located in the extracellular fluid compartment and are capable of responding to changes in the internal and external environments to coordinate a multiplicity of activities that maintain homeostasis. Diseases of the endocrine system are encountered in many animal species and present challenging diagnostic problems. The major pathogenic mechanisms responsible for disturbances in endocrine function include: 1) primary hyperfunction of an endocrine gland; 2) secondary hyperfunction; 3) primary hypofunction of an endocrine gland; 4) secondary hypofunction; 5) endocrine hyperactivity secondary to diseases of other organs; 6) hypersecretion by nonendocrine tumors of hormone-like substances; 7) failure of fetal endocrine function; 8) endocrine dysfunction due to failure of target cell response; 9) endocrine dysfunction resulting from abnormal degradation of hormone; and 10) iatrogenic syndromes of hormone-excess. For each major category, several specific disease problems have been selected to illustrate the morphologic and functional changes that characterize the response of a particular endocrine gland to disruption of function.

Animals↗
PubMedDate not supplied

[Individual characteristics of the organization of the human endocrine system].

Individual features of the endocrine system were studied in 26 healthy men, divided into 2 groups, according to the characteristics of EEG, electrocutaneous thresholds and the time response (TR) upon sound signals of 40 to 120 decibels. The subjects of the 1st group were characterized by the high energy of EEG delta- and theta-rhythms, low energy of alpha-rhythm, low thresholds and TR40 : TR120 ratio. The patients of the 2nd group had the opposite parameters. In both groups the blood plasma and urine catecholamine content, ACTH, TTH, 11-hydroxycorticosteroids, cortisol, aldosterone, thyroxine, triiodothyronine, testosterone and plasmatic insulin were determined by means of spectrofluorometry and radioimmunoassay. The elevation of the cortisol level after ACTH injection and of the TTH concentration following thyroliberin administration were investigated. Two polar variants of the endocrine system organization were revealed. The patients of the 1st group had an elevated activity of the sympathico-adrenal, hypophyseal-adrenal system and insular apparatus, comparatively lowered activity of the hypophyseal-thyroid system and gonads. The subjects of the 2nd group demonstrated an opposite character of the endocrine system. It is suggested that the individual peculiarities of the human endocrine system promote the development of obesity, Icenko-Cushing's disease, hypertension, thyrotoxicosis, acromegaly and bronchial asthma.

Acoustic Stimulation↗
PubMed2001

Alterations in development of reproductive and endocrine systems of wildlife populations exposed to endocrine-disrupting contaminants.

Wildlife and human populations are affected by contaminants in natural settings. This problem has been a growing concern over the last decade with the realization that various environmental chemicals can alter the development and functioning of endocrine organs, cells and target tissues. Documented disruptions or alterations in reproductive activity, morphology or physiology in wildlife populations have been correlated with contaminant-induced modifications in endocrine system functioning. Alterations of the endocrine system are complex, and not limited to a particular organ or molecular mechanism. For instance, contaminants have been shown to (1) act as hormone receptor agonists or antagonists, (2) alter hormone production at its endocrine source, (3) alter the release of stimulatory or inhibitory hormones from the pituitary or hypothalamus, (4) alter hepatic enzymatic biotransformation of hormones, and (5) alter the concentration or functioning of serum-binding proteins, altering free hormone concentrations in the serum. This review focuses on two of these alterations, altered hormone synthesis and hepatic biotransformation, as a number of recent studies indicate that these actions are important components of endocrine disruption in developing organisms. The possible role of contaminants in altering sex determination mechanisms is also examined.

Alligators and Crocodiles↗
PubMed1999

Apoptosis and cell death in the endocrine system.

Inflammatory diseases of the endocrine system--such as thyroiditis, diabetes, and Graves' disease--are considered to be autoimmune in origin. More recently, these and other autoimmune diseases have been associated with defects in Fas apoptosis. The mutation of the Fas or Fas ligand (FasL) has been observed in a minority of patients with autoimmune disease. However, dysfunction of the Fas apoptosis signaling pathway or production of soluble factors, including sFas and sFasL, may be more prevalent. Certain endocrine tissues, such as the testes, are immune privilege sites. Defects in Fas and FasL expression in immune privilege sites can trigger an inflammatory response. Other factors that trigger inflammatory diseases of the thyroid or islets may be loss of self tolerance, leading to an autoimmune response. An infectious trigger or other environmental agent can initiate organ damage, leading to release of new antigens that initiate the autoreactive process. We have developed a murine cytomegalovirus model of Sjögren's syndrome in which defects in the Fas/FasL pathway are necessary to enable chronic inflammation, even after the initial virus has been cleared. Another interaction between the endocrine system and apoptosis is by direct hormone interaction. This is exemplified by the orphan steroid receptor Nur77. Nur77 is important for T cell apoptosis after signaling through CD3. We have demonstrated that a dominant-negative Nur77 transgenic mouse exhibits a defect in thymic selection of T cells. Therefore, there are many potential mechanisms by which endocrine glands or hormones can affect the Fas apoptosis pathway, resulting in either cell death or a chronic inflammatory disease in the endocrine system, leading to hypothyroidism and diabetes. This inflammatory dysfunction can be reversed by a dominant-negative I kappa B that prevents nuclear translocation of NF-kappa B. We have developed antigen-specific, antigen-presenting cells that express high levels of FasL that can prevent tissue-specific inflammatory disease. Treatment with these cells prevents development of diabetes in NOD mice. Further understanding of the role and regulation of apoptosis in diseases of the endocrine system (e.g., diabetes, thyroiditis) should lead to better methods of treatment and prevention of these diseases.

Animals↗
PubMed1996

Nursing management of symptoms influenced by HIV infection of the endocrine system.

Examining the impact of endocrine disregulation is useful in managing symptoms of HIV infection in its later stages. Current studies indicate insults to the endocrine system from a variety of agents present in HIV infection. Establishing direct pathologic, causal effects is difficult; however, the functional domains of the endocrine system provide a good framework for nursing management of the symptoms of later-stage HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Endocrine-disrupting chemicals use distinct mechanisms of action to modulate endocrine system function.

The term endocrine-disrupting chemicals is used to define a structurally diverse class of synthetic and natural compounds that possess the ability to alter various components of the endocrine system and potentially induce adverse health effects in exposed individuals and populations. Research on these compounds has revealed that they use a variety of both nuclear receptor-mediated and non-receptor-mediated mechanisms to modulate different components of the endocrine system. This review will describe in vitro and in vivo studies that highlight the spectrum of unique mechanisms of action and biological effects of four endocrine-disrupting chemicals--diethylstilbestrol, genistein, di(n-butyl)phthalate, and methoxyacetic acid--to illustrate the diverse and complex nature of this class of compounds.

Acetates↗