Role of the Anterior Pituitary in the Development of a Fatty Liver

1958 ◽  
Vol 193 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Ira G. Wool ◽  
M. S. Goldstein

This study was undertaken to determine whether a fat mobilizing factor from the anterior pituitary is essential to the development of a fatty liver. The method employed was the administration of ethionine, an antimetabolite of methionine, to fasted female rats. Hypophysectomy led to a marked impairment in the ability to accumulate hepatic lipids. Cortisone alone or combined with thyroxine failed to restore this defect. Epinephrine administered to cortisone-maintained hypophysectomized rats led to the development of a fatty liver. While lipid accumulation in the liver can precede in the absence of a specific anterior pituitary fat mobilizing factor, the quantitative aspects do not exclude a possible physiological role for such a principle.

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 288
Author(s):  
Julie Massart ◽  
Karima Begriche ◽  
Jessica H. Hartman ◽  
Bernard Fromenty

Cytochrome P450 2E1 (CYP2E1) is pivotal in hepatotoxicity induced by alcohol abuse and different xenobiotics. In this setting, CYP2E1 generates reactive metabolites inducing oxidative stress, mitochondrial dysfunction and cell death. In addition, this enzyme appears to play a role in the progression of obesity-related fatty liver to nonalcoholic steatohepatitis. Indeed, increased CYP2E1 activity in nonalcoholic fatty liver disease (NAFLD) is deemed to induce reactive oxygen species overproduction, which in turn triggers oxidative stress, necroinflammation and fibrosis. In 1997, Avadhani’s group reported for the first time the presence of CYP2E1 in rat liver mitochondria, and subsequent investigations by other groups confirmed that mitochondrial CYP2E1 (mtCYP2E1) could be found in different experimental models. In this review, we first recall the main features of CYP2E1 including its role in the biotransformation of endogenous and exogenous molecules, the regulation of its expression and activity and its involvement in different liver diseases. Then, we present the current knowledge on the physiological role of mtCYP2E1, its contribution to xenobiotic biotransformation as well as the mechanism and regulation of CYP2E1 targeting to mitochondria. Finally, we discuss experimental investigations suggesting that mtCYP2E1 could have a role in alcohol-associated liver disease, xenobiotic-induced hepatotoxicity and NAFLD.


2005 ◽  
Vol 153 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Wilfried Allaerts ◽  
Hugo Vankelecom

Historically, the study of folliculo-stellate (FS) cells of the anterior pituitary dates back to the onset of electron microscopical observation of the pituitary gland. The morphological and electrophysiological characteristics, topographical distribution and contribution to intercellular junctions of these FS cells have been instrumental to the understanding of their putative function. Moreover, many studies have documented the role of FS cells as a source of newly discovered peptides, growth factors and cytokines. Quantitative immunohistochemical observation of FS cells in situ and functional in vitro studies, using either cultured FS cells or cells from an immortalized FS cell line, forwarded the notion of immunophenotypical and functional heterogeneity of the FS cell group. Double immunolabeling with a classical FS cell marker (S-100 protein) and with major histocompatibility complex class II markers characteristic for dendritic cells (DC) have shown a considerable overlap of FS cells with DC. The latter cells are immunocompetent cells belonging to the mononuclear phagocyte system. In this review, the FS cell heterogeneity is discussed with respect to the question of their embryological origin and developmental fate and with respect to the physiological relevance of functionally heterogeneous subpopulations. Recent findings of a myeloid origin of part of the interstitial cells of the anterior pituitary are confronted by other developmental paradigms of pituitary cell differentiation. The possibility that FS cells represent an adult stem cell population of the pituitary is critically examined. Also the physiological role of FS cells in the interferon-γ- and nitric oxide-mediated effects on pituitary hormone secretion is discussed. New approaches for the study of this enigmatic cell group using immortalized cell lines and new markers for an hitherto unrecognized pituitary cell population, the so-called ‘side population’, are evaluated.


1994 ◽  
Vol 266 (1) ◽  
pp. E57-E61 ◽  
Author(s):  
A. Giustina ◽  
M. Licini ◽  
M. Schettino ◽  
M. Doga ◽  
G. Pizzocolo ◽  
...  

The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)


1964 ◽  
Vol 46 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Claus Rerup

ABSTRACT The possibility of elaborating a sensitive test for the determination of CRF (Corticotrophin-releasing factor) was investigated in corticosteroid-blocked mice. Two synthetic peptides known to possess corticotrophin-releasing activity (CRA) in the rat, i. e. lysine-vasopressin and histidyl-seryl-lysine-vasopressin (CRA-41) were used as test substances. The results showed that it is possible to perform quantitative estimations of CR-activity and that both the peptides tested are true corticotrophin-releasing substances in mice. Lysine-vasopressin was more potent than its synthetic histidyl-seryl-analogue both on an absolute weight basis and in terms of pressor- or corticotrophin equivalents. Threshold doses for CR-activity of lysine-vasopressin in mice were calculated to be about 4 ng (nanograms). From the findings it appears that in mice, the main blocking action of the glucocorticoid dexamethasone is exerted at hypothalamic or higher centres, and not in the cells of the anterior pituitary gland. It is proposed to abandon arbitrary units for CR-activity and to use vasopressin or hypothalamic extracts as a standard for CRF-assay. The possibility of a physiological role of vasopressin as a transmitter substance for corticotrophin-release is briefly discussed.


2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Yong Zou ◽  
Zhengtang Qi

Nonalcoholic fatty liver disease (NAFLD) is globally prevalent and characterized by abnormal lipid accumulation in the liver, frequently accompanied by insulin resistance (IR), enhanced hepatic inflammation, and apoptosis. Recent studies showed that endoplasmic reticulum stress (ERS) at the subcellular level underlies these featured pathologies in the development of NAFLD. As an effective treatment, exercise significantly reduces hepatic lipid accumulation and thus alleviates NAFLD. Confusingly, these benefits of exercise are associated with increased or decreased ERS in the liver. Further, the interaction between diet, medication, exercise types, and intensity in ERS regulation is more confusing, though most studies have confirmed the benefits of exercise. In this review, we focus on understanding the role of exercise-modulated ERS in NAFLD and ERS-linked molecular pathways. Moderate ERS is an essential signaling for hepatic lipid homeostasis. Higher ERS may lead to increased inflammation and apoptosis in the liver, while lower ERS may lead to the accumulation of misfolded proteins. Therefore, exercise acts like an igniter or extinguisher to keep ERS at an appropriate level by turning it up or down, which depends on diet, medications, exercise intensity, etc. Exercise not only enhances hepatic tolerance to ERS but also prevents the malignant development of steatosis due to excessive ERS.


1961 ◽  
Vol 201 (6) ◽  
pp. 1176-1180 ◽  
Author(s):  
Alan Corbin ◽  
B. A. Schottelius

The possible role of four recognized hypothalamic constituents in activation and maturation of the hypophysial-reproductive organ complex of immature female albino rats was investigated. Normal and hypophysectomized rats and rats with bilateral destruction of an area extending from the ventromedial nucleus to mammillary body were studied. Animals were injected either with 70 milliunits of antidiuretic hormone (ADH), 70 milluniits of oxytocin, 25 µg of serotonin, or 2 µg of epinephrine every 5th day, from age 20 through 45 days, via a cannula permanently implanted in the 3rd ventricle of the brain. No response to ADH was observed. Oxytocin accelerated vaginal canalization and caused premature reproductive organ growth in normal recipients. Whereas lesioned untreated controls remained sexually retarded, vaginal opening and reproductive organ growth equivalent to 50-day-old sham-operated controls were induced in lesioned animals by oxytocin administration. Serotonin prevented maturation in normal controls, but was ineffective in lesioned animals. Hypophysectomized rats were unresponsive to any agent injected. The results imply that oxytocin may directly activate the hypophysis of immature female rats. Serotonin, on the other hand, inhibits the hypophysial-gonadal axis of these animals, but its effects probably are relayed via the hypothalamus.


1999 ◽  
Vol 23 (1) ◽  
pp. 57-66 ◽  
Author(s):  
C Keil ◽  
B Husen ◽  
J Giebel ◽  
G Rune ◽  
R Walther

In the present study we demonstrate for the first time the expression of glycodelin mRNA in the female and male genital tracts of rats using non-radioactive in situ hybridisation. Glycodelin fragment 1 (+41 to +141) shares 100% homology with the human gene sequence. In the ovary, glycodelin mRNA was restricted to granulosa cells. In the uterus, glycodelin mRNA was expressed in all epithelial cells of the endometrium. In the male reproductive tract, glycodelin mRNA was distributed in all epithelial cells of the epididymis, the prostate and the seminal vesicle. However, in the testis, glycodelin mRNA was predominantly found in spermatogonia and in spermatocytes of the seminiferous epithelium. The expression in several reproductive organs of rats offers an excellent tool to study further the physiological role of glycodelin, which is so far thought to act as an immunosuppressive factor.


2007 ◽  
Vol 292 (1) ◽  
pp. E7-E15 ◽  
Author(s):  
Annabelle Reaux-Le Goazigo ◽  
Rodrigo Alvear-Perez ◽  
Philippe Zizzari ◽  
Jacques Epelbaum ◽  
Marie-Thérèse Bluet-Pajot ◽  
...  

Apelin is a bioactive peptide recently identified as the endogenous ligand of the human orphan G protein-coupled receptor APJ. The presence of apelin-immunoreactive nerve fibers, together with the detection of apelin receptor mRNA in the parvocellular part of the paraventricular nucleus and the stimulatory action of apelin on corticotropin-releasing hormone release, indicate that apelin modulates adrenocorticotropin (ACTH) release via an indirect action on the hypothalamus. However, a direct action of apelin in the anterior pituitary cannot be excluded. Here, we provided evidence for the existence of an apelinergic system within the adult male rat pituitary gland. Double immunofluorescence staining indicated that apelin is highly coexpressed in the anterior pituitary, mainly in corticotrophs (96.5 ± 0.3%) and to a much lower extent in somatotropes (3.2 ± 0.2%). Using in situ hybridization combined with immunohistochemistry, a high expression of apelin receptor mRNA was also found in corticotrophs, suggesting a local interaction between apelin and ACTH. In an ex vivo perifusion system of anterior pituitaries, apelin 17 (K17F, 10−6 M) significantly increased basal ACTH release by 41%, whereas apelin 10 (R10F, 10−6 M), an inactive apelin fragment, was ineffective. In addition, K17F but not R10F induced a dose-dependent increase in K+-evoked ACTH release, with maximal increase being observed for a 10−6 M concentration. Taken together, these data outline the potential role of apelin as an autocrine/paracrine-acting peptide on ACTH release and provide morphological and neuroendocrine basis for further studies that explore the physiological role of apelin in the regulation of anterior pituitary functions.


Endocrinology ◽  
2014 ◽  
Vol 155 (3) ◽  
pp. 1091-1098 ◽  
Author(s):  
K.E. Beale ◽  
J.S. Kinsey-Jones ◽  
J.V. Gardiner ◽  
E.K. Harrison ◽  
E.L. Thompson ◽  
...  

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