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Results for “Endocrine System”

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At least 451 records · Page 25Linked to original sources

PubMed2004

The endocrine system during sepsis.

Endocrinopathy during sepsis can manifest as hyperglycemia and insulin resistance or as insufficient production of either adrenal corticosteroids or vasopressin. The results of a recent large clinical trial have demonstrated that tight glycemic control with insulin can confer survival benefit to selected intensive care unit patients. Relative impairment of adrenocortical reserve has been suggested to be an important contributor to the pathogenesis of shock in sepsis. Replacement doses of glucocorticoids and mineralocorticoids have been associated with improved survival in the subset of patients with blunted results on adrenocorticotropin hormone stimulation tests. Posterior pituitary production of vasopressin is diminished in septic shock while sensitivity to its vasopressor effects is enhanced. Clinical trials are underway to determine whether administration of vasopressin can improve outcomes in patients with septic shock. Whether the euthyroid sick syndrome represents an adaptive or a maladaptive response to severe illness remains unclear.

Animals↗

PubMed2002

[1,25-dihydroxyvitamin D3: the endocrine system meets the immune system].

1,25(OH)2D3, the activated form of vitamin D, is well known for its effects on calcium and bone metabolism, but also non-classical effects on cells of the immune system were described, in vivo as well as in vitro. Structural analogues have been developed with less calcemic effects, but at least comparable immune effects. Our group showed that treatment with 1,25(OH)2D3 can protect the NOD mouse, the murine model for type 1 diabetes, from diabetes in primary, secondary and tertiary prevention. This effect is based on shifts in cytokine profiles (Thelper1 to Thelper2), that occur specifically for the autoantigens, and on enhanced sensitivity of the autoreactive T lymphocytes to apoptotic signals thus leading to a better elimination of these potentially dangerous cells. 1,25(OH)2D3 and its analogues can therefore be considered as interventions aimed at the prevention or treatment of human type 1 diabetes.

Animals↗

PubMedDate not supplied

Dysfunction of the vitamin D endocrine system as common cause for multiple malignant and other chronic diseases.

Extensive research on the CYP27B1-encoded 25-(OH)D-1alpha-hydroxylase has contributed much to our understanding about how locally produced 1,25-(OH)2D3 exerts tissue-specific control of cellular growth, differentiation and function. Because many types of epithelial, mesenchymal and immune cells express the 25-(OH)D-1alpha-hydroxylase, many organ functions are necessarily affected by changes in the activity of the enzyme. It is hypothesized that this is likely to occur under conditions of hypovitaminosis D, i.e., at serum 25-(OH)D levels below 30 nM, because extra-renal 25-(OH) D-1alpha-hydroxylase activity is critically limited by the availability of its substrate. This can provide an explanation, on a molecular and cellular basis, for the many observations that significant associations exist between a compromised vitamin D status and the pathogenesis of frequent chronic diseases. In addition to skeletal disorders, vitamin D insufficiency is a risk factor for malignancies, particularly of the colon, breast and prostate gland, as well as for chronic inflammatory and autoimmune diseases (insulin-dependent diabetes mellitus, inflammatory bowel disease, multiple sclerosis, etc.).

Animals↗

PubMed2003

[Morphofunctional changes in the endocrine system of male rats during microgravity and suspension].

Morphofunctional changes in somatotrophs and gonadotrophs of the adenohypophysis and Leydig's cells in the testicles were investigated histologically and hystomorphometrically in male rats following microgravity or tail-suspension. Deficient loading of the musculoskeletal system in microgravity was shown to suppress the functional activity of somatotrophs, gonadotrophs and, seemingly, Leydig's cells. As a consequence, blood levels of the growth hormone and testosterone reduced in the space-flown rats. Reduction of the production of the main anabolic hormones is one of the causes for growth inhibition, prevalence of catabolism and consequent muscular atrophy and osteopenia. Simulation of the lack of weight loading inherent to the zero-g environment by suspension also leads to suppression of the somatotrophs activity, whereas the concentration and functional activity of gonadotrophs make a sharp rise. Proliferation of Leydig's cells in the testicles was noted to be very high despite desolation of the seminal canals and disintegration of the testicle epithelium. These findings drive to the conclusion that suspension affects deeply the spermiogenous and androgenous functions of the testicle which is not observed in animals exposed to microgravity. These differences evidence that genesis of the musculoskeletal atrophy in the suspended and space-flown rats was dissimilar.

Animals↗

PubMed2006

The acute effects of different whole body vibration amplitudes on the endocrine system of young healthy men: a preliminary study.

Whole body vibration (WBV) has been suggested as an alternative form of exercise producing adaptive responses similar to that of resistance training. Very limited information is available on the effects of different vibration parameters on anabolic hormones. In this study, we compared the acute effects of different WBV amplitudes on serum testosterone (T) and insulin growth factor-1 (IGF-1). Nine healthy young recreationally active adult males (age 22 +/- 2 years, height 181 +/- 6.3 cm, weight 77.4 +/- 9.5 kg) voluntarily participated in this randomized controlled (cross-over design) study. The subjects performed 20 sets of 1 min each of WBV exercise in the following conditions: Non-vibration condition (control), low amplitude vibration [low (30 Hz, 1.5 mm peak-to-peak amplitude)] and high amplitude vibration [high (30 Hz, 3 mm peak-to-peak amplitude)]. Blood samples were collected before, after 10 sets, at the end (20th set) and after 24 h of the exercise bout. WBV exercise did not produce significant changes in serum T and IGF-1 either with low or high amplitude when compared with the control condition. The results of this study demonstrate that a single session of WBV exposure with a frequency of 30 Hz and amplitudes of 1.5 and 3 mm does not noticeably alter serum T and IGF-1 levels.

Adult↗

PubMed2005

The Vitamin D endocrine system of the gut--its possible role in colorectal cancer prevention.

While Vitamin D insufficiency in the US and European population is rising, epidemiological studies suggest an inverse correlation between low serum levels of 25-hydroxyvitamin D(3) (25-OH-D(3)) and colorectal cancer incidence. The antimitotic, prodifferentiating and proapoptotic active metabolite 1alpha,25-dihydroxyvitamin D(3) (1,25-(OH)(2)-D(3)) is synthesized also by colonocytes, since these possess Vitamin D synthesizing (CYP27B1) and catabolic (CYP24) hydroxylases similar to the kidney. Early during colon tumor progression, expression of CYP27B1 and of the Vitamin D receptor increases, suggesting an autocrine/paracrine growth control in colon tissue as a physiological restriction against tumor progression. However, in human adenocarcinomas expression of the catabolic CYP24 is also enhanced when compared with adjacent normal mucosa. Therefore, to maintain colonic accumulation of 1,25-(OH)(2)-D(3) its catabolism needs to be restricted. Our studies in mice show that low nutritional calcium causes hyperproliferation of colon crypts and significant elevation of CYP24 expression, which can be completely abrogated by soy feeding. We suggest that phytoestrogens in soy, known to be estrogen receptor modulators, are responsible for decreased CYP24 expression. These results and our observation that 17beta-estradiol can elevate CYP27B1 expression in rectal tissue of postmenopausal women, may underlie the observed protective effect of estrogens against colorectal cancer in females.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1998

Intermittent lighting reduces the incidence of ascites in broilers: an interaction with protein content of feed on performance and the endocrine system.

An experiment with 840 day-old male broiler chicks (Ross) was initiated to investigate the effect of intermittent lighting schedules, combined with two isocaloric feeds differing in protein content, on ascites mortality. At 9 d of age, chicks were randomly distributed over two rooms: one room with a 23 h light(L):1 h dark (D) lighting schedule (CL), and another room with an intermittent lighting schedule (IL, 1L:3D). In each room, two isocaloric feeds differing in CP content, supplemented or not supplemented with 1.5 ppm triiodothyronine (T3), were provided. The experiment was repeated under identical conditions except that lighting schedules were changed between rooms. From Day 14 onwards, biweekly growth and feed intake were determined and feed conversion (FCR) was calculated. Daily mortality was recorded and necropsies were performed. Weekly blood samples were taken from 10 randomly chosen birds per experimental group for measurements of growth hormone (GH), thyroid hormones [thyroxine (T4) and triiodothyronine (T3)], and hematocrit values. Birds reared in IL manifested a more concave growth trajectory than those in CL, which was associated with a lower FCR and higher plasma GH levels during the finisher period. Mortality due to ascites was markedly increased by dietary T3 supplementation. In hyperthyroid chickens, ascites mortality was lower in IL than in CL and lower in birds fed normal protein than in those fed subnormal protein levels. Dietary T3 decreased plasma GH and T4 levels, whereas T3 levels were increased. It is concluded that IL or a higher protein content of the feed reduces the incidence of T3-induced ascites mortality. Possible causal mechanisms are discussed.

Animal Feed↗

PubMed2006

Effects on the male endocrine system of long-term treatment with gonadotropin-releasing hormone agonists and estrogens in male-to-female transsexuals.

We studied hormonal changes resulting from long-term treatment with gonadotropin-releasing hormone agonist and 17beta estradiol valerate in 40 healthy middle-aged male-to-female transsexuals over a period of two years. All of the participants received injections of 3.8 mg goserelin acetate every four weeks in combination with 6 mg oral 17beta estradiol valerate per day for cross-sex hormone treatment for male-to-female transsexuals. There was a significant reduction in the levels of serum luteinizing hormone and follicle-stimulating hormone to the hypogonadal stage. Mean testosterone levels decreased by 97% to 0.52 and 0.59 nmol/l after 12 months and 24 months, respectively. There was a significant reduction in dehydroepiandrosterone sulfate by 37% after 12 months and 43% after 24 months, and androstendione by 29% after 12 months and 27% after 24 months, respectively. Cortisol levels were reduced by 43% and 50%, respectively. Estrogen levels were significantly increased from 77.51 to 677 after 12 months and 661 pmol/l after 24 months. Sex hormone-binding globulin and corticoid-binding globulin levels were significantly increased after 12 and 24 months. There was a significant decrease in all measured androgen fractions and cortisol during long-term treatment with gonadotropin-releasing hormone agonist and 17beta estradiol valerate. Apart from suppression of testicular hormone production, one possible interpretation is that treatment with long-term gonadotropin-releasing hormone agonist and 17beta estradiol valerate influences adrenal hormone levels in healthy middle-aged male-to-female transsexuals. Cortisol serum levels may be decreased due to estrogen-induced increase in corticoid-binding globulin.

Adolescent↗

PubMed2003

Novel interactions of adiponectin with the endocrine system and inflammatory parameters.

Several markers of chronic immune activation have been found in association with obesity and insulin resistance. We aimed to study the interaction of adiponectin with chronic inflammation and known components of the insulin resistance syndrome. Insulin sensitivity (minimal model analysis) and plasma soluble fractions of TNF-alpha receptor 1 (sTNFR1) and 2 (sTNFR2), adrenal and thyroid function, and adiponectin were evaluated in 68 apparently healthy subjects. An additional group of type 2 diabetic patients (n = 19) similarly studied, except for insulin sensitivity, were also included in the analysis. As reported by others, serum adiponectin concentrations were higher in women than in men (13.55 +/- 9.79 vs. 8.64 +/- 7.83 mg/liter; P = 0.018). They were also higher in healthy subjects compared with diabetic patients (10.35 +/- 8.48 vs. 7.41 +/- 8.31 mg/liter; P = 0.021). As expected also, circulating adiponectin was significantly associated with waist to hip ratio (r = -0.28; P = 0.013), diastolic blood pressure (r = -0.25; P = 0.027), fasting plasma high-density lipoprotein cholesterol (r = 0.35; P = 0.001), triglycerides (r = -0.37; P = 0.001), and insulin sensitivity (r = 0.30; P = 0.011). Additionally, subjects in the higher quartile of circulating adiponectin had lower sTNFR2 concentrations (3.05 vs. 4.37 microg/liter; P = 0.012), a trend to lower sTNFR1 concentrations (1.76 vs. 2.20 microg/liter; P = 0.055), higher concentration of serum morning cortisol (16.86 vs. 13.52 microg/dl; P = 0.027), and higher serum free T(4) levels (1.31 vs. 1.20 ng/dl; P = 0.038). Multiple regression analysis models were constructed to predict adiponectin concentrations. Predictive variables in these models included insulin sensitivity, waist to hip ratio and free T(4), contributing to 17%, 10%, and 8% of adiponectin variance, respectively, These findings suggest that circulating adiponectin differentially modulates insulin action and that thyroid-axis, inflammatory cytokines, and the adrenal cortex might intervene in this modulation.

Adiponectin↗

PubMed1999

Physiological roles of the leptin endocrine system: differences between mice and humans.

Leptin is a 16-kDa cytokine secreted in humans primarily but not exclusively by adipose tissues. Its concentration in blood is usually proportional to body fat mass, but is higher in women than in men not only because of a different distribution of and greater fat mass in women, but also because testosterone reduces its level in men. Leptin features in different ways during the life span. It is synthesized in the ovary, transported in the oocyte, and made by both fetus and placenta, particularly during the last month of gestation. It is made by the lactating mammary gland and ingested by the newborn infant in its milk. The prime importance of leptin is realized at puberty when it is necessary for progression to a normal adult reproductive status in females. Fasting and chronic undernutrition result in a lower level of leptin in the blood. Lack of leptin results in hunger, ensuring that the individual eat to survive, and also inhibition of reproduction, until such time as food and fat stores are adequate to supply energy for pregnancy and lactation. Thus, leptin is important for survival of the individual and survival of the species. Although an extremely rare genetic absence of leptin induces hyperphagia and obesity in humans, as it does in mice, there appears to be little role for leptin in humans in ensuring that fat stores are not in excess of adequate, that is, in preventing obesity. The mouse differs from humans in many respects, in particular in the far more drastic ways it conserves energy when it very rapidly adapts to lack of food. These include not only suppression of reproduction but also lowering of its body temperature (torpor), suppressing its thyroid function, suppressing its growth, and increasing secretion of stress hormones (from the adrenal). This review concentrates on roles of leptin in human physiology and pathophysiology but also discusses why some observations on actions of leptin in mice are not applicable to humans.

Adipose Tissue↗

PubMed2003

Inertia of endocrine systems due to hormone binding to circulatory proteins.

It is often presumed that the main role of hormone binding to albumins and binding proteins (BPs) is to reduce oscillating levels of free hormone molecules and to transport steroid hormones. This paper is an attempt to define possible consequences of hormone molecules binding to carrier proteins in circulation. Binding to albumins and BPs prevents exact and quick control of hormone actions. Hormones without significant protein binding govern vital and fast acting regulatory mechanisms (blood glucose or calcium) in which any added inertia might be dangerous. In the presented model, the added inertia for a partially bound hormone (H) is defined as: H(bound)/H(free). Values, calculated from the reported data, range from 0.4 for GH to more than 2000 for T(4). In comparison to albumins, high-affinity BPs make more stable reserve that would cover periods of low or no hormone secretion. At the same time, hormone molecules are taken away from the blood level control and thus might be considered sequestrated. For hormones without protein binding, the well-perfused areas of the body, or the areas with increased capillary permeability, would be more exposed, making an uneven distribution among target tissues. For the hormone that binds blood proteins, places of secretion and tissue perfusion become unimportant, since the hormone is being liberated anywhere in the circulation (i.e., for strongly bound IGFs, IGF binding proteins do not just stabilize proinsulin actions of IGF-1, but also make all parts of body to be under the same exposure to liberated IGFs, an important feature to promote a symmetrical bone growth). Estrogens are known to stimulate liver secretion of different BPs. A possible explanation is that in the follicular phase there is a small initial mass of granulosa cells, and it takes time to saturate free estrogen carriers, before the normal free hormone level can be reached and FSH secretion inhibited. Less inert peptide inhibin might suppress FSH before free estrogens reach the required level. Without inhibin suppression, an increased FSH level with an increased number of growing follicles can be expected. Estrogens increased production of BPs augments inertia of the estrogen loop and possibly modulates the FSH/estrogen negative feedback.

Albumins↗

PubMed1989