oxytocin and Hypothyroidism

Hypopituitarism is defined as one or more partial or complete pituitary hormone deficiencies, which are related to the anterior and/or posterior gland and can have an onset in childhood or adulthood. The most common aetiology is a sellar or suprasellar lesion, often an adenoma, which causes hypopituitarism due to tumour mass effects, or the effects of surgery and/or radiation therapy. However, other clinical conditions, such as traumatic brain injury, and autoimmune and inflammatory diseases, can result in hypopituitarism, and there are also genetic causes of hypopituitarism. Furthermore, the use of immune checkpoint inhibitors to treat cancer is increasing the risk of hypopituitarism, with a pattern of hormone defects that is different from the classic patterns and depends on mechanisms that are specific for each drug. Moreover, autoantibody production against the pituitary and hypothalamus has been demonstrated in studies investigating the development or worsening of some cases of hypopituitarism. Finally, evidence suggests that posterior pituitary damage can affect oxytocin secretion. The aim of this Review is to summarize current knowledge on non-classic and emerging causes of hypopituitarism, so as to help clinicians improve early identification, avoid life-threatening events and improve the clinical care and quality of life of patients at risk of hypopituitarism.

Topics: Adenoma; Adrenocorticotropic Hormone; Autoimmune Hypophysitis; Brain Injuries, Traumatic; Dwarfism, Pituitary; Empty Sella Syndrome; Endocrine System Diseases; Genetic Diseases, Inborn; Humans; Hypoglycemia; Hypogonadism; Hypophysitis; Hypopituitarism; Hypothyroidism; Immune Checkpoint Inhibitors; Oxytocin; Pituitary Apoplexy; Pituitary Neoplasms; Subarachnoid Hemorrhage

Thyroid hormones play an essential role in metabolism regulation and circadian rhythm control. Recent studies approved their role in normal development and healthy function of central nervous system (CNS). The thyroid gland is a component of the hypothalamic-pituitary-thyroid axis disrupted during thyrotoxicosis and hypothyroidism, two main clinical conditions that induce more liability against dementia-related disease.. In the first step, this study evaluated the circular level of neuropeptide Y (NPY), leptin, oxytocin, and vasopressin in hyperthyroidism and hypothyroidism patients. In the second step, we investigated neurological and cognitive abnormalities by assessment of the hallmark proteins and peptides such as amyloid β (Aβ) variants, glycogen synthase kinase 3β (GSK-3β), and tau protein in thyroid-deficient samples.. The results show increased content of leptin hormone in patients with hypothyroidism who also manifested high levels of vasopressin. Underactivation and overactivation of the thyroid gland are accompanied by reduced circular oxytocin. We may conclude that thyroid deficiency is associated with neurohormone dysregulation. Interestingly, both patient groups exhibited significant increases in Aβ40 and Aβ42 levels relative to the control group, which was also accompanied by the rise in GSK-3β; this might be interpreted as cholinergic system dysfunction and cognitive impairment. The results revealed tau content increased considerably in thyrotoxicosis but did not change significantly in hypothyroidism compared to the control group.. Therefore, our results have shown that thyroid gland dysfunction is a risk factor for cognitive impairment, mainly through neuroendocrine dysregulation. This study provides a relationship between hyperthyroidism/hypothyroidism and biomarkers of neurological abnormalities in blood serum.

Topics: Amyloid beta-Peptides; Biomarkers; Cognitive Dysfunction; Glycogen Synthase Kinase 3 beta; Humans; Hyperthyroidism; Hypothyroidism; Leptin; Oxytocin; Thyrotoxicosis

What is the central question of this study? Does fetal hypothyroidism in rats alter uterine contractions and structure in the adult offspring? What is the main finding and its importance? Our study indicated that maternal hypothyroidism during pregnancy increased gestational length and decreased litter size. In addition, maternal hypothyroidism caused delayed puberty onset, irregular uterine contractions and histological changes in the uterus in the female offspring. This model might contribute to a better understanding of the cellular and molecular mechanisms involved in uterine contractions in fetal hypothyroidism, studies which are not possible in humans, and might help to establish therapeutic methods for these disorders observed in uterine contractions.. Thyroid hormones play an essential role in fetal growth. Hypothyroidism impairs reproductive function in both humans and animals. The aim of this study was to assess the effects of fetal hypothyroidism on uterine smooth muscle contraction and structure in the adult offspring. The control group of female Wistar rats consumed tap water, whereas the hypothyroid group received water containing 0.025% of 6-propyl-2-thiouracial throughout gestation from mating until delivery. Isometric contractility and histological changes in uterine tissue were evaluated in the adult female offspring. We tested the effects of carbachol (10

Topics: Animals; Carbachol; Female; Fetus; Hypothyroidism; Muscle Contraction; Muscle, Smooth; Oxytocin; Pregnancy; Rats; Rats, Wistar; Thyroid Gland; Thyroid Hormones; Uterine Contraction; Uterus

Acute intermittent porphyria (AIP) is a rare autosomal dominant metabolic disorder' affecting the production of heme, the oxygen-binding prosthetic group of hemoglobin. It is characterized by a deficiency of the enzyme hydroxymethylbilane synthase; without this cytoplasmic enzyme, heme synthesis cannot finish, and the metabolite porphobilinogen accumulates in the cytoplasm. Some additional factors must also be present such as drugs, hormones, dietary changes, infections diseases and surgery that trigger the appearance of symptoms, which include neurological disorders, abdominal pain, constipation, and muscle weakness. We present a perioperative course of a pregnant woman with porphyria in association with hypothyroidism and its anesthetic management.

Topics: Adult; Anesthesia, Spinal; Cephalopelvic Disproportion; Cesarean Section; Electrocardiography; Emergency Medical Services; Female; Humans; Hypothyroidism; Intraoperative Complications; Oxytocin; Perioperative Care; Porphyria, Acute Intermittent; Pregnancy; Pregnancy Complications

Hypophysiotropic thyrotropin-releasing hormone (TRH) neurons, the central regulators of the hypothalamic-pituitary-thyroid axis, are located in the hypothalamic paraventricular nucleus (PVN) in a partly overlapping distribution with non-hypophysiotropic TRH neurons. The distribution of hypophysiotropic TRH neurons in the rat PVN is well understood, but the localization of these neurons is unknown in mice. To determine the distribution and phenotype of hypophysiotropic TRH neurons in mice, double- and triple-labeling experiments were performed on sections of intact mice, and mice treated intravenously and intraperitoneally with the retrograde tracer Fluoro-Gold. TRH neurons were located in all parts of the PVN except the periventricular zone. Hypophysiotropic TRH neurons were observed only at the mid-level of the PVN, primarily in the compact part. In this part of the PVN, TRH neurons were intermingled with oxytocin and vasopressin neurons, but based on their size, the TRH neurons were parvocellular and did not contain magnocellular neuropeptides. Co-localization of TRH and cocaine- and amphetamine-regulated transcript (CART) were observed only in areas where hypophysiotropic TRH neurons were located. In accordance with the morphological observations, hypothyroidism increased TRH mRNA content of neurons only at the mid-level of the PVN. These data demonstrate that the distribution of hypophysiotropic TRH neurons in mice is vastly different from the pattern in rats, with a dominant occurrence of these neurosecretory cells in the compact part and adjacent regions at the mid-level of the PVN. Furthermore, our data demonstrate that the organization of the PVN is markedly different in mice and rats.

Topics: Animals; Hypothyroidism; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Thyrotropin-Releasing Hormone; Vasopressins

Anaphylactoid reaction to Syntocinon is rare, but has been described in the literature. The reactions described include patchy erythema, hypotension, bronchospasm and oxygen desaturation, but pulseless electrical activity following Syntocinon has not been reported. We present the case of a 34-year-old primigravida with essential hypertension, gestational diabetes and hypothyroidism with a twin pregnancy following in vitro fertilization. During elective caesarean delivery she developed a severe anaphylactic reaction to Syntocinon leading to pulseless electrical activity.

Topics: Adult; Anaphylaxis; Anesthesia, Spinal; Electrocardiography; Female; Humans; Hypertension; Hypothyroidism; Oxytocics; Oxytocin; Palpation; Pregnancy; Pregnancy Complications; Pregnancy, Multiple; Twins

The aim of the present investigations was to examine the effects of the states of hypothyroidism or hyperthyroidism on vasopressin (AVP) and oxytocin (OT) release under conditions of equilibrated water metabolism as well as of osmotic stimulation, brought about by the dehydration or hypertonic saline administration. The euhydrated and simultaneously hypothyroid rats showed decreased hypothalamic AVP and OT content and somewhat higher but not significant neurohypophysial AVP content. In these animals the raised OT (but not AVP) plasma level has been observed. In hyperthyroid rats drinking tap water ad libitum the neurohypophysial AVP and OT content significantly diminished; plasma OT concentration (but not AVP) was then elevated. The state of osmotic stimulation was the reason of different response of the hypothalamo-neurohypohysial system function in hypo- or hyperthyroid rats. Significant decreases of neurohypophysial AVP and OT content were found in both hypothyroid dehydrated as well as hypothyroid hypertonic saline-treatment rats as compared with hypothyroid euhydrated ones. On the contrary, in the state of hyperthyroidism AVP content in the neurohypophysis distinctly raised in dehydrated and salt-loaded rats; in these last neurohypophysial OT content increased as well. Plasma OT (but not AVP) distinctly diminished in hyperthyroid and simultaneously dehydrated or hypertonic saline injected rats in relation to hyperthyroid control subgroup. Data from the present study suggest that: 1). altered thyroid gland function affects vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in the state of equilibrated water metabolism; 2). the state of hypo- or hyperthyroidism modifies the response of AVP-ergic and OT-ergic neurons upon the osmoreceptors/osmodetectors stimulation. It may be supposed that OT-ergic neurons display greater than AVP-ergic neurons sensitivity upon the thyroid hormone influence.

Topics: Animals; Disease Models, Animal; Drinking; Hyperthyroidism; Hypothalamo-Hypophyseal System; Hypothyroidism; Male; Oxytocin; Pituitary-Adrenal System; Rats; Rats, Wistar; Vasopressins; Water; Water Deprivation

The present studies were designed to examine the regulation of leptin release in primary cultures of adipocytes from fed hypothyroid rats incubated with hormones for 24 hours. Leptin release was increased in the presence of dexamethasone, while the decrease in leptin mRNA content over a 24-hour incubation was reduced by dexamethasone. Dexamethasone did not affect the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA or 18S RNA content of adipocytes. Insulin increased leptin release by adipocytes in both the absence and presence of dexamethasone. Although insulin also prevented the loss of leptin mRNA, this effect was less than that observed for GAPDH mRNA or 18S RNA content. In isolated adipocytes, the loss of almost half the 18S RNA content over a 24-hour incubation was prevented in the presence of insulin but not oxytocin or epidermal growth factor (EGF). The specific beta3 catecholamine agonist CI 316,243 inhibited the effects of dexamethasone on leptin release and leptin mRNA accumulation, as did EGF, without affecting 18S RNA content. Oxytocin inhibited the increase in leptin release due to dexamethasone without affecting leptin mRNA levels. These data indicate that although dexamethasone and insulin are positive regulators of leptin release, only dexamethasone specifically prevented the loss of leptin mRNA in cultured rat adipocytes. In contrast, insulin, but not dexamethasone, prevented the marked loss in 18S RNA observed over a 24-hour incubation of rat adipocytes.

Topics: Adipocytes; Adrenergic beta-Agonists; Animals; Colforsin; Dexamethasone; Dioxoles; Epidermal Growth Factor; Glyceraldehyde-3-Phosphate Dehydrogenases; Hypothyroidism; Insulin; Leptin; Male; Oxytocin; Proteins; Rats; Rats, Sprague-Dawley; RNA, Messenger; RNA, Ribosomal, 18S; Tetradecanoylphorbol Acetate

Sustained hyperosmolality increases the levels of hypothalamic oxytocin (OT) and arginine vasopressin (AVP) messenger ribonucleic acids (mRNAs). Gonadectomy is known to abolish this response (12,18). In this study we investigated whether thyroidectomy would alter OT and AVP mRNA levels in the hypothalamic paraventricular nucleus (PVN) of the hyperosmotically stimulated rat. Male Sprague-Dawley rats underwent thyroidectomy (hypothyroid) or sham thyroidectomy (euthyroid) at 7 weeks of age. Three weeks later hypothyroid and euthyroid animals were administered 2% NaCl (6-11 days) or tap water and sacrificed at the end of the experiment. Northern blot hybridization was used to assess size and levels of hypothalamic OT and AVP mRNAs. Hypothyroid rats had significantly lower levels of serum thyroxine (T4) than their euthyroid cohorts (P < 0.0001). Both the euthyroid and the hypothyroid animals receiving 2% NaCl developed hypernatremia and increased the levels and the size of OT and AVP mRNAs compared to their tap water cohorts. We conclude that in contrast to gonadectomy, thyroidectomy does not alter the level of OT and AVP mRNAs in the hypothalamus of chronically hypernatremic male rats.

Topics: Animals; Arginine Vasopressin; Gene Expression Regulation; Hypernatremia; Hypothalamus; Hypothyroidism; Male; Oxytocin; Rats; Rats, Sprague-Dawley; RNA, Messenger; Thyroidectomy

In this paper we describe the modification of the galanin (GAL)-like immunostaining in the hypothalamus of rats, which were made hypothyroid at 52 days after birth. On 21st day after the surgical ablation of the thyroid gland, the staining of the GAL-immunoreactive fibers in the median eminence decreased and on the 84th day disappeared almost totally. The GAL-immunoreactive distribution in other areas of the hypothalamus, e.g. the anterior hypothalamus and the dorsomedial nucleus, is only slightly affected by the absence of thyroid hormones, whereas the GAL-staining of medulla oblongata (vagal complex) is equal in both control and hypothyroid rats. In hypothyroid colchicine-treated rats, we were unable to stain GAL-immunoreactive neurons in the paraventricular nucleus (PVN). Oxytocin- and vasopressin-like material was present in the magnocellular neurons and the staining pattern in hypothyroid rats was the same as that of control animals. Our data show a marked reduction in the expression of the GAL-like immunoreactivity of the PVN and median eminence of adult hypothyroid rats. The possible role of this deficit in the pathogenesis of the GH secretion impairment that is observed in hypothyroid rats is discussed.

Topics: Animals; Fluorescent Antibody Technique; Galanin; Hypothalamus; Hypothyroidism; Male; Median Eminence; Oxytocin; Paraventricular Hypothalamic Nucleus; Peptides; Rats; Rats, Inbred Strains; Vasopressins

Prenatal plus neonatal administration of methimazole (MMI), a procedure provoking marked hypothyroidism in rats, increased by about 100% the thymic content of oxytocin and severely (by approximately 80%) decreased the thymus weight, compared to euthyroid counterparts. Adult-onset, propylthiouracyl (PTU)-induced hypothyroidism, while provoking thymic involution, or thyroxine (T4) hyperthyroidism, did not affect oxytocin concentrations. Thymic involution and increases in thymus oxytoxin could also be obtained with repeated administration of the potent glucocorticoid dexamethasone. However, since corticosterone, unless subchronically injected at largely supraphysiological doses, was previously shown to have no influence on thymic parameters of young adult rats, a major involvement of the neonatal adrenal axis in oxytocin alterations could be excluded. It is suggested that the ontogenesis of thymic oxytocin production is under thyroid control.

Topics: Aging; Animals; Animals, Newborn; Dexamethasone; Female; Hyperthyroidism; Hypothyroidism; Male; Methimazole; Organ Size; Oxytocin; Propylthiouracil; Rats; Rats, Inbred Strains; Thymus Gland; Thyroxine

Arginine vasopressin (AVP) and oxytocin (OXT) were measured simultaneously by radioimmunoassay in neurohypophyses of rats immediately before birth (fetal day 22) onward to day 50 of life. The neurohypophysial content of AVP exceeded that of OXT by factor 17 at fetal day 22, by 20 immediately post natum, and by 2 at day 21 of life, respectively. As compared to day 0, the content at day 21 is considerably higher (AVP 24 fold, OXT 270 fold). The poor correlation between neurohypophysial AVP and OXT content suggests the possibility of a different onto-genetic development of both neuropeptide systems. Both AVP and OXT were detected in pooled rat plasma at various postnatal stages. Hypo- and hyperthyroidism induced experimentally during gestation did not result in a significant change in neuropeptide content of fetal neural lobes.

Topics: Age Factors; Animals; Arginine Vasopressin; Female; Fetus; Hypothyroidism; Oxytocin; Pituitary Gland, Posterior; Pregnancy; Rats; Rats, Inbred Strains

Topics: Deamino Arginine Vasopressin; Hyperthyroidism; Hypopituitarism; Hypothyroidism; Iodine Isotopes; Iodine Radioisotopes; Oxytocin; Pharmacology; Physiology; Pituitary Gland; Thyroid Function Tests; Vasopressins

Topics: Animals; Arginine Vasopressin; Electrolytes; Hypothyroidism; Ions; Oxytocin; Potassium; Rats; Sodium; Sodium, Dietary; Vasopressins