pituitrin and Anorexia

Topics: Anorexia; Arousal; Brain Mapping; Circadian Rhythm; Corticotropin-Releasing Hormone; Depression; Glucocorticoids; Humans; Hydrocortisone; Hypothalamic Hormones; Hypothalamo-Hypophyseal System; Hypothalamus; Magnetic Resonance Imaging; Models, Neurological; Models, Psychological; Mood Disorders; Neuropsychological Tests; Neurotransmitter Agents; Oxytocin; Paraventricular Hypothalamic Nucleus; Phototherapy; Pituitary-Adrenal System; Prefrontal Cortex; Receptors, Glucocorticoid; Receptors, Neurotransmitter; Sleep Initiation and Maintenance Disorders; Stress, Physiological; Stroke; Thyroid Gland; Tomography, Emission-Computed; Tomography, Emission-Computed, Single-Photon; Vasopressins

Topics: 17-Ketosteroids; Adrenal Glands; Adrenocorticotropic Hormone; Amenorrhea; Anorexia; Anorexia Nervosa; Basal Metabolism; Body Temperature Regulation; Cholesterol; Dopamine; Female; Gonadotropins; Growth Hormone; Humans; Hypothalamus; Prolactin; Starvation; Thyroid Gland; Vasopressins

Functional pancreatic neuroendocrine tumors (pNETs) rarely produce vasopressin. Here, we reported a case of pNET producing vasopressin in a 78-year-old man with hyponatremia.. The patient presented with anorexia approximately 4 years ago, and the laboratory test results indicated hyponatremia. He was hospitalized 3 times subsequently due to anorexia in the past 4 years, during which laboratory tests consistently indicated severe hyponatremia.. Upon admission, his serum osmolarity, urine osmolarity, urine sodium level, and 24-hour urine sodium level was 277 mOsm/kg H2O, 465 mOsm/kg H2O, 82.5 mmol/L, and 140.25 mmol, respectively. Gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography showed a high uptake lesion measuring approximately 1 cm in diameter in the pancreatic body, and the possibility of pNET was considered. Besides, laboratory tests showed that adrenocorticotropic hormone, follicle-stimulating hormone, and luteinizing hormone released by the pituitary was insufficient in the case of low levels of cortisol, estradiol, progesterone, and testosterone. Thus, the diagnosis of the syndrome of inappropriate antidiuresis (SIAD) was considered along with hypopituitarism.. The patient underwent surgery, and pNET was confirmed by pathology examination. The immunohistochemical study showed that the tumor cells were positive for somatostatin receptors 2 and vasopressin.. In the last follow-up 17 months after surgery, the patient was in good condition, taking methylprednisolone 4 mg every other day, and had been free of anorexia or hyponatremia episodes.. This case illustrated the potential ectopic production of vasopressin resulting in SIAD in pNETs, highlighting the adoption of gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography and vasopressin immunohistochemical staining in the evaluation of the etiology of SIAD.

Topics: Adrenal Cortex Hormones; Aged; Anorexia; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Neuroendocrine Tumors; Pancreatic Neoplasms; Vasopressins

Evidence in rats suggests that central oxytocin (OT) signaling pathways contribute to suppression of food intake during dehydration (i.e., dehydration anorexia). The present study examined water deprivation-induced dehydration anorexia in wild-type and OT -/- mice. Mice were deprived of food alone (fasted, euhydrated) or were deprived of both food and water (fasted, dehydrated) for 18 h overnight. Fasted wild-type mice consumed significantly less chow during a 60-min refeeding period when dehydrated compared with their intake when euhydrated. Conversely, fasting-induced food intake was slightly but not significantly suppressed by dehydration in OT -/- mice, evidence for attenuated dehydration anorexia. In a separate experiment, mice were deprived of water (but not food) overnight for 18 h; then they were anesthetized and perfused with fixative for immunocytochemical analysis of central Fos expression. Fos was elevated similarly in osmo- and volume-sensitive regions of the basal forebrain and hypothalamus in wild-type and OT -/- mice after water deprivation. OT-positive neurons expressed Fos in dehydrated wild-type mice, and vasopressin-positive neurons were activated to a similar extent in wild-type and OT -/- mice. Conversely, significantly fewer neurons within the hindbrain dorsal vagal complex were activated in OT -/- mice after water deprivation compared with activation in wild-type mice. These findings support the view that OT-containing projections from the hypothalamus to the hindbrain are necessary for the full expression of compensatory behavioral and physiological responses to dehydration.

Topics: Animals; Anorexia; Blood Volume; Dehydration; DNA; Eating; Food Deprivation; Genotype; Hindlimb; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Oxytocin; Proto-Oncogene Proteins c-fos; Rhombencephalon; Vasopressins

It is known that water deprivation or injection of hypertonic saline induces anorexia. The present study examined the possible involvement of vasopressin in the suppression of food intake during high plasma osmolality. Intraperitoneal injection of vasopressin (20 microg/kg) into male rats significantly suppressed food intake for 1 hr. This anorectic effect of vasopressin was reversed by simultaneous injection of a peptide antagonist for V(1) receptor (40 microg/kg), but not for V(2) receptor (40 microg/kg). Intraperitoneal injection of hypertonic saline (20% NaCl, 2 ml/kg) similarly suppressed food intake for 2 hr, which was associated with a transient increase in plasma vasopressin concentrations. This hypertonic saline-induced suppression of food intake was blocked by a V(1) receptor antagonist. Vasopressin (40 ng/2 microl) directly administered into the third ventricle of the brain also suppressed food intake for 1 hr. These results suggest that vasopressin participates in the suppression of food intake during high plasma osmolality, the action of which is mediated by V(1) receptors in the brain.

Topics: Analysis of Variance; Animals; Anorexia; Antidiuretic Hormone Receptor Antagonists; Disease Models, Animal; Eating; Male; Osmolar Concentration; Rats; Rats, Wistar; Receptors, Vasopressin; Sodium Chloride; Time Factors; Vasopressins

The anorectic effect of IP injection of amylin (1 microgram/kg) was abolished by simultaneous IP injection of the amylin receptor antagonist calcitonin gene-related peptide-(8-37) [CGRP(8-37), 10 micrograms/kg]. The IP injection of pancreatic glucagon (400 micrograms/kg) at dark onset also reduced food intake in 24-h food-deprived rats, and this effect was also totally blocked by coadministration of CGRP(8-37) (10 micrograms/kg). In another feeding paradigm with glucagon (540 micrograms/kg IP 3 h into the light phase in 3 h-prefed rats), however, the anorectic effect of glucagon was not significantly antagonized by CGRP(8-37). The anorectic effect of cholecystokinin (CCK) (0.25 microgram/kg) and bombesin (BBS) (2 micrograms/kg) was partly neutralized by CGRP(8-37). In contrast, the anorectic effect of vasopressin (VP) (2.5 micrograms/kg) was not influenced by CGRP(8-37). As glucagon has been shown previously to increase the secretion of amylin, we conclude that the anorectic effect of peripherally administered glucagon is mediated by the release of amylin, at least under certain conditions. This may also be true for CCK and BBS, as these peptides are insulinotropic and may therefore be presumed to increase amylin release.

Topics: Amyloid; Animals; Anorexia; Bombesin; Calcitonin Gene-Related Peptide; Cholecystokinin; Glucagon; Humans; Islet Amyloid Polypeptide; Male; Peptide Fragments; Rats; Receptors, Islet Amyloid Polypeptide; Receptors, Peptide; Vasopressins