pituitrin and Starvation

Starvation-induced alterations of neuropeptide activity probably contribute to neuroendocrine dysfunctions in anorexia nervosa. For example, CRH alterations contribute to hypercortisolemia and NPY alterations may contribute to amenorrhea. Alterations of these peptides as well as opioids, vasopressin, and oxytocin activity could contribute to other characteristic psychophysiological disturbances, such as reduced feeding, in acutely ill anorexics. Such neuropeptide disturbances could contribute to the vicious cycle that has been hypothesized to occur in anorexia nervosa. That is, the consequences of malnutrition perpetuate pathological behavior.

Topics: Anorexia Nervosa; Corticotropin-Releasing Hormone; Feeding Behavior; Humans; Neuropeptide Y; Neuropeptides; Neurosecretory Systems; Opioid Peptides; Oxytocin; Starvation; 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

Topics: Adipose Tissue; Adrenocorticotropic Hormone; Animals; Anxiety; Cold Temperature; Epinephrine; Fatty Acids; Glucagon; Growth Hormone; Hibernation; Human Growth Hormone; Hypophysectomy; Lipid Metabolism; Melanocyte-Stimulating Hormones; Norepinephrine; Peptides; Pharmacology; Physiology, Comparative; Pregnancy; Research; Species Specificity; Starvation; Thyrotropin; Urine; Vasopressins

Preventing reproduction during nutritional deprivation is an adaptive process that is conserved and essential for the survival of species. In mammals, the mechanisms that inhibit fertility during starvation are complex and incompletely understood. Here we show that exposure of female mice to fibroblast growth factor 21 (FGF21), a fasting-induced hepatokine, mimics infertility secondary to starvation. Mechanistically, FGF21 acts on the suprachiasmatic nucleus (SCN) in the hypothalamus to suppress the vasopressin-kisspeptin signaling cascade, thereby inhibiting the proestrus surge in luteinizing hormone. Mice lacking the FGF21 co-receptor, β-Klotho, in the SCN are refractory to the inhibitory effect of FGF21 on female fertility. Thus, FGF21 defines an important liver-neuroendocrine axis that modulates female reproduction in response to nutritional challenge.

Topics: Animals; Energy Metabolism; Female; Fibroblast Growth Factors; Hypothalamus; Infertility, Female; Kisspeptins; Klotho Proteins; Luteinizing Hormone; Membrane Proteins; Mice; Mice, Inbred C57BL; Mice, Knockout; Proestrus; Reproduction; Signal Transduction; Starvation; Suprachiasmatic Nucleus; Vasopressins

In the present study, we have examined in Wistar rats the effects of food or water deprivation of 3 days on the hypophyso-adrenal axis, vasopressinergic system and activity of A1 noradrenergic brain stem cell group, which is involved in the control of the hypothalamic neuro-endocrine activity. Levels of adrenocorticotropic hormone (ACTH) and vasopressin (AVP) were determined by radio-immunoassay, and corticosterone level was determined by fluorimetric method. Plasma levels of ACTH and corticosterone were greatly increased in both groups of rats. In water-deprived rats, plasma AVP (13.83 +/- 1.63 vs. 3.03 +/- 0.23 pg/ml) and osmolality levels were significantly elevated with a marked decrease of AVP hypophysis content (272 +/- 65 vs. 1098 +/- 75 ng/mg protein), but not in food-deprived rats in which osmolality did not change and AVP remained stocked (2082 +/- 216 ng/mg protein) in the hypophysis without release in the plasma (1.11 +/- 0.23 pg/ml). These observations indicated that both food-deprivation and water-deprivation stimulated the pituitary adrenal axis thereby suggesting a stress state. AVP production is stimulated both by fluid and food restriction but is secreted with differential effects: during food restriction AVP secretion is limited to supporting the hypothalamic pituitary-adrenal system.

Topics: Animals; Dehydration; Hypothalamo-Hypophyseal System; Male; Norepinephrine; Pituitary-Adrenal System; Rats; Rats, Wistar; Starvation; Vasopressins

1. The cytoskeletal depolymerizing agent, colchicine, prevents the hepatic alpha 1-adrenoceptor-mediated stimulation of respiration, H+ and Ca2+ release to the effluent perfusate, intracellular alkalosis, and glycogenolysis. Unlike the other parameters, colchicine does not perturb the alpha 1-agonist-induced stimulation of gluconeogenesis or phosphorylase 'a' activation, and enhances the increase in portal pressure response. The lack of effect of colchicine on the hepatic alpha 2-adrenoceptor-mediated effects indicates that its actions are alpha 1-specific. 2. Colchicine enhances the acute alpha 1-adrenoceptor-mediated intracellular Ca2+ mobilization and prevents the activation of protein kinase C. This differential effect on the two branches of the alpha 1-adrenoceptor signalling pathway is a distinctive feature of the colchicine action. 3. The lack of effect of colchicine in altering the alpha 1-adrenoceptor ligand binding affinity suggests that it might interact with some receptor-coupled regulatory element(s). 4. The acuteness of the colchicine effect and the ability of its isomer beta-lumicolchicine to prevent all the alpha 1-adrenoceptor-mediated responses but the increase in vascular resistance, indicate that its action cannot be merely ascribed to its effects in depolymerizing tubulin. 5. Colchicine perturbs the hepatic responses to vasoactive peptides. It enhances the vasopressin-induced rise of cytosolic free Ca2+ in isolated hepatocytes and prevents the sustained decrease of Ca2+ in the effluent perfusate. It also inhibits the stimulation of glycogenolysis, without altering the stimulation of gluconeogenesis. 6. It is concluded that there are at least two major alpha 1-adrenoceptor signalling pathways. One is colchicine-sensitive, independent of variations in free cytosolic Ca2+, and protein kinase C-dependent; the other one is colchicine-insensitive, dependent on variations in free cytosolic Ca2+, and protein kinase C-independent.

Topics: Animals; Calcium; Cells, Cultured; Colchicine; Cytosol; Hydrogen-Ion Concentration; Kinetics; Liver; Lumicolchicines; Male; Oxygen Consumption; Phosphorylases; Protein Kinase C; Rats; Rats, Wistar; Receptors, Adrenergic, alpha-1; Starvation; Vasoconstrictor Agents; Vasopressins

1. The vasopressin mRNA in the adult male rat hypothalamus is modulated in two distinct ways by a dehydration stimulus. In addition to the well-established increase in transcript abundance, it has recently been demonstrated that the vasopressin mRNA poly(A) tail increases in length. 2. We have studied the ontogeny of poly(A) tail length modulation in neonates in response to milk deprivation and found that poly(A) tail length changes are age dependent. In neonates older than 12 days of age, the vasopressin mRNA poly(A) tail length increased with milk deprivation and this effect became more marked in older animals. However, in rats 5 to 9 days old, milk deprivation resulted in a detectable though not significant decrease in vasopressin mRNA poly(A) tail length. 3. As milk deprivation is a combination of dehydration and starvation, we investigated the effect of the latter stimulus in more mature animals. We found that starvation modifies the length of the vasopressin mRNA poly(A) tail in a manner opposite that due to dehydration. 4. Our data indicate a novel mode of regulation of the vasopressin mRNA, namely, poly(A) tail shortening. This system provides a model for future studies concerning the adaptive role of poly(A) tail length modulation in response to physiological stimuli.

Topics: Adaptation, Physiological; Age Factors; Animals; Animals, Newborn; Dehydration; Female; Hypothalamus; Male; Osmolar Concentration; Poly A; Rats; Rats, Sprague-Dawley; RNA, Messenger; Starvation; Vasopressins; Weight Loss

The short-term effect of L-tri-iodothyronine (T3) on hepatic Ca2+ uptake from perfusate was compared with changes induced by T3 on cellular respiration and glucose output in isolated perfused livers from fasted and fed rats. The same parameters were also studied after the addition of glucagon or vasopressin. T3 (1 microM) induced Ca2+ uptake from the perfusate into the liver within minutes, and the time course was similar to that for stimulation of respiration and gluconeogenesis in livers from fasted rats, and for the stimulation of respiration and glucose output in livers from fed rats. The effects were dose-dependent in the range 1 microM-0.1 nM. Similar changes in the same parameters could be observed with glucagon and vasopressin, but with a completely different time course. Also, the influence of the T3 analogues L-thyroxine (L-T4), 3,5-di-iodo-L-thyronine (L-T2) and 3,3',5-tri-iodo-D-thyronine (D-T3) on hepatic energy metabolism was examined. Whereas D-T3 had practically no effect, L-T4 and L-T2 caused changes in Ca2+ uptake, O2 consumption and gluconeogenesis in livers from fasted rats similar to those with T3. It is concluded that changes in mitochondrial and cytosolic Ca2+ concentrations are involved in the stimulation of respiration and glucose metabolism observed with T3, glucagon and vasopressin.

Topics: Animals; Calcium; Glucagon; In Vitro Techniques; Liver; Male; Perfusion; Rats; Rats, Inbred Strains; Starvation; Time Factors; Triiodothyronine; Vasopressins

Vasopressin was found to be an effective inhibitor of protein labelling in isolated liver cells. Its effect shows the following distinct characteristics: (1) in contrast with alpha-adrenergic agonists, its effect is observable under a wide range of cellular Ca2+-loading conditions; (2) it is not influenced by the nutritional state of the animal. The lack of vasopressin effect on valine production, and its ability to decrease protein labelling from near-saturation concentrations of [3H]valine, indicate that the observed variations in protein labelling reflect actual changes in the rate of protein synthesis. The action of vasopressin is primarily exerted on the initiation step of protein synthesis and this effect is accompanied by a decreased activity of eukaryotic initiation factor 2. Activators of protein kinase C showed similar but not additive effects on protein synthesis, as did vasopressin. It seems plausible to conclude that protein kinase C activation may play an important regulatory role in hepatic protein synthesis as a transducer of hormonal and perhaps other type of signals.

Topics: Animals; Calcium; Dose-Response Relationship, Drug; Enzyme Activation; Eukaryotic Initiation Factor-2; In Vitro Techniques; Liver; Male; Peptide Chain Initiation, Translational; Peptide Initiation Factors; Protein Biosynthesis; Protein Kinase C; Proteins; Rats; Rats, Inbred Strains; Starvation; Tritium; Valine; Vasopressins

Effects of water-deprivation on several metabolic parameters and on plasma aldosterone concentration have been investigated in male Brattleboro rats homozygous for hypothalamic diabetes insipidus (DI) and in male Long-Evans rats (LE) as controls. Two separate experiments were performed over a period of 72 hours: 1) to determine the global effect of water-deprivation, water deprived rats were compared with hydrated animals, 2) to elucidate the specific effect of dehydration alone, water-deprived rats were compared with similar food-restricted, but water-supplied DI and LE rats. In hydrated animals, plasma aldosterone concentration was close to 50% less in DI rats than in LE rats. After 72 hours, plasma aldosterone values increased mainly because of dehydration and this increase was greater in DI rats than in LE rats. At the same time, plasma aldosterone concentration remained lower in DI rats compared to LE rats. The changes in plasma aldosterone concentration after dehydration and possible reasons for the impairment of aldosterone production in DI rats are discussed.

Topics: Adrenal Glands; Aldosterone; Animals; Male; Organ Size; Rats; Rats, Brattleboro; Starvation; Urine; Vasopressins; Water Deprivation

The effects of vasopressin on the metabolism of starved rats were investigated by using a constant-infusion regimen (50 pmol/kg body wt. per min, after an initial loading dose of 150 pmol/kg body wt.). 2. Blood ketone bodies decreased by 50% in 10 min, and this was accompanied by a 60% decrease in the plasma non-esterified fatty acids. 3. Blood glucose increased by 0.9 mM within 5 min and decreased to control values over the 40 min infusion. Small increases in lactate and pyruvate also occurred. 4. Plasma insulin was not increased by vasopressin infusion. 5. The net decrease in blood ketone bodies caused by vasopressin was similar when somatostatin was infused simultaneously (1 nmol/kg body wt. per min). 6. Hepatic ketone bodies were significantly decreased by vasopressin, as was the 3-hydroxybutyrate/acetoacetate ratio. A small increase in the hepatic concentration of several glycolytic intermediates also occurred. 7. Vasopressin did not decrease the ketonaemia produced by infusions of octanoate or long-chain triacylglycerol in rats that had been pre-treated with the anti-lipolytic agent 3,5-dimethylpyrazole. 8. In comparison with vasopressin, the infusion of adrenaline or glucose had much smaller effects in decreasing the ketonaemia of starvation, despite the 4-fold increase in plasma insulin, at 10 min, with the glucose infusion. 9. The primary metabolic effect of vasopressin in the starved rat appears to be that of decreased supply of non-esterified fatty acid to the liver. It is suggested that vasopressin has a direct anti-lipolytic effect in adipose tissue.

Topics: Animals; Epinephrine; Glucose; Infusions, Parenteral; Ketone Bodies; Lipid Metabolism; Liver; Male; Rats; Rats, Inbred Strains; Somatostatin; Starvation; Vasopressins

Adrenaline, noradrenaline, vasopressin and angiotensin increased 14CO2 production from [1-14C]oleate by hepatocytes from fed rats but not by hepatocytes from starved rats. The hormones did not increase 14CO2 production when hepatocytes from fed rats were depleted of glycogen in vitro. Increased 14CO2 production from ]1-14C]oleate in response to the hormones was observed when hepatocytes from starved rats were incubated with 3-mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase. 3-Mercaptopicolinate inhibited uptake and esterification of [1-14C]oleate, slightly increased 14CO2 production from [1-14C]oleate and greatly increased the [3-hydroxybutyrate]/[acetoacetate] ratio. In the presence of 3-mercaptopicolinate 14CO2 production in response to the catecholamines was blocked by the alpha-antagonist phentolamine and required extracellular Ca2+. The effects of vasopressin and angiotensin were also Ca2+-dependent. The actions of the hormones of 14CO2 production from [I-14C]oleate by hepatocytes from starved rats in the presence of 3-mercaptopicolinate thus have the characteristics of the response to the hormones found with hepatocytes from fed rats incubated without 3-mercaptopicolinate. The stimulatory effects of the hormones on 14CO2 production from [1-14C]oleate were not the result of decreased esterification (as the hormones increased esterification) or increased beta-oxidation. It is suggested that the effect of the hormones to increase 14CO2 production from [1-14C]oleate are mediated by CA2+-activation of NAD+-linked isocitrate dehydrogenase, the 2-oxoglutarate dehydrogenase complex, and/or electron transport. The results also demonstrate that when the supply of oxaloacetate is limited it is utilized for gluconeogenesis rather than to maintain tricarboxylic acid-cycle flux.

Topics: Angiotensin II; Animals; Carbon Dioxide; Epinephrine; Female; In Vitro Techniques; Liver; Norepinephrine; Oleic Acid; Oleic Acids; Picolinic Acids; Rats; Rats, Inbred Strains; Starvation; Stimulation, Chemical; Vasopressins

14CO2 production from [l-14C]oleate, [l-14C]butyrate and [U-14C]proline by isolated rat hepatocytes was studied. In hepatocytes from fed rats, fatty acid and proline oxidation are stimulated in parallel by adrenaline, noradrenaline, vasopressin and angiotensin II. In contrast in hepatocytes from 24 h-starved rats these hormones stimulate proline oxidation whereas oleate and butyrate oxidation is hormone-insensitive. This suggests that 14CO2 production from [U-14C]proline and [l-14C]oleate is subject to independent endocrine control. In support of this in hepatocytes from fed rats, glucagon and dibutyryl cyclic AMP stimulate 14CO2 production from proline but inhibit 14CO2 production from [l-14C]oleate. The pathway of hepatic proline oxidation is discussed and it is suggested that 2-oxoglutarate dehydrogenase is one site of endocrine control of proline oxidation.

Topics: Angiotensin II; Animals; Butyrates; Butyric Acid; Carbon Dioxide; Citric Acid Cycle; Epinephrine; Glucagon; Liver; Norepinephrine; Oleic Acid; Oleic Acids; Oxidation-Reduction; Picolinic Acids; Proline; Rats; Starvation; Vasopressins

Earlier observations that food restriction for a short period of time in the morning produced an altered circadian rhythm of plasma corticosterone having the peak just before feeding time, and that the elevated plasma corticosterone levels declined promptly immediately after food presentation were confirmed. After a 14-day restricted feeding schedule, where food was given from 11:00 to 13:00, if food was not given, elevated levels of plasma corticosterone were sustained for at least 1 hr and then declined gradually. On the other hand, if food was given 2 hr earlier than the scheduled time, the peak at 11:00 disappeared. The conditioned peak of plasma corticosterone was maintained for at least 3 days after the restricted feeding schedule if hypertonic saline, but not tap water, was given without food in male rats and ovariectomized female ones. When female rats were treated with lysine vasopressin for 5 days 10 min before the food presentation, highly elevated levels of plasma corticosterone were found at the time of food presentation. However, administration of cortisol 2 hr before the feeding time blocked the effect of vasopressin. The results suggest that vasopressin is involved in the acquisition and consolidation of the conditioned circadian rhythm of plasma corticosterone induced by restricted feeding.

Topics: Animals; Circadian Rhythm; Corticosterone; Eating; Hydrocortisone; Male; Rats; Starvation; Vasopressins

Topics: Angiotensin II; Animals; Diabetes Mellitus; Epinephrine; Fatty Acids, Nonesterified; Glucagon; Glucose; Glycerides; Hormones; Insulin; Liver; Liver Glycogen; Nucleotides, Cyclic; Obesity; Oxytocin; Parathyroid Hormone; Protein Kinases; Starvation; Stress, Physiological; Vasopressins

Topics: Animals; Glucose; Glycerol; Lactates; Liver; Liver Glycogen; Perfusion; Pyruvates; Rats; Serine; Starvation; Vasopressins

Topics: Animals; Body Composition; Body Water; Dogs; Humans; Mathematics; Parenteral Nutrition; Potassium; Potassium Deficiency; Radioisotope Dilution Technique; Regression Analysis; Sepsis; Sodium; Sodium Isotopes; Starvation; Surgical Procedures, Operative; Tritium; Uremia; Vasopressins

Topics: Acetates; Animals; Blood Glucose; Epinephrine; Fatty Acids, Nonesterified; Female; Growth Hormone; Heparin; Homeostasis; Insulin; Male; Malonates; Nicotinic Acids; Propionates; Pyrazoles; Radioimmunoassay; Salicylates; Sheep; Starvation; Triglycerides; Vasopressins

Topics: Aminohippuric Acids; Animals; Chlorides; Dehydration; Dietary Proteins; Glomerular Filtration Rate; Glucose; Hydrolases; Kidney; Kidney Concentrating Ability; Mannitol; Phosphoenolpyruvate Carboxykinase (GTP); Potassium; Regional Blood Flow; Sheep; Sodium; Starvation; Transferases; Urea; Vasopressins

1. Vasopressin (anti-diuretic hormone, [8-arginine]vasopressin) stimulated the breakdown of glycogen in perfused livers of fed rats, at concentrations (50-600muunits/ml) that have been reported in the blood of intact rats, especially during acute haemorrhagic shock. 2. In perfused livers from starved rats, vasopressin (30-150muunits/ml) stimulated gluconeogenesis from a mixture of lactate, pyruvate and glycerol. 3. Vasopressin prevented accumulation of liver glycogen in the perfused liver of starved rats, or in starved intact rats. 4. The action of vasopressin on hepatic carbohydrate metabolism thus resembles that of glucagon; the minimum effective circulating concentrations of these hormones are of the same order (100pg/ml). 5. The stimulation of hepatic glucose output by vasopressin is discussed in connexion with the release of glucose and water from the liver.

Topics: Animals; Gluconeogenesis; Glucose; Glycerol; Lactates; Liver; Liver Glycogen; Male; Perfusion; Pyruvates; Rats; Shock, Hemorrhagic; Starvation; Vasopressins; Water

Topics: Animals; Desoxycorticosterone; Drinking; Kidney; Kidney Tubules; Male; Natriuresis; Potassium; Rabbits; Sodium; Starvation; Time Factors; Urea; Urination; Vasopressins; Water; Water-Electrolyte Balance

Topics: Animals; Autoradiography; Body Weight; Buffers; Carbon Isotopes; DNA; Hypothalamo-Hypophyseal System; Hypothalamus; In Vitro Techniques; Microscopy, Electron; Nerve Tissue Proteins; Neuroglia; Neurosecretion; Nucleotidyltransferases; Pituitary Gland, Posterior; Rats; Ribonucleases; RNA; Starvation; Tritium; Uracil Nucleotides; Vasopressins; Water Deprivation

Topics: Angiotensin II; Animals; Drinking; Hypothalamus; Injections; Nephrectomy; Rats; Renin; Starvation; Thirst; Time Factors; Vasopressins

Topics: Adrenal Glands; Animals; Chickens; Dehydration; Female; Poultry Diseases; Starvation; Thyroid Gland; Thyroxine; Vasopressins

Topics: Adrenal Glands; Adrenalectomy; Animals; Body Weight; Desoxycorticosterone; Drinking; Male; Rats; Starvation; Urine; Vasopressins; Water

Topics: Animals; Dehydration; Diabetes Insipidus; Hypothalamus; Potassium; Rats; Sodium; Starvation; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Arginine Vasopressin; Dogs; Humans; Potassium; Starvation; Urea; Vasopressins

Topics: Hypothalamo-Hypophyseal System; Hypothalamus; Pituitary Gland; Starvation; Vasopressins

Topics: Diuresis; Glucose; Humans; Kidney; Kidney Tubules; Male; Mannitol; Pharmacology; Sodium; Starvation; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Arginine Vasopressin; Dehydration; Rats; Starvation; Thyroid Gland; Vasopressins