oxytocin 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: Amino Acids; Anesthetics; Animals; Circadian Rhythm; Estrogens; Estrus; Female; Labor, Obstetric; Lactation; Oxytocin; Pregnancy; Prolactin; Seasons; Starvation; Stress, Physiological; Thyroid Hormones; Thyrotropin-Releasing Hormone; Tranquilizing Agents

This study describes the responses of the vasotocinergic and isotocinergic systems to food deprivation and re-feeding processes in immature gilthead sea bream (Sparus aurata). The animals were subjected to the following experimental treatments: (1) normal feeding (control), (2) food deprivation for 21 days; and (3) re-feeding for 7 days, beginning 14 days after starvation. The animals were sampled at 0, 7, 14 and 21 days from the beginning of the trial. The pituitary and plasma arginine vasotocin (AVT) and isotocin (IT) levels and the hypothalamic pro-vasotocin and pro-isotocin mRNA expression levels were measured. In addition, the mRNA levels of three receptors, avtr v1, avtr v2 and itr, were analyzed in target organs associated with (1) the integration and control of different physiological pathways related to stress and food intake (i.e., the hypothalamus), (2) hormonal release into the bloodstream (i.e., the pituitary), and (3) metabolism and its control (i.e., the liver). The metabolic parameters in the liver were also determined. The hepatosomatic index decreased, and hepatic metabolites were mobilized beginning in the early stages of starvation. Moreover, an over-compensation of these parameters occurred when the fish were re-fed after starvation. In terms of the vasotocinergic and isotocinergic systems, feed restriction induced a clear time-dependent regulation among metabolic organization, stress regulation and orexigenic processes in the mature hormone concentration and pro-peptide and receptor mRNA expression. Our results reveal the important role of the AVT/IT endocrine systems in the orchestration of fish physiology during starvation and re-feeding and indicate their involvement in both central and peripheral organs.

Topics: Animal Nutritional Physiological Phenomena; Animals; Eating; Fish Proteins; Gene Expression Regulation; Hypothalamus; Liver; Oxytocin; Pituitary Gland; Receptors, Vasopressin; RNA, Messenger; Sea Bream; Starvation; Time Factors; Vasotocin

Hunger is a complex behavioural state that elicits intense food seeking and consumption. These behaviours are rapidly recapitulated by activation of starvation-sensitive AGRP neurons, which present an entry point for reverse-engineering neural circuits for hunger. Here we mapped synaptic interactions of AGRP neurons with multiple cell populations in mice and probed the contribution of these distinct circuits to feeding behaviour using optogenetic and pharmacogenetic techniques. An inhibitory circuit with paraventricular hypothalamus (PVH) neurons substantially accounted for acute AGRP neuron-evoked eating, whereas two other prominent circuits were insufficient. Within the PVH, we found that AGRP neurons target and inhibit oxytocin neurons, a small population that is selectively lost in Prader-Willi syndrome, a condition involving insatiable hunger. By developing strategies for evaluating molecularly defined circuits, we show that AGRP neuron suppression of oxytocin neurons is critical for evoked feeding. These experiments reveal a new neural circuit that regulates hunger state and pathways associated with overeating disorders.

Topics: Agouti-Related Protein; Animals; Arcuate Nucleus of Hypothalamus; Axons; Eating; Feeding Behavior; Female; Food Deprivation; gamma-Aminobutyric Acid; Hunger; Male; Mice; Models, Neurological; Neural Pathways; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Pro-Opiomelanocortin; Starvation; Synapses

Topics: Animals; Body Weight; Female; Lactation; Mammary Glands, Animal; Milk Ejection; Oxytocin; Pregnancy; Rats; Rats, Inbred Strains; Starvation

Topics: Animals; Aprotinin; Caseins; Cytosol; Female; Insulin; Insulysin; Kinetics; Liver; Male; Oxytocin; Perfusion; Proinsulin; Protein Deficiency; Rats; Somatostatin; Starvation

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; Animals, Newborn; Female; Lactation; Methods; Milk; Oxytocin; Pregnancy; Rats; Starvation; Time Factors

Topics: Acid-Base Equilibrium; Acidosis; Alkalosis; Anesthesia, Obstetrical; Bicarbonates; Carbon Dioxide; Female; Glucose; Humans; Hydrogen-Ion Concentration; Hyperventilation; Labor, Obstetric; Lactates; Maternal-Fetal Exchange; Muscle Contraction; Oxytocin; Parity; Partial Pressure; Pregnancy; Pyruvates; Starvation; Time Factors