Determining the etiology and possible treatment strategies for numerous diseases requires a comprehensive understanding of compensatory mechanisms in physiological systems. The vagus nerve acts as a key interface between the brain and the peripheral internal organs. We set out to identify mechanisms compensating for a lack of neuronal communication between the immune and the central nervous system (CNS) during infection. We assessed biochemical and central neurotransmitter changes resulting from subdiaphragmatic vagotomy and whether they are modulated by intraperitoneal infection. We performed a series of subdiaphragmatic vagotomy or sham operations on male Wistar rats. Next, after full, 30-day recovery period, they were randomly assigned to receive an injection of Escherichia coli lipopolysaccharide or saline. Two hours later, animal were euthanized and we measured the plasma concentration of prostaglandin E2 (with HPLC-MS), interleukin-6 (ELISA), and corticosterone (RIA). We also had measured the concentration of monoaminergic neurotransmitters and their metabolites in the amygdala, brainstem, hippocampus, hypothalamus, motor cortex, periaqueductal gray, and prefrontal medial cortex using RP-HPLC-ED. A subset of the animals was evaluated in the elevated plus maze test immediately before euthanization. The lack of immunosensory signaling of the vagus nerve stimulated increased activity of discrete inflammatory marker signals, which we confirmed by quantifying biochemical changes in blood plasma. Behavioral results, although preliminary, support the observed biochemical alterations. Many of the neurotransmitter changes observed after vagotomy indicated that the vagus nerve influences the activity of many brain areas involved in control of immune response and sickness behavior. Our studies show that these changes are largely eliminated during experimental infection. Our results suggest that in vagotomized animals with blocked CNS, communication may transmit via a pathway independent of the vagus nerve to permit restoration of CNS activity for peripheral inflammation control.

This study examined the effects of acute restraint stress in the presence or absence of naltrexone on the circulating concentrations of insulin, glucose, Met-enkephalin and corticosterone in 14-week-old chickens [design: 2 sex × 2 stress/non-stress × 2 +/− naltrexone]. In chickens (five male and five females per treatment) subjected to restraint for 30 min, there were increases in the plasma concentrations of corticosterone and Met-enkephalin. The plasma concentrations of insulin and glucose were also increased in the chickens during restraint. Moreover, there were increases in the plasma concentrations of insulin and glucose in the chickens. The patterns of expression of the proenkephalin gene (PENK) in both the anterior pituitary gland and the adrenal gland were very similar to that of plasma Met-enkephalin. There were relationships between the plasma concentrations of corticosterone, Met-enkephalin, insulin and glucose after 30 min of restraint. The effects of naltrexone treatment on both untreated and stressed chickens were also examined, with naltrexone attenuating the stress-induced increases in the plasma concentrations of corticosterone, Met-enkephalin and glucose but not in those of insulin. The present study demonstrates that stress increases insulin secretion in chickens but also induces insulin resistance.

Introduction: Obesity is a highly prevalent disease in the world associated with the disorders of endocrine system. Recently, it may be concluded that the only effective treatment of obesity remains bariatric surgery. The aim of the review was to compare the concepts of appetite hormonal regulation, reasons of obesity development and bariatric procedures published over the last decade. Material and methods: The reviewed publications had been chosen on the base on: 1. reasons and endocrine consequences of obesity; 2. development of surgery methods from the first bariatric to present and future less aggressive procedures; 3. impact of surgery on the endocrine status of patient. Results: The most serious endocrine disturbances during obesity are dysfunctions of hypothalamic circuits responsible for appetite regulation, insulin resistance, changes in hormones activity and abnormal activity of adipocytes hormones. The currently recommended bariatric surgeries are Roux-en-Y gastric bypass, sleeve gastrectomy and adjustable gastric banding. Bariatric surgical procedures, particularly combination of restrictive and malabsorptive, decrease the body weight and eliminate several but not all components of metabolic syndrome. Conclusions: 1.Hunger and satiety are mediated by an interplay of nervous and endocrine signals. 2. Healthy adipose tissue secretion of adipokines is coordinated in an anti-inflammatory, insulin-sensitizing and cardioprotective pattern. However, with increasing fat mass this secretion pattern is changed into a proinflammatory, insulin resistant, atherogenic and fatal systemic environment . 3. Bariatric surgery is not a solution of the obesity problem for everyone. 4. Long term postsurgical observations of the hormonal profile changes are necessary and should be obligatory. Introduction: Obesity is a highly prevalent disease in the world associated with the disorders of endocrine system. Recently, it may be concluded that the only effective treatment of obesity remains bariatric surgery. The aim of the review was to compare the concepts of appetite hormonal regulation, reasons of obesity development and bariatric procedures published over the last decade. Material and methods: The reviewed publications had been chosen on the base on: 1. reasons and endocrine consequences of obesity; 2. development of surgery methods from the first bariatric to present and future less aggressive procedures; 3. impact of surgery on the endocrine status of patient. Results: The most serious endocrine disturbances during obesity are dysfunctions of hypothalamic circuits responsible for appetite regulation, insulin resistance, changes in hormones activity and abnormal activity of adipocytes hormones. The currently recommended bariatric surgeries are Roux-en-Y gastric bypass, sleeve gastrectomy and adjustable gastric banding. Bariatric surgical procedures, particularly combination of restrictive and malabsorptive, decrease the body weight and eliminate several but not all components of metabolic syndrome. Conclusions: 1.Hunger and satiety are mediated by an interplay of nervous and endocrine signals. 2. Healthy adipose tissue secretion of adipokines is coordinated in an anti-inflammatory, insulin-sensitizing and cardioprotective pattern. However, with increasing fat mass this secretion pattern is changed into a proinflammatory, insulin resistant, atherogenic and fatal systemic environment . 3. Bariatric surgery is not a solution of the obesity problem for everyone. 4. Long term postsurgical observations of the hormonal profile changes are necessary and should be obligatory.

The present review summarizes the state of knowledge of endogenous opioids in birds. Endogenous opioid peptides acts in a neuromodulatory, hormonal and paracrine manner to mediate analgesic and other physiological functions. These peptides act through specific G-protein coupled receptors. Opioid receptors consist of a family of four closely-related proteins. The three types of opioid receptors are the mu (MOR or μ), delta (DOR or δ), and kappa (KOR or κ) opioid receptor proteins. The role of the fourth member of the opioid receptor family, the nociceptin or orphanin FQ receptor (ORL), is not clear. The ligands for opioid receptors are: β –endorphin (MOR), Met- enkephalin, Leu-enkephalin (DOR) and dynorphin (KOR), together with probably endomorphins 1 and 2. In spite of long history of research on endogenous opioid peptides, there are no studies of endogenous opioids per se in wild birds and few in poultry species. β-endorphin is present in all birds investigated and there is close agreement between the structures of β-endorphin in different birds. Plasma concentrations of β-endorphin are increased by ether stress in geese. There is evidence that β-endorphin plays a role in the control of luteinizing hormone release in chickens. Met-enkephalin is present in tissues such as the retina, hypothalamus, pituitary gland, and adrenals together with circulation of birds. Stresses such as crowding and withholding water increase circulating concentrations of Met-enkephalin in chickens. The structures of chicken dynorphin A and B have been deduced from cDNA. What is missing are comprehensive studies of plasma concentrations and expression of the full array of endogenous opioids in multiple avian species under different situations. Also, what is not known is the extent to which circulating or locally released or intra-cellular Met-enkephalin influence physiological process in birds. Thus, there is considerable scope for investigation of the physiology of endogenous opioids in birds.

It was hypothesized that there is cross-talk between the classical constituents of the hypothalamo-pituitary-adrenocortical axis (HPA) and Met-enkephalin in the HPA axis. The study examined effects of isolation stress, sex, and age on concentrations of native Met-enkephalin and pro-enkephalin (PENK) gene expression in tissues of the HPA (hypothalamus, pituitary gland and adrenal cortex) in 3-, 6- and 9-month old female and male lambs. In addition, the effects of isolation stress on in vitro release Met-enkephalin from fragments of the hypothalamus or adrenal cortex were examined. Isolation stress was followed by decreases in the concentration of Met-enkephalin in both the pituitary gland and adrenal cortex. There were also increases in the hypothalamic concentration of Met-enkephalin together with increases in PENK gene expression in the HPA in 6- and 9-months old females and males. There were reductions in release of Met-enkephalin from hypothalamic and adrenocortical tissue in vitro after isolation stress. In the presence of naltrexone, there were increases in basal release in vitro of Met-enkephalin from hypothalamic tissue from control and stressed female lambs but a decrease in tissue from stressed male lambs. In a somewhat similar manner, the presence of naltrexone was associated with increases in the basal release of Met-enkephalin from adrenocortical tissue from control female lambs but a decrease with tissue from stressed female and both stressed and control male lambs.

The effects of stressors were examined on Met-enkephalin-related parameters and plasma concentrations of corticosterone in 14-week-old female chickens. Water deprivation for 24 h was accompanied by a tendency for increased plasma concentration of Met-enkephalin while plasma concentrations of corticosterone were elevated in water-deprived birds. Concentrations of Met-enkephalin were reduced in the anterior pituitary gland and adrenal gland in water-deprived pullets while proenkephalin (PENK) expression was increased in both tissues. There were changes in the plasma concentrations of Met-enkephalin and corticosterone in pullets subjected to either feed withholding or crowding. Concentrations of Met-enkephalin were increased in the anterior pituitary gland but decreased in adrenal glands in pullets subjected to crowding stress. The increase in the plasma concentrations of Met-enkephalin was ablated when the chickens were pretreated with naltrexone. However, naltrexone did not influence either basal or crowding on plasma concentrations of corticosterone. In vitro release of Met-enkephalin from the anterior pituitary or adrenal tissues was depressed in the presence of naltrexone. It was concluded that Met-enkephalin was part of the neuroendocrine response to stress in female chickens. It was concluded that stress influenced the release of both Met-enkephalin and corticosterone, but there was not complete parallelism.