neuropeptide-y and Burns

Burn injury is a severe form of trauma associated with pain, metabolic abnormalities, susceptibility to infections, muscle loss, mental and emotional distress. Conventional therapies as well as some recent approaches for the treatment of burned patients are currently in use. Nutritional therapy is also suggested as a supplementary option in major burns. Within this context, hormones involved in the regulation of appetite will have a paramount importance. The aim is to evaluate the interactions among ghrelin, some inflammatory parameters and the burn injury. Asprosin is also involved into this discussion due to its ghrelin-like actions. Aside from the consideration of insulin as well as stress hormones (cortisol, epinephrine, norepinephrine), an orexigenic, anti-inflammatory hormone, ghrelin affecting both metabolic and inflammatory systems is also involved in the protocols designed for burn treatment. Ghrelin's actions exerted by way of growth-hormone secretagogue receptor, neuropeptide Y, agouti-related protein, proopiomelanocortin and gamma amino butyric acid are being investigated. Asprosin, one of the remarkably few hormones identified as appetite stimulator, acts as another orexigenic hormone by using almost the same signalling pathways as those of ghrelin. Interleukin-6 should also be evaluated both as a reliable biomarker of inflammation and also with its inhibitory effects on TNF-α within the scope of burn injury. In conclusion, treatment protocols during burn injury may be designed to raise decreased concentrations of ghrelin and to repress increased levels of inflammatory agents such as TNF-α. IL-6 may be evaluated from an entirely different aspect. The potential therapeutic use of asprosin may be considered within an integrative approach with a focus on cachexia-anorexia developed in severe burn trauma.

Topics: Animals; Anorexia; Burns; Cachexia; Cytokines; Epinephrine; Fibrillin-1; Ghrelin; Hormones; Humans; Inflammation; Interleukin-10; Interleukin-6; Mice; Microfilament Proteins; Models, Theoretical; Neurons; Neuropeptide Y; Peptide Fragments; Peptide Hormones; Treatment Outcome; Tumor Necrosis Factor-alpha

Hypermetabolism and anorexia are significant problems associated with major burn trauma. Recent studies have shown that hypothalamic corticotropin releasing factor (CRF) elevates metabolic rate, while neuropeptide Y (NPY) reduces it. CRF also elicits anorexia, while NPY stimulates feeding. We hypothesized that elevation of CRF and decrease of NPY may be mediators of these negative effects of burn trauma. Therefore, we assessed concentrations of CRF and NPY in hypothalamus of burned rats one, three, and twenty-one days after a 30% body surface area, full-thickness, open flame burn. In addition we determined whether a biochemical lesion of CRF receptors using 3rd ventricle injections of a saporin-CRF conjugated peptide would decrease resting energy expenditure (REE). We found a three-day period of anorexia, with REE significantly increasing three days after the burn trauma. Concentrations of NPY were increased in the PVN-containing dorsomedial region of the hypothalamus 1 and 3 days after burn trauma, but were increased further in the day 1 pair-fed rats suggesting this change was a consequence of the anorexia. Levels of CRF were decreased in the ventromedial region of the hypothalamus in day 1 and day 3 burned and PF rats. Treatment with the saporin-CRF conjugate normalized REE and reduced CRF receptor-2 density in the hypothalamus of burned rats, and blocked CRF-induced hypermetabolism in sham-burned rats. Although these results suggest a role of CRF receptors in mediating burn-induced hypermetabolism, CRF itself may not be the principle ligand, as suggested by the significant elevation of hypothalamic urocortin 15 days after burn injury.

Topics: Animals; Anorexia; Burns; Corticotropin-Releasing Hormone; Disease Models, Animal; Energy Metabolism; Hypothalamus; Immunotoxins; Male; N-Glycosyl Hydrolases; Neuropeptide Y; Plant Proteins; Rats; Rats, Sprague-Dawley; Ribosome Inactivating Proteins, Type 1; Saporins

To investigate the influence of the changes in the levels of calcitonin gene-related peptide (CGRP) and neuropeptide Y (NPY) on cardiac function of severe burn patients during shock stage.. Sixty severe burn patients with total burn surface area larger than 30% were enrolled as experiment group (E group) , and they received fluid resuscitation and debridement during shock stage. Sixty healthy volunteers were enrolled as control group (C group). The changes in the plasma level of CGRP, NPY and cTnT in E and C groups were observed at 1, 3, 6, 12, 24, 48 post-burn hours (PBH). The correlation among the CGRP, NPY and cTnT in the C group were analyzed.. At 3 PBH, the plasma level of CGRP in E group (28 +/- 6) ng/L was lower than that in C group (55 +/- 7) ng/L , and it reached the lowest level at 12 PBH (15 +/- 4)ng/L . It was still lower than that in C group at 48 PBH (P < 0.05). The levels of NPY and cTnT in E group were significantly increased at 1PBH [(136 +/- 20) ng/L, (0.41 +/- 0.08) microg/L] compared with that in C group[ (86 +/- 13) ng/L, (0.16 +/- 0.06) microg/L], peaking at 12PBH [(189 +/- 31) ng/L, (1.78 +/- 0. 47) microg/L], and remaining higher than those in C group at 48PBH. There exhibited obvious negative correlation between the changes in the level of CGRP and cTnT ( r = -0.76, P < 0.01), while obvious positive correlation was found between the changes in level of NPY and cTnT ( r = 0.79, P < 0.01).. The decrease in CGRP level and the increase in NPY level might play important roles in myocardial injury during shock stage of severe burn patients.

Topics: Adult; Burns; Calcitonin Gene-Related Peptide; Female; Humans; Male; Middle Aged; Myocardium; Neuropeptide Y; Shock, Traumatic; Troponin T

An intact nociceptor system of primary afferent sensory nerves is important for the initiation of the inflammatory process and successful tissue repair. Dysfunction of this system could be a contributing factor for delayed wound healing in humans. We examined the levels of vasodilators [substance P (SP), calcitonin gene-related peptide (CGRP)] and a vasoconstrictor peptide [neuropeptide Y (NPY)] in the peripheral blood samples of patients with burns covering from 20 to 75% of body surface area. Thirteen patient samples were obtained immediately on admission (OA), which was within 12 h of the thermal injury, and 24 h post-admission (PA). Enzyme immunoassay techniques were used for the measurement of the neuropeptides. In addition, an inflammatory marker, tumour necrosis factor-alpha (TNF-alpha), and a myofibrillar protein, creatine kinase (CK), were examined and compared with levels in 13 control subjects. CGRP was high OA and the levels were maintained PA (P < 0.05). SP was also significantly high at both sampling times (P < 0.05). Although TNF-alpha and NPY were somewhat higher in the patients' samples than in the control samples, these levels were not statistically significant (P = NS). CK was higher OA (P < 0.01) than PA (P < 0.04), compared to controls. Plasma levels of SP and CGRP increased significantly in patients with thermal injuries. These peptides may yet be another group of neuromodulators playing a significant role in immune, pain, inflammatory and wound healing in burns.

Topics: Adult; Aged; Aged, 80 and over; Burns; Calcitonin Gene-Related Peptide; Female; Humans; Male; Middle Aged; Neuropeptide Y; Substance P

It has recently been hypothesized that both the sensory and sympathetic nervous system contribute to the inflammatory reaction. A scalding model was developed in anaesthetized rats to investigate the contribution of neuropeptides in heat-induced edema localized to the hindpaw. After immersing the paw in water at 60 degrees C for 10, 20, 30 and 60 s, edemic reactions were registered as change of paw volume in a plethysmograph and hindpaw perfusates collected to measure the content of neuropeptides by radioimmunoassay. A scalding period of 30 s induced the most prominent edemic reaction. There was a marked increase of the sensory neuropeptide neurokinin A and the sympathetic related transmitter neuropeptide Y in hindpaw perfusates after scalding. The effect of peripheral nerve ligation on edemic reaction and on the release of neuropeptides was investigated in rats scalded for 30 s at 60 degrees C. There was a significant decrease of edema formation in the scalded nerve ligated paw as compared with the scalded paw on the non-ligated side. Neurokinin A was not detected in nerve ligated rats before or after scalding, whereas mononeuropathic rats showed increased concentrations of neuropeptide Y. The present results indicate that the sensory as well as the sympathetic nervous system, possibly through the release of neuropeptides, may contribute to scald-induced edema.

Topics: Animals; Burns; Disease Models, Animal; Edema; Ganglia, Sensory; Hindlimb; Hot Temperature; Ligation; Male; Neurokinin A; Neuropeptide Y; Neuropeptides; Plethysmography; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System