calcitonin and Vomiting

The analgesic properties of salmon calcitonin for the treatment of atypical facial pain (AFP) were investigated. An initial open-label trial of salmon calcitonin in subjects with refractory AFP was followed with a randomized, double-blind, placebo-controlled crossover trial of salmon calcitonin in the management of AFP. Salmon calcitonin (100 IU in 1 mL saline) was administered in an open-label fashion to 13 subjects with refractory AFP five times per week for 6 weeks. In the subsequent randomized investigation, salmon calcitonin (100 IU in 1 mL saline) or placebo (1 mL saline) was delivered three times per week for 3 weeks, with a 1-week washout prior to crossover. The percentage of subjects dropping out (57%) exceeded that reported in other pain studies using calcitonin. Therefore, it was imperative to halt the study for ethical reasons. There was no difference in outcome measures (P > .05) in subjects administered either active drug or placebo, and a high incidence of side effects led to dropout in subjects taking salmon calcitonin. Although salmon calcitonin may have analgesic properties, it is not efficacious for AFP, largely because of the side effects.

Topics: Adult; Aged; Analgesics; Calcitonin; Chronic Disease; Double-Blind Method; Facial Pain; Female; Humans; Male; Middle Aged; Nausea; Pain Measurement; Vomiting

The behavioral mechanisms and the neuronal pathways mediated by amylin and its long-acting analog sCT (salmon calcitonin) are not fully understood and it is unclear to what extent sCT and amylin engage overlapping or distinct neuronal subpopulations to reduce food intake. We here hypothesize that amylin and sCT recruit different neuronal population to mediate their anorectic effects.. Viral approaches were used to inhibit calcitonin gene-related peptide (CGRP) lateral parabrachial nucleus (LPBN) neurons and assess their role in amylin's and sCT's ability to decrease food intake in mice. In addition, to test the involvement of LPBN CGRP neuropeptidergic signaling in the mediation of amylin and sCT's effects, a LPBN site-specific knockdown was performed in rats. To deeper investigate whether the greater anorectic effect of sCT compared to amylin is due do the recruitment of additional neuronal pathways related to malaise multiple and distinct animal models tested whether amylin and sCT induce conditioned avoidance, nausea, emesis, and conditioned affective taste aversion.. Our results indicate that permanent or transient inhibition of CGRP neurons in LPBN blunts sCT-, but not amylin-induced anorexia and neuronal activation. Importantly, sCT but not amylin induces behaviors indicative of malaise including conditioned affective aversion, nausea, emesis, and conditioned avoidance; the latter mediated by CGRP. Together, the present study highlights that although amylin and sCT comparably decrease food intake, sCT is distinctive from amylin in the activation of anorectic neuronal pathways associated with malaise.

Topics: Animals; Anorexia; Appetite Depressants; Calcitonin; Calcitonin Gene-Related Peptide; Islet Amyloid Polypeptide; Mice; Nausea; Neurons; Rats; Vomiting

Effects of synthetic eel (E-), salmon (S-), and human (H-) calcitonin (CT) on gastrointestinal motility were studied in conscious beagle dogs, which had been implanted with strain gauge force transducers. Intramuscular administration of E-, S-, or H-CT interrupted gastric migrating motor complexes, digestive pattern, and gastric emptying. The order of potency was E-CT = S-CT > H-CT. Motor inhibition induced by CT occurred independently of plasma immunoreactive motilin levels or hypocalcemia. In addition, E-CT and S-CT induced vomiting without a retrograde giant contraction (RGC) during the postprandial state. Apomorphine or CuSO4 initiated RGC prior to vomiting. RGC induced by apomorphine was inhibited by pretreatment with E-CT as well as hexamethonium, atropine, or surgical vagotomy. E-CT showed no inhibitory effect on nicotine stimulated contraction of isolated guinea-pig ileum. These results suggest that peripherally administered CT inhibits canine gastrointestinal motility at the central nervous system level by lowering vagal activity.

Topics: Analgesics; Animals; Calcitonin; Calcium; Dogs; Female; Gastric Emptying; Gastrointestinal Motility; Humans; Male; Motilin; Muscle Contraction; Parasympathetic Nervous System; Stomach; Synaptic Transmission; Transducers, Pressure; Vagotomy; Vomiting