calcitonin and Nausea

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 reports of the effect of calcitonin on pituitary function are confusing and often refer to uncontrolled studies. We have now carried out a double-blind placebo-controlled trial of intravenous and subcutaneous salmon calcitonin on anterior pituitary function in 17 healthy volunteers. Visual analogue scores for the nausea and vomiting seen after salmon calcitonin correlated with the rise in ACTH and, secondarily, cortisol. Calcitonin had no effect on growth hormone, prolactin, thyrotrophin, luteinizing hormone or follicle stimulating hormone. It is concluded that the stimulation of ACTH secretion following a single dose of salmon calcitonin is probably the result of the stress of nausea rather than a direct effect on the pituitary.

Topics: Adrenocorticotropic Hormone; Adult; Calcitonin; Double-Blind Method; Humans; Hydrocortisone; Male; Nausea; Pituitary Gland, Anterior; Pituitary Hormones, Anterior

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

The ability of amylin, a pancreatic β-cell-derived neuropeptide, to promote negative energy balance has been ascribed to neural activation at the area postrema. However, despite amylin binding throughout the brain, the possible role of amylin signaling at other nuclei in the control of food intake has been largely neglected. We show that mRNA for all components of the amylin receptor complex is expressed in the ventral tegmental area (VTA), a mesolimbic structure mediating food intake and reward. Direct activation of VTA amylin receptors reduces the intake of chow and palatable sucrose solution in rats. This effect is mediated by reductions in meal size and is not due to nausea/malaise or prolonged suppression of locomotor activity. VTA amylin receptor activation also reduces sucrose self-administration on a progressive ratio schedule. Finally, antagonist studies provide novel evidence that VTA amylin receptor blockade increases food intake and attenuates the intake-suppressive effects of a peripherally administered amylin analog, suggesting that amylin receptor signaling in the VTA is physiologically relevant for food intake control and potentially clinically relevant for the treatment of obesity.

Topics: Amylin Receptor Agonists; Animals; Calcitonin; Dose-Response Relationship, Drug; Drug Interactions; Eating; Male; Microinjections; Motor Activity; Nausea; Peptide Fragments; Rats; Receptors, Islet Amyloid Polypeptide; Reinforcement Schedule; Reward; RNA, Messenger; Self Administration; Sucrose; Ventral Tegmental Area

One hundred and four patients with Paget's disease of bone received treatment with a calcium/thiazide regimen, salmon calcitonin, or ethane-1-hydroxy-1, 1-diphosphonate (EHDP). Most patients commenced therapy with the calcium/thiazide regimen; in 67% of these, the disease was satisfactorily controlled for some years. When the response was unsatisfactory, calcitonin was given. This was frequently effective, but produced troublesome nausea in 28% of patients. When these side effects were unacceptable, or the response was not adequate, EHDP was given, unless the patient appeared to be at risk of fracture. It is suggested that the calcium/thiazide regimen has a place in the management of Paget's disease; that calcitonin is more frequently effective, but has a high incidence of unpleasant, though not serious, side effects; and that EHDP is a useful agent in the treatment of Paget's disease, but must be administered with care, and does carry a small risk of pathological fracture.

Topics: Aged; Alkaline Phosphatase; Calcitonin; Calcium; Chlorthalidone; Dose-Response Relationship, Drug; Etidronic Acid; Female; Fractures, Bone; Humans; Kinetics; Male; Middle Aged; Nausea; Osteitis Deformans; Risk