Anorectic effect of amylin is not transmitted by capsaicin-sensitive nerve fibers

Abstract

Abdominal vagal and splanchnic afferents play an important role in the control of food intake in that they transmit various satiety signals to the central nervous system. Inasmuch as previous studies have shown that the anorectic effect of intraperitoneally injected amylin was not abolished by subdiaphragmatic vagotomy, the aim of the present study was to elucidate the role of splanchnic afferents in mediating amylin’s anorectic effect after intraperitoneal injection. Rats were pretreated intraperitoneally with the neurotoxin capsaicin, which destroys primary sensory (vagal and splanchnic) afferents. Sham-treated rats served as control. Capsaicin-pretreatment had no influence on the anorectic effects of amylin (5 μg/kg) and the related peptide, calcitonin gene-related peptide (CGRP; 5 μg/kg), in 24-h food-deprived rats. Abolition of cholecystokinin’s (3 μg/kg) anorectic effect agrees with previous studies and confirmed the effectiveness of the capsaicin pretreatment. In conclusion, the anorectic effects of intraperitoneally injected amylin and CGRP are not mediated by capsaicin-sensitive primary sensory neurons. Both anorectic peptides are, therefore, most likely to act within the central nervous system. Previous studies suggest that the relevant receptors might be located in neurons of the area postrema-nucleus of the solitary tract region.

Treating hypertension while protecting the vulnerable islet in the cardiometabolic syndrome

“…It inhibits hepatic production and release of glucose after a meal [54] and inhibits glucagon and somatostatin secretion, slowing the secretion of insulin [4]. Amylin contributes to the perception of satiety and may have a site of action within the central nervous system [58]. It has binding sites within the renal cortex [54,59], where it promotes renin secretion [59,60].…”

Gut hormones such as amylin and GLP-1 in the control of eating and energy expenditure

“…25,30,[37][38][39][40] This evidence is, for example, based on experiments, showing that amylin's effect is abolished in rats with AP lesions but not by disrupting afferent nerve signaling from the periphery to the brain. [41][42][43][44] Further, APadministered amylin antagonists blocked the anorectic action of peripheral amylin. 25 Recent experiments indicate that the AP may not be the only primary receptive site for the action of peripheral amylin or its analogs, and that the ventral tegmental area (VTA) may also have a role in this respect.…”

Phenylpyrazolone derivatives inhibit gastric emptying in rats by a capsaicin-sensitive afferent pathway

“…After pretreatment the animals were kept in the laboratory, fed by their dams (4 animals per dam) for 4 weeks, and then for an additional 4/5 weeks after weaning, receiving ration and water ad libitum in individual cages. To determine the neurotoxic effect of Cps, sensitivity to pain was assessed on the day preceding the determination of GE by the eye-wiping test in both groups using a 1% NaOH solution as an eye irritant (8).…”