Leptin-induced satiation mediated by abdominal vagal afferents

Peters, James H.; McKay, B. M.; Simasko, Steven M.; Ritter, Robert C.

doi:10.1152/ajpregu.00716.2004

Cited by 87 publications

(78 citation statements)

References 22 publications

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“…These effects were particularly pronounced over the second hour of the dark phase; i.e., after the rats had eaten their first meals. Important for consideration of the effects of peripherally elevated levels of leptin is that these can be signaled directly in the CNS (i.e., through increased transport of leptin across the blood-brain barrier) and additionally via vagal afferent fibers [32][33][34]. Since CAP rats lack a substantial part of their vagal afferent innervation, yet have an increased sensitivity to leptin with respect to food intake modulation, it is likely that leptin's enhanced anorexigenic actions are mediated via interaction with CNS pathways.…”

Section: Discussionmentioning

confidence: 99%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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Several mechanisms involved in ingestive behavior and neuroendocrine activity rely on vagal afferent neuronal signaling. Seemingly contradictory to this idea are observations that vagal afferent neuronal ablation by neonatal capsaicin (CAP) treatment has relatively small effects on glucose homeostasis and long-term regulation of energy balance. It may be proposed that humoral endocrine factors and/or their sensitivities compensate for the loss of vagal afferent information, particularly when subjects face disturbances in ambient fuel levels. Therefore, male adult rats neonatally treated with CAP or with the vehicle (VEH) underwent intravenous glucose tolerance tests (IVGTTs) during which blood fuel levels, and circulating adipose, pancreatic, and adrenal hormones were assessed. CAP rats displayed similar hyperglycemia as VEH rats, but with markedly reduced plasma insulin and corticosterone responses. These results indicate that CAP rats have increased insulin sensitivity during hyperglycemic episodes, and lower plasma levels of corticosterone in CAP rats relative to VEH rats could underlie this effect. After the IVGTT, CAP rats had increased plasma adiponectin and reduced plasma resistin levels, and these alterations in adipose hormones might be relevant for post-ingestive metabolic processes. In a second experiment, anorexigenic efficacies of cholecystokinin and leptin were assessed. While VEH rats, but not CAP rats, responded with reduced food intake to i.p. injected cholecystokinin, only CAP rats responded to i.v. infused leptin with a reduction in food intake. It is concluded that reduced HPA axis activity and/or increased leptin signaling could underlie compensations in fuel handling and energy balance following CAP treatment.

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Section: Discussionmentioning

confidence: 99%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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“…Vagal stimulation results in gastric mucosal leptin secretion, but no increase in plasma leptin concentration (Sobhani et al, 2002), suggesting that gastric leptin is secreted during the cephalic phase of gastric secretions, and acts in a paracrine fashion. Leptin receptor mRNA is present in vagal afferent neurons that innervate the gastric fundus, suggesting that leptin may have direct stimulatory effects on vagal afferents (Peters et al, 2005). Infusions of leptin into the celiac artery, but not the jugular vein, significantly reduced intake of a sucrose solution by rats (Peters et al, 2005).…”

Section: A Role For Cephalic Phase Responses In Appetite and Satiety?mentioning

confidence: 99%

“…Leptin receptor mRNA is present in vagal afferent neurons that innervate the gastric fundus, suggesting that leptin may have direct stimulatory effects on vagal afferents (Peters et al, 2005). Infusions of leptin into the celiac artery, but not the jugular vein, significantly reduced intake of a sucrose solution by rats (Peters et al, 2005).…”

Section: A Role For Cephalic Phase Responses In Appetite and Satiety?mentioning

confidence: 99%

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

2008

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Anticipatory physiological regulation is an adaptive strategy that enables animals to respond faster to physiologic and metabolic challenges. The cephalic phase responses are anticipatory responses that prepare animals to digest, absorb and metabolize nutrients. They enable the sensory aspects of the food to interact with the metabolic state of the animal to influence feeding behavior. The anticipatory digestive secretions and metabolic adjustments in response to food cues are key adaptations that affect digestive and metabolic efficiency and aid in controlling the resulting elevation of metabolic fuels in the blood. Cephalic phase responses enable digestion, metabolism and appetite to be regulated in a coordinated fashion. These responses have significant effects on meal size. For example, if the cephalic phase insulin response is blocked the result is poor glucose control and smaller meals. Cephalic phase responses also are linked to motivation to feed, and may play a more direct role in regulating meal size beyond the permissive one of ameliorating negative consequences of feeding. For example, the orexigenic peptide ghrelin appears to display a cephalic phase response, rising before expected meal times. This anticipatory ghrelin response increases appetite; interestingly it also enhances fat absorption, linking appetite with digestion and metabolism.

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“…Normal meal termination involves activation of the vagus nerve. 4 Inflation of the stomach with a balloon, which increases vagal activity, causes an immediate decrease of hunger in fasting, healthy humans. 5 In animal studies, intra-abdominal vagal stimulation by electrical pacing over 1 month reduces food intake and body mass at the expense of body fat without a change in metabolic rate.…”

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confidence: 99%

Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation

et al. 2007

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Fourteen patients were treated over 2 years with cervical vagus nerve stimulation (VNS) for adjunctive therapy of severe, treatment-resistant depression. Here, we report the serendipitous observation that this treatment was associated with highly significant, gradual weight loss despite the patients' report of not dieting or exercising. The weight loss was proportional to the initial BMI, that is, the more severe the obesity, the greater the weight loss. Weight loss did not correlate with changes in mood symptoms. The vagus nerve carries visceral information to and from the brain; modulation of its activity may alter eating behavior. Chronic cervical VNS may merit controlled study for the treatment of severe obesity. Table 1. Psychiatric diagnoses were determined using a structured clinical interview (SCID). 1 One patient had bipolar depression; all others had recurrent, unipolar, major depression. These severely depressed patients (mean Hamilton 2 depression score 29, range 24-37) had failed standard treatments: average duration of illness, 24 years; average duration of current episode, 2.5 years; average number of failed, but adequate, medications trials, 4. The medications on intake and psychiatric co-morbidities are also listed in Table 1.The VNS device (NCP Model 101, Cyberonics Inc., Houston, TX, USA) was approved in 2005 for the adjunctive therapy of severe depression refractory to conventional therapies. It consists of a pacemaker-like device implanted subcutaneously just below the left clavicle. An electrode from the device courses subcutaneously and attaches to the trunk of the left vagus nerve about half way between the clavicle and the mastoid. The right vagus is not used typically because of greater vagal side effects upon the heart. The device is programmed to deliver preset stimuli using an external, magnetic, programming wand. The protocol and device parameters have been previously described. 3 The output current frequently varied either up or down depending upon the patients' side effects and depression symptoms, since the precise relationship between dose and efficacy remains unsettled. At 1 year, the current outputs varied between 0.25 and 1.5 mA. The stimulation frequency was 30 Hz with a pulse width of 500 ms, except for two patients who had 250 ms. The device cycled continuously with stimulation on for 30 s and off for 5 min.After continuous VNS therapy for 6-12 months, several obese patients showed marked weight loss. The mean weight on intake was 91 kg (s.d. 727, range 46-137 kg) with a body mass index (BMI) of 43 kg/m 2 (s.d. 75, range 18-49 kg/m 2 ). The average weight loss at 1 year was 7 kg (s.d. 73, range -6 to þ 24) with mean drop in BMI at 1 year of 2 kg/m 2 (s.d. 73, range -2 to þ 8). The heaviest patient weighed initially 137 kg (BMI 49 kg/m 2 ) and after 1 year of VNS, 114 kg (BMI 40 kg/m 2 ), a decrease of 23 kg. Figure 1 shows that the decrease in BMI at 1 year of individual patients was

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Leptin-induced satiation mediated by abdominal vagal afferents

Cited by 87 publications

References 22 publications

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Anticipatory physiological regulation in feeding biology: Cephalic phase responses

Weight loss during chronic, cervical vagus nerve stimulation in depressed patients with obesity: an observation

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