scholarly journals Non-invasive stimulation of vagal afferents reduces gastric frequency

2019 ◽  
Author(s):  
Vanessa Teckentrup ◽  
Sandra Neubert ◽  
João C. P. Santiago ◽  
Manfred Hallschmid ◽  
Martin Walter ◽  
...  

AbstractMetabolic feedback between the gut and the brain relayed via the vagus nerve contributes to energy homeostasis. We investigated in healthy adults whether non-invasive stimulation of vagal afferents impacts energy homeostasis via efferent effects on metabolism or digestion. In a randomized crossover design, we applied transcutaneous auricular vagus nerve stimulation (taVNS) while recording efferent metabolic effects using simultaneous electrogastrography (EGG) and indirect calorimetry. We found that taVNS reduced gastric myoelectric frequency (p =.008), but did not alter resting energy expenditure. We conclude that stimulating vagal afferents induces gastric slowing via vagal efferents without acutely affecting net energy expenditure at rest. Collectively, this highlights the potential of taVNS to modulate digestion by activating the dorsal vagal complex. Thus, taVNS-induced changes in gastric frequency are an important peripheral marker of brain stimulation effects.

Cephalalgia ◽  
2017 ◽  
Vol 37 (13) ◽  
pp. 1285-1293 ◽  
Author(s):  
Romain Nonis ◽  
Kevin D’Ostilio ◽  
Jean Schoenen ◽  
Delphine Magis

Background Benefits of cervical non-invasive vagus nerve stimulation (nVNS) devices have been shown in episodic cluster headache and preliminarily suggested in migraine, but direct evidence of vagus nerve activation using such devices is lacking. Vagal somatosensory evoked potentials (vSEPs) associated with vagal afferent activation have been reported for invasive vagus nerve stimulation (iVNS) and non-invasive auricular vagal stimulation. Here, we aimed to show and characterise vSEPs for cervical nVNS. Methods vSEPs were recorded for 12 healthy volunteers who received nVNS over the cervical vagus nerve, bipolar electrode/DS7A stimulation over the inner tragus, and nVNS over the sternocleidomastoid (SCM) muscle. We measured peak-to-peak amplitudes (P1-N1), wave latencies, and N1 area under the curve. Results P1-N1 vSEPs were observed for cervical nVNS (11/12) and auricular stimulation (9/12), with latencies similar to those described previously, whereas SCM stimulation revealed only a muscle artefact with a much longer latency. A dose-response analysis showed that cervical nVNS elicited a clear vSEP response in more than 80% of the participants using an intensity of 15 V. Conclusion Cervical nVNS can activate vagal afferent fibres, as evidenced by the recording of far-field vSEPs similar to those seen with iVNS and non-invasive auricular stimulation.


2020 ◽  
Vol 245 (1) ◽  
pp. 165-178 ◽  
Author(s):  
Terese M Zidon ◽  
Jaume Padilla ◽  
Kevin L Fritsche ◽  
Rebecca J Welly ◽  
Leighton T McCabe ◽  
...  

Loss of ovarian hormones leads to increased adiposity and insulin resistance (IR), increasing the risk for cardiovascular and metabolic diseases. The purpose of this study was to investigate whether the molecular mechanism behind the adverse systemic and adipose tissue-specific metabolic effects of ovariectomy requires loss of signaling through estrogen receptor alpha (ERα) or estrogen receptor β (ERβ). We examined ovariectomized (OVX) and ovary-intactwild-type (WT), ERα-null (αKO), and ERβ-null (βKO) female mice (age ~49 weeks; n = 7–12/group). All mice were fed a phytoestrogen-free diet (<15 mg/kg) and either remained ovary-intact (INT) or were OVX and followed for 12 weeks. Body composition, energy expenditure, glucose tolerance, and adipose tissue gene and protein expression were analyzed. INT αKO were ~25% fatter with reduced energy expenditure compared to age-matched INT WT controls and βKO mice (all P < 0.001). Following OVX, αKO mice did not increase adiposity or experience a further increase in IR, unlike WT and βKO, suggesting that loss of signaling through ERα mediates OVX-induced metabolic dysfunction. In fact, OVX in αKO mice (i.e., signaling through ERβ in the absence of ERα) resulted in reduced adiposity, adipocyte size, and IR (P < 0.05 for all). βKO mice responded adversely to OVX in terms of increased adiposity and development of IR. Together, these findings challenge the paradigm that ERα mediates metabolic protection over ERβ in all settings. These findings lead us to suggest that, following ovarian hormone loss, ERβ may mediate protective metabolic benefits.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Nicté Figueroa-Vega ◽  
Elva L Perez-Luque ◽  
Juan M Malacara

Abstract Background: The uncoupling proteins (UCPs) belong to the mitochondrial inner membrane anion carrier superfamily and play an important role in energy homeostasis. UCP-1 is expressed mostly in brown adipose tissue (BAT) and act in the thermogenesis and regulation of energy expenditure. UCP-2 has a role in the metabolism of fatty acids direct and indirectly path insulin secretion. UCP-3 is specific of skeletal muscle and BAT and may affects the adaptive and translocation of fatty acids. Genetic polymorphisms in these proteins have been associated with obesity, as rs1800592 (-3826 A/G) in UCP-1 gene. The rs659366 (-866GA) UCP-2 has being associated with high expression of its RNAm, decrease of obesity risk, and increase of energy expenditure. The rs1800849 (-55CT) UCP-3 has been associated with low risk of type 2 Diabetes Mellitus, but its association with body mass index is controversial. Objective: To analyze the association of the polymorphisms rs1800592 UCP-1, rs659366 UCP-2, and rs1800849 UCP-3 with BMI and resting energy expenditure (REE). Material and Methods: We included 120 subjects with BMI&gt;30kg/m2 and 100 subjects with BMI between18.5 -24.9 kg/m2, aged 20 to 50 years. Anthropometric data were recorded and the REE was measure for indirect calorimetric. Fasting glucose and lipid profile were assessed. Leptin, insulin and acylated-ghrelin were quantified by ELISA. Genomic DNA was extracted using comercial kit. Genotyping for three polymorphisms was performed by allelic discrimination using Taqman probes. Results: All the three polymorphisms of UCPs showed distribution in accordance with Hardy-Weinberg equilibrium. The weight, BMI, glucose, triglycerides, leptin, insulin, HOMA-IR, and REE levels were signitifcantly higher in obese subjects. There was a strong correlation between REE with BMI (r=0.42, p&lt;0.00001) and with insulin levels (r=0.229, p=0.001) in all group. No differences in genotypic and allelic frequencies of rs1800592 UCP-1, rs659366 UCP-2 and rs180084 UCP-3 polymorphisms between obese and lean subjects. No differences among the genotypes rs1800592 UCP-1 and rs1800849 UCP-3 with metabolic variables. In rs659366 UCP-2 polymorhism, the REE and glucose concentrations were lower in carriers of rs659366AA genotype (F=3.11, p=0.046; F=2.97, p=0.053, respectively) in whole group. In obese subjects with rs659366AA UCP-2 genotype, the REE was significantly low (F=4.15, P=0.017). Conclusion. In this work the obese subjects with rs659366AA genotype had low REE. We found low glucose concentrations in the carries of rs659366 AA genotype.


1991 ◽  
Vol 260 (3) ◽  
pp. E345-E352 ◽  
Author(s):  
N. K. Fukagawa ◽  
L. G. Bandini ◽  
P. H. Lim ◽  
F. Roingeard ◽  
M. A. Lee ◽  
...  

Resting energy expenditure (EE) has recently been shown to be reduced in elderly human subjects even after adjustment for body size and composition. The present study extended this examination of EE in relation to age by comparing the thermic effect of a protein meal in young men (YM 20-26 yr, n = 9), old men (OM 70-89 yr, n = 9), and old women (OW 67-75 yr, n = 6). EE was measured before and from 1 to 6 h after presentation of 60 g protein and of a control noncaloric meal on separate occasions. Despite substantial differences in body size and composition, the protein-induced increment in EE was similar in all groups [maximum increase: YM 0.21 +/- 0.05, OM 0.17 +/- 0.12, and OW 0.17 +/- 0.04 (SE) kcal/min]. Although fasting plasma norepinephrine (NE) levels differed among all three groups (YM less than OM less than OW), NE concentrations were not affected by protein ingestion. Because protein administration acutely promotes synthesis of dopamine (DA) and serotonin (5-HT), which are both capable of stimulating EE, blockade of extraneuronal synthesis of DA and 5-HT with carbidopa, a competitive inhibitor of aromatic-L-amino acid decarboxylase, failed to suppress (and actually increased) postprandial EE. These data demonstrate that not all mechanisms responsible for EE decline with age and that protein-induced changes in EE are more a function of the oral load itself than of the size, age, or antecedent diet of the individual ingesting the protein.


2019 ◽  
Vol 8 (6) ◽  
pp. 878 ◽  
Author(s):  
Juan Añón-Hidalgo ◽  
Victoria Catalán ◽  
Amaia Rodríguez ◽  
Beatriz Ramírez ◽  
Adrián Idoate-Bayón ◽  
...  

Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor (TGF)-β superfamily which declines with age and has been proposed as an anti-aging factor with regenerative effects in skeletal muscle in mice. However, recent data in humans and mice are conflicting, casting doubts about its true functional actions. The aim of the present study was to analyze the potential involvement of GFD11 in energy homeostasis in particular in relation with thyroid hormones. Serum concentrations of GDF11 were measured by enzyme-linked immunosorbent assay (ELISA) in 287 subjects. A highly significant positive correlation was found between GDF11 and thyroid-stimulating hormone (TSH) concentrations (r = 0.40, p < 0.001). Neither resting energy expenditure (REE) nor REE per unit of fat-free mass (REE/FFM) were significantly correlated (p > 0.05 for both) with GDF11 levels. In a multiple linear regression analysis, the model that best predicted logGDF11 included logTSH, leptin, body mass index (BMI), age, and C-reactive protein (logCRP). This model explained 37% of the total variability of logGDF11 concentrations (p < 0.001), with only logTSH being a significant predictor of logGDF11. After segregating subjects by TSH levels, those within the low TSH group exhibited significantly decreased (p < 0.05) GDF11 concentrations as compared to the normal TSH group or the high TSH group. A significant correlation of GDF11 levels with logCRP (r = 0.19, p = 0.025) was found. GDF11 levels were not related to the presence of hypertension or cardiopathy. In conclusion, our results show that circulating concentrations of GDF11 are closely associated with TSH concentrations and reduced in subjects with low TSH levels. However, GDF11 is not related to the regulation of energy expenditure. Our data also suggest that GDF11 may be involved in the regulation of inflammation, without relation to cardiac function. Further research is needed to elucidate the role of GDF11 in metabolism and its potential involvement in thyroid pathophysiology.


1999 ◽  
Vol 86 (2) ◽  
pp. 517-522 ◽  
Author(s):  
J. de Metz ◽  
F. Sprangers ◽  
E. Endert ◽  
M. T. Ackermans ◽  
I. J. M. ten Berge ◽  
...  

To evaluate whether interferon-γ (IFN-γ) is involved in the interaction between the immune and endocrine systems in vivo, we studied six healthy subjects twice in a placebo-controlled trial: once after administration of recombinant human IFN-γ and, on another occasion, after administration of saline. The rate of appearance of glucose was determined by infusion of [6,6-2H2]glucose and resting energy expenditure by indirect calorimetry. Human leukocyte antigen-DR gene expression on monocytes and serum neopterin increased after administration of IFN-γ ( P < 0.05 vs. control). IFN-γ increased serum interleukin-6 levels significantly. Levels of tumor necrosis factor-α remained below detection limits. IFN-γ increased plasma concentrations of ACTH and cortisol ( P < 0.05 vs. control), IFN-γ did not alter concentrations of growth hormone, (nor)epinephrine, insulin, C peptide, glucagon, or insulin-like growth factor I. IFN-γ did not alter plasma concentrations of glucose and free fatty acids nor the rate of appearance of glucose. IFN-γ increased resting energy expenditure significantly. We conclude that IFN-γ is a minor stimulator of the endocrine and metabolic pathways. Therefore, IFN-γ by itself is probably not a major mediator in the interaction between the immune and the endocrine and metabolic systems.


2020 ◽  
Vol 13 (2) ◽  
pp. 470-473 ◽  
Author(s):  
Vanessa Teckentrup ◽  
Sandra Neubert ◽  
João C.P. Santiago ◽  
Manfred Hallschmid ◽  
Martin Walter ◽  
...  

2008 ◽  
Vol 99 (5) ◽  
pp. 1068-1075 ◽  
Author(s):  
A. Khossousi ◽  
C. W. Binns ◽  
S. S. Dhaliwal ◽  
S. Pal

Overweight and obesity is one of the risk factors for developing CVD. At present, very little is known about the acute effects of dietary fibre on lipids, glucose and insulin, resting energy expenditure and diet-induced thermogenesis in overweight and obese individuals. This study examined the postprandial metabolic effects of dietary fibre in overweight and obese men. Ten overweight and obese men consumed a mixed meal accompanied by either a high-fibre or low-fibre supplement on two separate visits, in a random order, 1 week apart. Two isoenergetic breakfast meals with similar composition were consumed by ten overweight/obese men. The meals contained either a low (3 g) or high (15 g) amount of fibre, low-fibre meal (LFM) and high-fibre meal (HFM) respectively. Analysis was carried out using paired t test and ANOVA. Serum TAG incremental area under the curve during 6 h of the postprandial period was significantly lower after the consumption of HFM compared with LFM. At the first hour of the postprandial period, plasma apo B48 concentration after consumption of HFM was significantly lower compared with LFM. The resting energy expenditure and diet-induced thermogenesis after both meals was similar during 6 h of the postprandial period. Collectively, these findings suggest that a single acute dose of dietary fibre in the form of psyllium supplement can decrease arterial exposure to TAG and modify chylomicron responses in the postprandial period.


2013 ◽  
Vol 289 (3) ◽  
pp. 1779-1787 ◽  
Author(s):  
Qian Zhang ◽  
Bin Liu ◽  
Ying Cheng ◽  
Qingshu Meng ◽  
Tingting Xia ◽  
...  

Leptin signaling in the hypothalamus is crucial in energy homeostasis. We have previously shown that dietary deprivation of the essential amino acid leucine in mice stimulates fat loss by increasing energy expenditure. The involvement of leptin signaling in this regulation, however, has not been reported. Here, we show that leucine deprivation promotes leptin signaling in mice maintained on an otherwise normal diet and restores leptin responses in mice maintained on a high fat diet, a regimen known to induce leptin resistance. In addition, we found that leucine deprivation stimulated energy expenditure, and fat loss was largely blocked in db/db mice homozygous for a mutation in leptin receptor and a knock-in mouse line Y3F with abrogation of leptin receptor Tyr1138-mediated signal transducer and activator transcript 3 signaling. Overall, our studies describe a novel link between hypothalamic leptin signaling and stimulation of energy expenditure under leucine deprivation.


1980 ◽  
Vol 58 (7) ◽  
pp. 823-829 ◽  
Author(s):  
Steve Iscoe ◽  
Stephen Vanner

The effects on respiratory periodicity of electrical stimulation of the cut central end of a vagus nerve were studied in anaesthetized, vagotomized, paralyzed, and ventilated rabbits. Electrical activity of a phrenic nerve was used to determine inspiratory and expiratory durations (Ti and Te). The central cut end of one vagus nerve was electrically stimulated during the entire inspiratory phase of every 10th respiratory cycle and Ti and Te of that respiratory cycle and the following 8 were measured. When only the fastest conducting afferents (pulmonary stretch receptor afferents) were stimulated, reductions in Ti and Te were restricted to the stimulated cycle. When stimulus intensity was increased, activating higher threshold, more slowly conducting afferents (including those of irritant receptors), Te but not necessarily Ti decreased, increasing the frequency of phrenic bursts (respiratory frequency). The recovery of Te following stimulation was exponential, with a time constant of 3–7 s which varied inversely with control respiratory frequency. The effects on Ti and Te on higher intensity stimulation suggest either that coupling between inspiratory and expiratory neurones in the brainstem respiratory oscillator can be "looser" than currently hypothesized or a separate population of expiratory neurones, with a short-term memory (three time constants or [Formula: see text]), mediates the observed effects.


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