The vagus nerve, food intake and obesity

Berthoud, Hans‐Rudolf

doi:10.1016/j.regpep.2007.08.024

Cited by 263 publications

(215 citation statements)

References 175 publications

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“…The AUC of the plasma glucose levels in the V group tended to be lower than that in the C group, but the (CCK) is secreted from the I cells in the duodenum and jejunum [17]. CCK stimulates pancreatic enzyme secretion and gall bladder contraction and delays gastric emptying and food intake via the stimulation of the vagus nerve [18,19]. Ghrelin, a 28-amino acid acylated peptide, is an orexigenic peptide secreted by the stomach [20].…”

Section: Resultsmentioning

confidence: 99%

Effects of miglitol, vildagliptin, or their combination on serum insulin and peptide YY levels and plasma glucose, cholecystokinin, ghrelin, and obestatin levels

et al. 2014

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α-Glucosidase inhibitors (αGIs) decrease plasma glucose and serum insulin levels in healthy subjects [1,2] and reduce the development of type 2 diabetes in subjects with impaired glucose tolerance (IGT) [3,4]. αGIs reportedly enhance active glucagon-like peptide-1 (GLP-1) responses and reduce total glucosedependent insulinotropic polypeptide (GIP) responses [5][6][7][8]. Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin or vildagliptin, increase active GLP-1 and GIP by inhibiting DPP-4 enzymatic activity and improve hyperglycemia in a glucose-dependent fashion by increasing serum insulin and decreasing serum glucagon levels in diabetic patients [9].Because miglitol and sitagliptin enhance plasmaEffects of miglitol, vildagliptin, or their combination on serum insulin and peptide YY levels and plasma glucose, cholecystokinin, ghrelin, and obestatin levels abstract. We previously reported that combination therapy with an α-glucosidase inhibitor (αGI) and a dipeptidyl peptidase-4 (DPP-4) inhibitor increased active glucagon-like peptide-1 (GLP-1) levels and decreased total glucose-dependent insulinotropic polypeptide (GIP) levels, compared with monotherapy, in non-diabetic men. However, the peptide YY (PYY), cholecystokinin (CCK), ghrelin, and obestatin levels in patients receiving a combination of αGIs and DPP-4 inhibitors have not been previously reported. We evaluated the effect of miglitol, vildagliptin, or their combination on these parameters. Miglitol and/or vildagliptin were administered according to four different intake schedules in eleven non-diabetic men (C: no drug, M: miglitol; V: vildagliptin, M+V: miglitol+vildagliptin). Blood samples were collected at 0, 30, 60, and 120 min after the start of breakfast. The plasma glucose, serum insulin, serum total PYY (PYY 1-36 and PYY 3-36 ), plasma CCK, plasma active ghrelin, and plasma obestatin levels were measured. The area under the curve (AUC) of the serum total PYY level in the M group was significantly greater than that in the C group, and the AUC of the serum total PYY level in the M+V group was significantly lower than that in the M group. The combination therapy did not change the AUC of the plasma CCK, plasma active ghrelin, plasma obestatin, and ghrelin/obestatin levels, compared with the control. The results of our study suggested that combination therapy with miglitol and vildagliptin had no effect on appetite regulation hormones, such as total PYY, CCK, active ghrelin, and obestatin, compared with the levels in the control group.

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Section: Resultsmentioning

confidence: 99%

Effects of miglitol, vildagliptin, or their combination on serum insulin and peptide YY levels and plasma glucose, cholecystokinin, ghrelin, and obestatin levels

et al. 2014

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“…[11][12][13] Food intake induces gastric accommodation and stimulates the ANS. 29,30 An increased blood volume after meal ingestion induces vasopressin release through the supraoptic and paraventricular nuclei of the hypothalamus. 31 The paraventricular nuclei also have neurons releasing corticotrophin-releasing hormone and noradrenaline.…”

Section: Discussionmentioning

confidence: 99%

Increased Postprandial Colonic Motility and Autonomic Nervous System Activity in Patients With Irritable Bowel Syndrome: A Prospective Study

Tanaka

Kanazawa

Palsson

et al. 2018

J Neurogastroenterol Motil

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Background/AimsThe prevalence and severity of irritable bowel syndrome (IBS) declines with age, but the cause of this is unknown. This study tested 2 hypotheses: (1) autonomic nervous system responses to eating and bowel distention, measured by heart rate variability (HRV), differs by age in IBS patients and (2) HRV is correlated with colonic motility and IBS symptoms. MethodsOne hundred and fifty-six Rome III positive IBS patients and 31 healthy controls underwent colonic manometry with bag distention in the descending colon, followed by ingestion of an 810-kcal meal. HRV, evaluated by low frequency (%LF; 0.04-0.15 Hz) component, high frequency (%HF; 0.15-0.40 Hz) component, and the LF/HF ratio, was measured during colonic distention and after the meal. Motility index and subjective symptom scores were simultaneously quantified. ResultsBoth colonic distention and eating decreased %HF and increased the LF/HF ratio, and both indices of autonomic nervous system correlated with age. In IBS patients, %HF negatively correlated with the postprandial motility index after adjusting for age. The %HF and LF/HF ratios also correlated with psychological symptoms but not bowel symptoms in IBS patients. ConclusionDecreased vagal activity is associated with increase in age and greater postprandial colonic motility in patients with IBS, which may contribute to postprandial symptoms. (J Neurogastroenterol Motil 2018;24:87-95)

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“…In animals and humans, appetitive drive and food intake are affected by signals from inside the body and the environment and are under hormonal control together with sympathetic and parasympathetic nervous system inputs (Berthoud, 2008). Environmental signals affecting food intake interact almost exclusively with corticolimbic brain areas (especially with hypothalamic and brainstem structures involved in the control of food intake and energy balance) and are modulated by metabolic signals (Berthoud, 2012).…”

Section: Regulation Of Lipid Metabolism In the Laying Henmentioning

confidence: 99%

Fatty Liver Haemorrhagic Syndrome in Laying Hens: Field and Experimental Investigations

Shini¹

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Field and experimental investigations were conducted to study the fatty liver haemorrhagic syndrome (FLHS) in caged laying hens. The main goal of the research was to gain a greater understanding of the aetiology and pathogenesis of this non-infectious disease. The disease is characterized by excessive accumulation of fat in the liver and abdominal cavity, subsequent liver rupture, haemorrhage and sudden death of hens. It has been shown that the balance between hepatic synthesis and secretion of lipids is the key point that regulates hepatic and extrahepatic fat deposition in hens. Liver fat accumulation can be increased by many factors, especially nutrition, housing conditions, and inflammatory challenges. A description of normal and abnormal lipid metabolism in the hen, and consequences for hen health and disease (including FLHS) is given in the literature review (Chapter 2).The initial study examined mortality of layer flocks kept in three different housing systems (cage, barn and free range) on the Gatton Campus, University of Queensland (Chapter 4). It was shown that there were no significant differences in mortality rates of hens (6.1%, 6.4% and 5.8%, for cages, barns and free range, respectively) between the housing systems but the causes of death were different. The most common cause of death in hens kept in cages was FLHS with 74% of dead hens dying from the condition. In contrast, FLHS only accounted for 0 to 5% of hen mortality in the other systems. Post-mortem of dead hens and body weight monitoring of flocks throughout the laying cycle were recommended as tools to predict FLHS.An epidemiological survey (Chapter 5) of caged flocks in South-Eastern Queensland was undertaken to explore the prevalence of FLHS in commercial layer flocks. From necropsies of dead birds from 7 flocks of different ages, it was found that approximately 40% of hens died due to FLHS. This result indicated that FLHS continues to be the major cause of mortality in commercial caged laying hens kept in either controlled environment sheds or naturally ventilated sheds. As part of the epidemiological study, a questionnaire was circulated among farms and the responses revealed that there is a general lack of knowledge of FLHS in the industry.The study of the pathogenesis of FLHS is very difficult as it occurs sporadically and over an extended period of time in the field. In the studies in Chapter 6, an oestradiol (E 2 ) hen model was used to study the condition. The administration of exogenous E 2 reproduced the disease in 30 wk old laying hens, and was associated with significant changes in E 2 plasma levels and metabolic iv profiles, increased liver weights, and macroscopic (fat depositions, haemorrhages and haematomas) and microscopic alterations. Hens exposed to E 2 and fed ad libitum diet experienced severe FLHS and had a higher incidence of FLHS than hens that had their feed intake restricted by 10%. One interesting observation from this study (not reported from other investigators) was the alteration of total leukocyte n...

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The vagus nerve, food intake and obesity

Cited by 263 publications

References 175 publications

Effects of miglitol, vildagliptin, or their combination on serum insulin and peptide YY levels and plasma glucose, cholecystokinin, ghrelin, and obestatin levels

Effects of miglitol, vildagliptin, or their combination on serum insulin and peptide YY levels and plasma glucose, cholecystokinin, ghrelin, and obestatin levels

Increased Postprandial Colonic Motility and Autonomic Nervous System Activity in Patients With Irritable Bowel Syndrome: A Prospective Study

Fatty Liver Haemorrhagic Syndrome in Laying Hens: Field and Experimental Investigations

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