Cholecystokinin regulates satiation independently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy

Ripken, Dina; Wielen, Nikkie van der; Meulen, Jan van der; Schuurman, T.; Witkamp, Renger F.; Hendriks, H.; Koopmans, S.J.

doi:10.1016/j.physbeh.2014.11.031

Cited by 22 publications

(22 citation statements)

References 49 publications

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“…), and CCKA receptor antagonist prevents satiation in both vagotomized and intact pigs (Ripken et al . ). It remains to be determined whether this is because at higher doses the circulating levels of CCK are high enough that they are able to activate receptors on vagal afferent neurons and axons beyond the terminals, or whether a vagally independent mechanism is activated.…”

Section: Targeting the Vagus Nerve With Pharmacotherapy For The Treatmentioning

confidence: 97%

Role of the vagus nerve in the development and treatment of diet‐induced obesity

Lartigue

2016

The Journal of Physiology

201

144

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This review highlights evidence for a role of the vagus nerve in the development of obesity and how targeting the vagus nerve with neuromodulation or pharmacology can be used as a therapeutic treatment of obesity. The vagus nerve innervating the gut plays an important role in controlling metabolism. It communicates peripheral information about the volume and type of nutrients between the gut and the brain. Depending on the nutritional status, vagal afferent neurons express two different neurochemical phenotypes that can inhibit or stimulate food intake. Chronic ingestion of calorie-rich diets reduces sensitivity of vagal afferent neurons to peripheral signals and their constitutive expression of orexigenic receptors and neuropeptides. This disruption of vagal afferent signalling is sufficient to drive hyperphagia and obesity. Furthermore neuromodulation of the vagus nerve can be used in the treatment of obesity. Although the mechanisms are poorly understood, vagal nerve stimulation prevents weight gain in response to a high-fat diet. In small clinical studies, in patients with depression or epilepsy, vagal nerve stimulation has been demonstrated to promote weight loss. Vagal blockade, which inhibits the vagus nerve, results in significant weight loss. Vagal blockade is proposed to inhibit aberrant orexigenic signals arising in obesity as a putative mechanism of vagal blockade-induced weight loss. Approaches and molecular targets to develop future pharmacotherapy targeted to the vagus nerve for the treatment of obesity are proposed. In conclusion there is strong evidence that the vagus nerve is involved in the development of obesity and it is proving to be an attractive target for the treatment of obesity.

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Section: Targeting the Vagus Nerve With Pharmacotherapy For The Treatmentioning

confidence: 97%

Role of the vagus nerve in the development and treatment of diet‐induced obesity

Lartigue

2016

The Journal of Physiology

201

144

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“…Depending on the amount and composition of the diet, CCK is secreted by the I cells in the duodenal and jejunal mucosa and also by neurons in the enteric nervous system. Clutter et al (72) measured plasma CCK-8 in pigs, at fasting about 2 pmol/l increasing to 10 pmol/l at mixed meal feeding whereas Ripken et al (73) reported concentrations of 0·5 pmol/l and 2 pmol/l for fasting and postprandial, respectively. The major effects of CCK are stimulation of gall bladder contraction, delay of gastric emptying and stimulation of pancreatic secretion (63) .…”

Section: Nutrition Research Reviewsmentioning

confidence: 99%

“…Corring & Chayvialle (71) ; Clutter et al (72) ; Ripken et al (73) ; Feinle et al (76) ; Seimon et al (77) ; Blom et al (78) ; Mossner et al (79) GLP-1 About 3-fold About 3-fold Very high. Quantitative and qualitative changes are similar Souza da Silva et al (95) ; Hooda et al (96) ; Knapper et al (97) ; Blom et al (78) ; Lavin et al (98) ; Verdich et al (99) PYY 1-to 2-fold About 4-fold Low.…”

Section: Comparisons Between Pigs and Humans In Nutritional Chemosensingmentioning

confidence: 99%

Critical review evaluating the pig as a model for human nutritional physiology

et al. 2016

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The present review examines the pig as a model for physiological studies in human subjects related to nutrient sensing, appetite regulation, gut barrier function, intestinal microbiota and nutritional neuroscience. The nutrient-sensing mechanisms regarding acids (sour), carbohydrates (sweet), glutamic acid (umami) and fatty acids are conserved between humans and pigs. In contrast, pigs show limited perception of high-intensity sweeteners and NaCl and sense a wider array of amino acids than humans. Differences on bitter taste may reflect the adaptation to ecosystems. In relation to appetite regulation, plasma concentrations of cholecystokinin and glucagon-like peptide-1 are similar in pigs and humans, while peptide YY in pigs is ten to twenty times higher and ghrelin two to five times lower than in humans. Pigs are an excellent model for human studies for vagal nerve function related to the hormonal regulation of food intake. Similarly, the study of gut barrier functions reveals conserved defence mechanisms between the two species particularly in functional permeability. However, human data are scant for some of the defence systems and nutritional programming. The pig model has been valuable for studying the changes in human microbiota following nutritional interventions. In particular, the use of human flora-associated pigs is a useful model for infants, but the long-term stability of the implanted human microbiota in pigs remains to be investigated. The similarity of the pig and human brain anatomy and development is paradigmatic. Brain explorations and therapies described in pig, when compared with available human data, highlight their value in nutritional neuroscience, particularly regarding functional neuroimaging techniques.

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“…Based on the blood samples before the food intake, homeostasis model assessment of insulin resistance (HOMA-IR) was calculated as HOMA-IR = glucose (mmol/L) × insulin (mU/L)/22.5. In this study, we acquired the data for the satiety sate at 30 minutes after liquid intake, which reported to reach the peak levels 36 37 .…”

Section: Methodsmentioning

confidence: 99%

Altered baseline brain activity differentiates regional mechanisms subserving biological and psychological alterations in obese men

Zhang

Tian

et al. 2015

Sci Rep

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Obesity as a chronic disease is a major factor for insulin resistance and Type 2 diabetes, which has become a global health problem. In the present study, we used resting state functional MRI to investigate the amplitude of low frequency fluctuations of spontaneous signal during both hunger and satiety states in 20 lean and 20 obese males. We found that, before food intake, obese men had significantly greater baseline activity in the precuneus and lesser activity in dorsal anterior cingulate cortex (dACC) relative to lean subjects. Furthermore, after food intake, obese males had significantly lesser activity in dACC than lean males. We further found a significant positive correlation between precuneus activation and hunger ratings before food intake, while dACC activity was negatively correlated with plasma insulin levels before and after food intake. These results indicated that both precuneus and dACC may play an important role in eating behavior. While precuneus rather seemed to mediate subjective satiety, dACC levels rather reflected indirect measures of glucose utilization.

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Cholecystokinin regulates satiation independently of the abdominal vagal nerve in a pig model of total subdiaphragmatic vagotomy

Cited by 22 publications

References 49 publications

Role of the vagus nerve in the development and treatment of diet‐induced obesity

Role of the vagus nerve in the development and treatment of diet‐induced obesity

Critical review evaluating the pig as a model for human nutritional physiology

Altered baseline brain activity differentiates regional mechanisms subserving biological and psychological alterations in obese men

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