Nervous regulation of insulin release by the intestinal vagal glucoreceptors

Mei, N.; Arlhac, Aurore; Boyer, A.

doi:10.1016/0165-1838(81)90038-2

Cited by 50 publications

(8 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reflexes mediated by the autonomic nervous system are now also thought to be involved. 17 Gibby and Hales 9 have recently questioned the whole concept of alimentary augmentation of insulin secretion, i.e., the enteroinsular axis, which was developed to explain the occurrence of higher circulating plasma insulin levels when hyperglycemia was produced by oral rather than by i.v. glucose.…”

Section: Discussionmentioning

confidence: 99%

Insulin and C-Peptide Levels After Oral and Intravenous Glucose: Contribution of Enteroinsular Axis to Insulin Secretion

Hampton¹,

Tredger²,

Cramb

1986

Diabetes

View full text Add to dashboard Cite

Peripheral venous plasma insulin and C-peptide concentrations were measured in 10 healthy volunteers, given either 100 g glucose orally or sufficient intravenous (i.v.) glucose to produce similar glucose concentrations when measured in arterialized blood. The incremental areas under both the insulin and C-peptide curves were significantly increased after oral as compared with i.v. glucose administration by 229% and 138%, respectively. Arteriovenous plasma glucose differences were higher after oral glucose administration and were positively correlated with plasma insulin concentrations. Plasma gastric inhibitory polypeptide (GIP) and insulin concentrations were measured in seven healthy volunteers given oral glucose loads ranging from 25 to 200 g. Both the magnitude and duration of the GIP and insulin responses after oral glucose ingestion were dose dependent. These results suggest that the main cause of the increase in peripheral insulin levels after large oral carbohydrate loads is augmented insulin secretion rather than reduced hepatic extraction, indicating the possibility that an enteroinsular factor does exist, in accordance with the "incretin" concept. They also emphasize the need to document both arterial and venous glucose concentrations for the correct interpretation of experiments investigating glucose homeostasis.

show abstract

Section: Discussionmentioning

confidence: 99%

Insulin and C-Peptide Levels After Oral and Intravenous Glucose: Contribution of Enteroinsular Axis to Insulin Secretion

Hampton¹,

Tredger²,

Cramb

1986

Diabetes

View full text Add to dashboard Cite

show abstract

“…The gastrointestinal tract features glucoreceptors and osmoreceptors (13,25), as well as sweet-taste receptors (12). Intestinal glucoreceptors take part in glucoregulation by mediating nervous control of insulin release via the vagus nerve (26) and glucoseinduced increases in pancreatic islet blood flow (6). These mechanisms, which rely on vagal pathways, are bypassed by direct infusion of glucose into the blood stream.…”

Section: Discussionmentioning

confidence: 99%

Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

Smeets¹,

Vidarsdottir²,

Graaf³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

View full text Add to dashboard Cite

Smeets PA, Vidarsdottir S, de Graaf C, Stafleu A, van Osch MJ, Viergever MA, Pijl H, van der Grond J. Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion. Am J Physiol Endocrinol Metab 293: E754-E758, 2007. First published June 12, 2007; doi:10.1152/ajpendo.00231.2007.-We previously showed that hypothalamic neuronal activity, as measured by the blood oxygen level-dependent (BOLD) functional MRI signal, declines in response to oral glucose intake. To further explore the mechanism driving changes in hypothalamic neuronal activity in response to an oral glucose load, we here compare hypothalamic BOLD signal changes subsequent to an oral vs. an intravenous (iv) glucose challenge in healthy humans. Seven healthy, normal-weight men received four interventions in random order after an overnight fast: 1) ingestion of glucose solution (75 g in 300 ml) or 2) water (300 ml), and 3) iv infusion of 40% glucose solution (0.5 g/kg body wt, maximum 35 g) or 4) infusion of saline (0.9% NaCl, equal volume). The BOLD signal was recorded as of 8 min prior to intervention (baseline) until 30 min after. Glucose infusion was associated with a modest and transient signal decline in the hypothalamus. In contrast, glucose ingestion was followed by a profound and persistent signal decrease despite the fact that plasma glucose levels were almost threefold lower than in response to iv administration. Accordingly, glucose ingestion tended to suppress hunger more than iv infusion (P Ͻ 0.1). We infer that neural and endocrine signals emanating from the gastrointestinal tract are critical for the hypothalamic response to nutrient ingestion. functional magnetic resonance imaging; glucose homeostasis; insulin; incretins THE BLOOD OXYGEN LEVEL-DEPENDENT (BOLD) signal, produced by functional magnetic resonance imaging (fMRI), is a noninvasive measure of neuronal activity (19, 30,35). We (36, 37) have recently shown that the BOLD signal in the upper part of the hypothalamus of healthy, normal-weight humans consistently declines in response to an oral glucose load, which strongly suggests that glucose ingestion blunts hypothalamic neuronal activity in these subjects. The hypothalamus plays a critical role in the control of energy balance. Neural circuits in hypothalamic nuclei perceive and integrate endocrine and metabolic cues reflecting bodily energy content to coordinate behavior and fuel flux so as to maintain energy homeostasis (28, 34). Thus, adaptations of hypothalamic neuronal activity driven by nutrient ingestion may serve to guard energy equilibrium in the face of an environmental challenge.The mechanism linking glucose intake and changes in hypothalamic neuronal activity in humans is currently unknown. Various metabolic and endocrine cues are worthwhile to consider. Circulating levels of glucose can be sensed by specialized neurons in the arcuate and ventromedial nuclei of the hypothalamus, and these neurons project to other key nuclei (21). Alternatively, insulin inhibits NPY neuronal activit...

show abstract

“…Additionally, the state of the animal was routinely controlled by monitoring the heart rate with an EKG pre-amplifier and by visual observation of the pupil. Finally, in some experiments, the blood glucose level, which is a good physiological index (see Mei, Arlhac & Boyer, 1981), was estimated from time to time with the glucose oxidase method. For this purpose, samples of 100 F1 of carotid blood were taken.…”

Section: Surgical Preparationmentioning

confidence: 99%

“…However, they are able to detect more specific stimuli such as gentle stroking of the mucosae. The physiological role of these receptors is believed to be to provide information on bolus consistency and a large majority are vagal in origin (see Paintal, 1973; Leek, 1977;Mei, 1981). The other endings situated in the stomach or in the duodeno-jejunum, are connected to splanchnic fibres (Ranieri et al 1973;Ranieri, Crousillat & Mei, 1975; Morrison, 1973;Floyd et al 1976).…”

Section: Introductionmentioning

confidence: 99%

Vagal mechanoreceptors located in the lower oesophageal sphincter of the cat.

Clerc¹,

Mei²

1983

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. In anaesthetized cats, sixty-two vagal sensory units with afferent endings in the lower oesophageal sphincter were recorded by means of extracellular glass micro-electrodes implanted in the nodose ganglion.2. All the receptors had non-medullated fibres, with conduction velocities ranging from 0O8 to 1-2 m/s. From the direct stimulation of the lower oesophageal sphincter, three types of mechanoreceptors were identified. 3. Thirty-one were activated by natural stimuli: tonic contraction of the sphincter and distension elicited by the passage of a bolus. Artificial stimulation effected by digital compression was also effective. These receptors were similar to muscular endings already described in the-digestive tract. Their main characteristic, i.e. their slow adaptation, suggests that they act as sensors of sphincter opening and closure. This was corroborated by observations obtained during distension of the cervical or thoracic oesophagus; a maximum decrease occurred in the lower oesophageal sphincter mechanoreceptor discharge when the distension was produced between 9 and 12 cm from the lower oesophageal sphincter.4. Twenty-nine endings were found in the superficial layers mucosaee). Contrary to the muscular receptors, the mucosal receptors were not affected by normal contractions or distensions of the lower oesophageal sphincter. They were activated only by strong stimuli like digital compression or distension achieved with a balloon. In addition, mucosal stroking was a potent stimulus. Whatever the stimulus used, the mucosal receptors showed rather rapidly adapting discharges. These receptors should be considered to be sensors of bolus consistency.5. Two mechanoreceptors, located in the serous membrane ofthe lower oesophageal sphincter, were identified by touching or by stretching. Their discharges showed that they belonged to the rapidly adapting type.6. A comparison of the three types of receptors found in the lower oesophageal sphincter is made with known digestive endings and their possible role is discussed.

show abstract

Nervous regulation of insulin release by the intestinal vagal glucoreceptors

Cited by 50 publications

References 33 publications

Insulin and C-Peptide Levels After Oral and Intravenous Glucose: Contribution of Enteroinsular Axis to Insulin Secretion

Insulin and C-Peptide Levels After Oral and Intravenous Glucose: Contribution of Enteroinsular Axis to Insulin Secretion

Oral glucose intake inhibits hypothalamic neuronal activity more effectively than glucose infusion

Vagal mechanoreceptors located in the lower oesophageal sphincter of the cat.

Contact Info

Product

Resources

About