Stimulation of intestinal glucoreceptors in rats increases pancreatic islet blood flow through vagal mechanisms

Carlsson, Per‐Ola; Iwase, Masanori; Jansson, Leif

doi:10.1152/ajpregu.1999.276.1.r233

Cited by 17 publications

(19 citation statements)

References 18 publications

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“…In previous work [4,5,6], changes in glucose-dependent islet blood flow preferentially depend on nerve-mediated signals. Therefore, the islet blood flow response to hypoglycaemia was further evaluated by administration of 2-deoxy glucose, which by interfering with neuronal glucose metabolism induces a selective neuronal glucopenia [22,23].…”

Section: Discussionmentioning

confidence: 93%

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

et al. 2003

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Aims/hypothesis. The aim of this study was to evaluate the effects of induced hypoglycaemia on pancreatic-islet blood flow in normal rats and in the GK rat, an animal model of Type 2 diabetes which normally has an increased islet blood perfusion. Methods. A 50% reduction in blood glucose concentrations was achieved by intravenous administration of a rapidly acting insulin (15 IU/kg body weight). Blood flows were measured by a non-radioactive microsphere technique. Results. A pronounced decrease in islet blood flow was observed in all animals, but preferentially in the Type 2 diabetic GK rats. When a similar dose of insulin was given to whole-pancreas transplanted rats only islet blood flow in the native pancreas was decreased, whereas that of the transplanted, i.e. denervated, pancreas was unchanged. Administration of 2-deoxy-Dglucose, which induces intracellular glucopenia especially in neurons, also decreased islet blood flow despite a systemic hyperglycaemia. Conclusion/interpretation. Hypoglycaemia leads to a preferential decrease in pancreatic-islet blood perfusion. The effect is probably mediated by the central nervous system, since 2-deoxy D-glucose-induced neuronal glucopenia caused a similar decrease in blood flow. The effects of islet blood flow are not likely to be mediated by nervous stimulation of the adrenal glands, with an associated release of catecholamines, because the transplanted pancreas was not affected by hypoglycaemia. The decreased islet blood perfusion could possibly diminish the output of insulin from the islets, thereby preventing a further decrease in blood glucose concentrations. [Diabetologia (2003[Diabetologia ( ) 46:1124[Diabetologia ( -1130

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Section: Discussionmentioning

confidence: 93%

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

et al. 2003

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“…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

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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...

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“…The arterial blood perfusion of the whole pancreas, islets, duodenum, colon, adrenal glands, and kidneys was then measured with a microsphere technique (12). Briefly, a total of 1.5-2.0 ϫ 10 5 nonradioactive microspheres (EZ-Trac; Triton Microspheres, San Diego, CA), with a diameter of 10 m, was injected via the catheter with its tip in the ascending aorta during 10 s. Starting 5 s before the microsphere injection, and continuing for a total of 60 s, an arterial blood sample was collected by free flow from the catheter in the femoral artery at a rate of ϳ0.40 ml/min.…”

mentioning

confidence: 99%

“…Arterial blood was collected from the carotid catheter for determination of blood glucose and serum insulin concentrations as given below. The animals were then killed, and the pancreas and adrenal glands were removed in toto, blotted, weighed, and treated with a freeze-thawing technique, which visualized the pancreatic islets and microspheres (12). Approximately 100 mg each of the duodenum (around the papilla), colon (descending part), and left kidney (slice through the center) were also removed and treated in the same way.…”

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confidence: 99%

KATP Channels and Pancreatic Islet Blood Flow in Anesthetized Rats

et al. 2003

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K ATP channels are important for insulin secretion and depolarization of vascular smooth muscle. In view of the importance of drugs affecting K ATP channels in the treatment of diabetes, we investigated the effects of these channels on splanchnic blood perfusion in general and pancreatic islet blood flow in particular. We treated anesthetized Sprague-Dawley rats with the K ATP channel openers diazoxide or NNC 55-0118 or the K ATP channel closer glipizide. Both diazoxide and NNC 55-0118 dose-dependently increased total pancreatic and islet blood flow in the presence of moderate hyperglycemia, but had no effects on the blood perfusion of other splanchnic organs. Diazoxide markedly lowered the mean arterial blood pressure and thus increased vascular conductance in all organs studied. NNC 55-0118 had much smaller effects on the blood pressure. Glipizide did not affect total pancreatic blood flow, but decreased islet blood flow by 50% in the presence of hypoglycemia. We conclude that K ATP channels actively participate in the blood flow regulation of the pancreatic islets and that substances affecting such channels may also influence islet blood flow.

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Stimulation of intestinal glucoreceptors in rats increases pancreatic islet blood flow through vagal mechanisms

Cited by 17 publications

References 18 publications

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

Hypoglycaemia induces decreased islet blood perfusion mediated by the central nervous system in normal and Type 2 diabetic GK rats

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

KATP Channels and Pancreatic Islet Blood Flow in Anesthetized Rats

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