Effect of enteral vs. parenteral glucose delivery on  initial splanchnic glucose uptake in nondiabetic humans

Vella, Adrian; Shah, Pankaj; Basu, Rita; Basu, Ananda; Camilleri, Michael; Schwenk, W.; Rizza, Robert A.

doi:10.1152/ajpendo.00178.2001

Cited by 22 publications

(20 citation statements)

References 62 publications

(89 reference statements)

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“…It is clear, however, based on the measurement of net splanchnic glucose balance in humans (6)(7)(8) and net hepatic glucose balance in dogs (9,10), that neither hyperinsulinemia nor hyperglycemia can independently induce much net hepatic glucose uptake (NHGU 6 ). NHGU remains modest (2.8-11.1 mmol$kg 21 $min 21 ) even when hyperinsulinemia and hyperglycemia (resulting from glucose infusion into a peripheral vein) are combined (6,7,9,11,12). On the other hand, when similar levels of hyperinsulinemia and hyperglycemia are brought about by oral or enteral glucose delivery, the resulting rates of NHGU are as great as 25-27.8 mmol$kg 21 $min 21 (13,14).…”

Section: Current Status Of Knowledgementioning

confidence: 99%

Regulation of Hepatic Glucose Uptake and Storage In Vivo

Moore

Coate

Winnick

et al. 2012

Advances in Nutrition

280

224

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In the postprandial state, the liver takes up and stores glucose to minimize the fluctuation of glycemia. Elevated insulin concentrations, an increase in the load of glucose reaching the liver, and the oral/enteral/portal vein route of glucose delivery (compared with the peripheral intravenous route) are factors that increase the rate of net hepatic glucose uptake (NHGU). The entry of glucose into the portal vein stimulates a portal glucose signal that not only enhances NHGU but concomitantly reduces muscle glucose uptake to ensure appropriate partitioning of a glucose load. This coordinated regulation of glucose uptake is likely neurally mediated, at least in part, because it is not observed after total hepatic denervation. Moreover, there is evidence that both the sympathetic and the nitrergic innervation of the liver exert a tonic repression of NHGU that is relieved under feeding conditions. Further, the energy sensor 5'AMP-activated protein kinase appears to be involved in regulation of NHGU and glycogen storage. Consumption of a high-fat and high-fructose diet impairs NHGU and glycogen storage in association with a reduction in glucokinase protein and activity. An understanding of the impact of nutrients themselves and the route of nutrient delivery on liver carbohydrate metabolism is fundamental to the development of therapies for impaired postprandial glucoregulation.

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Section: Current Status Of Knowledgementioning

confidence: 99%

Regulation of Hepatic Glucose Uptake and Storage In Vivo

Moore

Coate

Winnick

et al. 2012

Advances in Nutrition

280

224

View full text Add to dashboard Cite

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“…This response was inhibited by somatostatin infusion and dependent upon GLP-1 receptor activation (4). Prior work observed an inhibitory or no effect of the portal signal on glucose clearance using somatostatin with insulin and glucose replacement to allow careful matching of the insulin and insulin concentrations (7,20,28). However, the use of somatostatin may have blocked an augmentation of the peripheral glucose uptake seen with portal glucose delivery.…”

mentioning

confidence: 99%

Impact of portal glucose delivery on glucose metabolism in conscious, unrestrained mice

Chueh¹,

Malabanan²,

McGuinness³

2006

American Journal of Physiology-Endocrinology and Metabolism

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Previous studies in mice suggest that portal venous infusion of glucose at a low rate paradoxically causes hypoglycemia; this does not occur in dogs, rats, and humans. A possible explanation is that fasting status in the mouse studies may have altered the response. We sought to determine whether the response to portal glucose delivery in the mouse was similar to that seen in other species and whether it was dependent on fasting status. Studies were performed on chronically catheterized conscious mice. Catheters were placed into the portal and jugular veins and carotid artery 5 days before study. After a 5-or 16-h fast, glucose was infused into either the portal (PO) or the jugular vein (JU) for 6 h at 25H]glucose was infused into the JU to measure glucose turnover. In 5-h-fasted mice, PO and JU exhibited similar increases in arterial blood glucose from 155 Ϯ 11 to 173 Ϯ 19 and 147 Ϯ 8 to 173 Ϯ 10 mg/dl, respectively. Endogenous glucose production decreased and arterial insulin increased to the same extent in both PO and JU. A similar response was observed in 16-h-fasted mice; however, the proportion of hepatic glycogen synthesis occurring by the indirect pathway was increased by fasting. In summary, portal glucose delivery in the mouse did not cause hypoglycemia even when the duration of the fast was extended. The explanation of the differing response from previous reports in the mouse is unclear. portal vein; hyperglycemia; fasting THE LIVER PLAYS A MAJOR ROLE in blood glucose homeostasis by being able to rapidly transition from a site of glucose production in the fasting state to a site of glucose utilization in the fed state. The magnitude of hepatic glucose utilization during feeding is dependent on both the plasma insulin and glucose levels and the route of glucose delivery. In fact, significant hepatic glucose utilization is not observed if only hyperglycemia and hyperinsulinemia are present, but an intraportal or intraduodenal glucose infusion prompts substantial hepatic glucose uptake (24). Portal vein glucose delivery is known to produce a signal ("portal signal"), which enhances net hepatic glucose uptake and hepatic glycogen deposition in humans (9, 29) and rats (7,12,27). The portal signal also impairs peripheral glucose utilization in dogs and rats (20), thus augmenting the importance of the liver in whole body glucose disposal following a meal.A series of studies in the mouse suggested that delivery of glucose into the portal vein at a rate of 25 g⅐g Ϫ1 ⅐min Ϫ1 , which is similar to the basal endogenous glucose production (EGP) paradoxically induced hypoglycemia (5, 6). Hypoglycemia was precipitated by an activation of peripheral glucose clearance. This response was inhibited by somatostatin infusion and dependent upon GLP-1 receptor activation (4). Prior work observed an inhibitory or no effect of the portal signal on glucose clearance using somatostatin with insulin and glucose replacement to allow careful matching of the insulin and insulin concentrations (7,20,28). However, the use of somatosta...

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“…L'augmentation de l'utilisation du glucose par l'intestin lui-même explique essentiellement cette différence et non le stockage en glycogène hépatique qui est comparable quelle que soit la voie d'administration. Cela contredit des données anciennes obtenues chez l'animal et remet en cause la pré-sence d'un capteur de glucose (glucose-sensor) portal [20].…”

Section: Incrétine Et Nutrition Entérale Effet Sur La Glycémieunclassified

Incrétines et nutrition entérale

et al. 2011

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Contrairement à la nutrition parentérale, la nutrition entérale provoque la sécrétion d'hormones digestives dont les incrétines. Ces hormones, le GLP-1 (glucagon-like peptide-1) et le GIP (glucose dependent insulinotropic polypeptide), potentialisent la sécrétion d'insuline et inhibent la sécrétion de glucagon. Leur sécrétion est dépendante de l'absorption des nutriments, notamment des lipides qui sont les plus forts stimulateurs de leur sécrétion. Leurs actions ne se limitent pas à la sécrétion d'insuline. GIP et GLP-1 améliorent aussi l'insulinosensibilité. Le GIP, en stimulant la lipogenèse adipocytaire, représente un vrai système intégratif entéroadi-pocytaire favorisant l'anabolisme. GIP et GLP-1 inhibent la sécrétion acide gastrique, ralentissent le transit en agissant sur la motricité intestinale, améliorent la vascularisation mésen-térique et la trophicité digestive. Le GLP-1, hormone du frein iléal, ralentit la vidange gastrique, ce qui ralentit l'absorption des glucides et diminue leur effet sur la glycémie. Compte tenu de ces différentes propriétés, la nutrition entérale, en stimulant ces hormones, a un effet bénéfique sur l'équilibre glycémique. Cet effet est également observé lorsqu'elle est associée à la nutrition parentérale. Les effets favorables de la nutrition entérale sur l'inflammation intestinale, sur la vascularisation et la cicatrisation, observés en pratique clinique, pourraient être en grande partie liés à ces effets hormonaux, qui sont très probablement prolongés et accentués du fait de la durée d'administration. Il est également probable que ces effets soient variables selon le site d'administration. Pour citer cette revue : Réanimation 20 (2011). Mots clés Incrétines · Nutrition entérale · Glucagon-like peptide-1 · Glucose-dependent insulinotropic polypeptideAbstract In contrast to parenteral nutrition, enteral nutrition induces the secretion of gastro-intestinal hormones including incretines. Glucagon-like peptide-1 (GLP-1) and glucose dependent insulinotropic polypeptide (GIP) potentiate insulin production but also inhibit glucagon secretion. GIP and GLP-1 secretion depends upon nutriment absorption and especially lipids that highly stimulate their production. However, their action is not limited to insulin secretion. GIP and GLP-1 also improve sensitivity to insulin. By stimulating adipocytal lipogenesis, GIP appears to be a real entero-adipocytal integrative system that improves anabolism. GIP and GLP-1 inhibit acid gastric secretion, slow down transit by altering intestinal motility, and improve mesentric vascularisation and digestive trophicity. GLP-1, the hormone of ileal break, slows down gastric emptying, which decreases carbohydrate absorption, limiting their impact on blood glucose level. If considering the properties of the hormones which secretion is mediated by incretins, enteral nutrition may improve blood glucose balance. Improvement also occurs when enteral nutrition is associated with parenteral nutrition. Favourable impact of enteral nutrition on intestinal inflammat...

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Effect of enteral vs. parenteral glucose delivery on initial splanchnic glucose uptake in nondiabetic humans

Cited by 22 publications

References 62 publications

Regulation of Hepatic Glucose Uptake and Storage In Vivo

Regulation of Hepatic Glucose Uptake and Storage In Vivo

Impact of portal glucose delivery on glucose metabolism in conscious, unrestrained mice

Incrétines et nutrition entérale

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