Route of nutrient delivery affects insulin sensitivity and liver glucose transporter expression in rat

Colomb, V.; Leturque, Armelle; Guihot, G.; Loizeau, M.; Lavie, S.; Colomer, S.; Ricour, C.; Girard, Jean

doi:10.1152/ajpendo.1995.269.5.e827

Cited by 13 publications

(11 citation statements)

References 23 publications

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“…The Vanderbilt group has subsequently provided convincing evidence that hepatic glucose uptake in the presence of matched glucose, insulin, and glucagon concentrations is greater during intraportal than intravenous infusion (3,25,33,47,49,50). This observation has subsequently been confirmed by other investigators in both rats (10,13,17,30) and dogs (31,34). These studies strongly support the existence of a portal signal.…”

mentioning

confidence: 77%

“…Although to our knowledge the study of DeFronzo et al (19) is the only one that has compared the effects of enteral vs. intravenous glucose administration on splanchnic glucose uptake in humans, numerous studies have addressed this question in animals (8,10,17,25,30,31,34). Ishida et al (34) demonstrated that hepatic glucose uptake in dogs was greater after oral or intraportal glucose than after intravenous glucose infusion.…”

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confidence: 99%

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

Vella

Shah

Basu

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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Effect of enteral vs. parenteral glucose delivery on initial splanchnic glucose uptake in nondiabetic humans. Am J Physiol Endocrinol Metab 283: E259-E266, 2002. First published March 27, 2002 10.1152/ajpendo.00178.2001.-To determine if enteral delivery of glucose influences splanchnic glucose metabolism, 10 subjects were studied when glucose was either infused into the duodenum at a rate of 22 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 and supplemental glucose given intravenously or when all glucose was infused intravenously while saline was infused intraduodenally. Hormone secretion was inhibited with somatostatin, and glucose (ϳ8.5 mmol/l) and insulin (ϳ450 pmol/l) were maintained at constant but elevated levels. Intravenously infused [6,6-2 H2]glucose was used to trace the systemic appearance of intraduodenally infused [3-3 H]glucose, whereas UDP-glucose flux (an index of hepatic glycogen synthesis) was measured using the acetaminophen glucuronide method. Despite differences in the route of glucose delivery, glucose production (3.5 Ϯ 1.0 vs. 3.3 Ϯ 1.0 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and glucose disappearance (78.9 Ϯ 5.7 vs. 85.0 Ϯ 7.2 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) were comparable on intraduodenal and intravenous study days. Initial splanchnic glucose extraction (17.5 Ϯ 4.4 vs. 14.5 Ϯ 2.9%) and hepatic UDP-glucose flux (9.0 Ϯ 2.0 vs. 10.3 Ϯ 1.5 mol ⅐ kg Ϫ1 ⅐ min Ϫ1 ) also did not differ on the intraduodenal and intravenous study days. These data argue against the existence of an "enteric" factor that directly (i.e., independently of circulating hormone concentrations) enhances splanchnic glucose uptake or hepatic glycogen synthesis in nondiabetic humans. splanchnic glucose metabolism; postprandial hyperglycemia; acetaminophen glucuronide; hepatic glycogen synthesis; enteric signal GLUCOSE CONCENTRATIONS RARELY exceed 8.0-9.0 mmol/l in healthy nondiabetic humans. This is because of a complex interplay in the regulation of glucose metabolism between splanchnic and extrasplanchnic tissues. After carbohydrate ingestion, the splanchnic bed limits the amount of glucose that must be disposed of by peripheral tissues by a variety of mechanisms (20,22,24). These include metabolism of a portion of the ingested glucose by the gut, stimulation of hepatic glucose uptake, and suppression of hepatic (and perhaps renal) glucose production (1, 12, 36). The route of glucose delivery is also important. It is well established that glucose tolerance is better during enteral than during intravenous glucose delivery. This is in part because of increased insulin secretion mediated by neural (commonly referred to as the cephalic phase) and incretin pathways (4,7,21,60). It is less clear whether enteral glucose administration directly (i.e., independently of changes in hormone concentrations) enhances splanchnic glucose uptake in humans.Several studies suggest that it may. DeFronzo et al. (19) used the hepatic catheterization technique in an effort to determine whether the route of glucose delivery influences splanchnic glucose balance. They reported that net splanchnic...

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confidence: 77%

mentioning

confidence: 99%

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

Vella

Shah

Basu

et al. 2002

American Journal of Physiology-Endocrinology and Metabolism

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“…We can hypothesize that GLP-1 secretion has not been stimulated from birth in these children because of intestinal resection, mucosal dysfunction, or lack of oral intake. The role of this incretin in enhancing insulin release and hepatic glucose uptake has been well documented (27,28). GLP-1 has also been implicated in the postnatal maturation and trophicity of ␤ cells, at least in rodent models (29 -31).…”

Section: Insulin Release and Parenteral Nutritionmentioning

confidence: 99%

Lower Insulin Secretory Response to Glucose Induced by Artificial Nutrition in Children: Prolonged and Total Parenteral Nutrition

et al. 2007

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Long-term parenteral nutrition (TPN) in children is associated with sustained hyperinsulinemia due to a high nutriment infusion flow 12 h/24 h, with plausible lipotoxicity secondary to repeated lipid infusions and with changes in incretin hormone release. The aim of this study was to test whether long-term TPN can lead to an alteration in ␤-cell function. Thirteen children (age 9.5 Ϯ 3.9 y) on total TPN without obvious alternation in glucose tolerance were included. ␤-Cell function was quantified with an intravenous glucose tolerance test (IVGTT) and a graded glucose infusion. R isk factors for type 2 diabetes have been well identified for years. Among them, lipotoxicity, chronic hyperinsulinemia, and alteration in the enteroinsular axis have been debated (1-3). Clinical situations, such long-term long-term parenteral nutrition (TPN), encompassing these metabolic conditions are not frequently studied. In theory, they could lead to alteration in glucose homeostasis or insulin release. In one pediatric cohort followed in two children's hospitals in Paris, the appearance of some cases of chronic and unremitting hyperglycemia during infusion, requiring insulin, suggested that TPN could promote glucose homeostasis disorders.In examples like intestinal mucosa deficiency or neonatal extended intestinal resections, TPN has dramatically changed the prognosis (4,5). Adequate nutrition is now provided to these children as daily home care. However, TPN is a nonphysiologic route of nutrient delivery. Nutrient mixtures are infused nightly over 10 -14 h in sick children in whom caloric needs are equal or greater than in healthy children. High glucose and insulin secretagogue nutrients induce chronic hyperinsulinemia lasting approximately 12 h per day (6). High lipid infusion rates could promote peripheral and central lipotoxicity. Moreover, some intestinal diseases have been shown to be associated with an alternation in incretin hormone release (7).Insulin release in children on TPN was evaluated in one study 10 y ago (8). It was measured during an intravenous glucous tolerance test (IVGTT) and a hyperglycemic clamp. No obvious alterations in insulin release were observed. Patients had an insulin response to IVGTT similar to that of control children of the same age. Insulin release was greater than that in healthy young adults during a hyperglycemic clamp. However, patients were not observed among standardized metabolic conditions. Many of them were not totally dependent on TPN. Indeed, ␤-cell failure could not be reported there.The aim of the study was to test whether metabolic conditions associated with long-term TPN could lead to an alteration ␤-cell function before any obvious alteration in glucose tolerance. METHODSPatients. Thirteen children on long-term TPN were included. Inclusion criteria were the following: children on PN since birth and for at least 5 y, Ͼ80% of their daily caloric intake via the parenteral route, no obvious alternation in glucose tolerance as defined by fasting glycemia (before the beginn...

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“…In these patients, hyperinsulinemia or increased peptide-C levels have been reported (25,26). Insulin resistance has also been shown in rats receiving continuous PN who presented with marked hyperinsulinemia in spite of the absence of hyperglycemia (24). Human studies have also suggested that substrate competition during PN can lead to insulin resistance (27).…”

Section: Discussionmentioning

confidence: 98%

“…Glucose perfusion has been shown to stimulate insulin secretion (23). Further, in rats receiving continuous PN, plasma FFA were significantly increased as well as some amino acids that have been shown to be potent insulin secretagogues (24). In humans, however, few data are available regarding the effects of long-term PN on insulin secretion and sensitivity.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Function and Mechanical Properties of the Common Carotid Artery in Children on Parenteral Nutrition

et al. 2004

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Route of nutrient delivery affects insulin sensitivity and liver glucose transporter expression in rat

Cited by 13 publications

References 23 publications

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

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

Lower Insulin Secretory Response to Glucose Induced by Artificial Nutrition in Children: Prolonged and Total Parenteral Nutrition

Endothelial Function and Mechanical Properties of the Common Carotid Artery in Children on Parenteral Nutrition

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