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Parenteral nutrition intravenous fat emulsions product shortage considerations.
A.S.P.E.N. Intravenous Fat Emulsion National Shortage Task Force, Vanek VW, Allen P, Harvey Banchik LP, Bistrian B, Collier S, Driscoll DF, Gura K, Houston DR, Miles J, Mirtallo J, Mogensen KM, Seidner D
(2013) Nutr Clin Pract 28: 528-9
MeSH Terms: Adult, Child, Deficiency Diseases, Dietary Fats, Fat Emulsions, Intravenous, Fatty Acids, Essential, Humans, Infant, Newborn, Parenteral Nutrition, Parenteral Nutrition Solutions, Parenteral Nutrition, Total, Practice Guidelines as Topic
Added September 30, 2015
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12 MeSH Terms
Continuous low-dose fructose infusion does not reverse glucagon-mediated decrease in hepatic glucose utilization.
Johnson PM, Chen SS, Santomango TS, Williams PE, Lacy DB, McGuinness OP
(2011) Metabolism 60: 867-73
MeSH Terms: Animals, Body Weight, Dogs, Female, Fructose, Glucagon, Glucokinase, Glucose, Glycolysis, Hemodynamics, Hormones, Hypoglycemic Agents, Insulin, Liver, Male, Organ Size, Pancreatectomy, Parenteral Nutrition, Total, Phosphofructokinase-1
Show Abstract · Added December 10, 2013
An adaptation to continuous total parenteral nutrition (TPN; 75% of nonprotein calories as glucose) is the liver becomes a major consumer of glucose with lactate release as a by-product. The liver is able to further increase liver glucose uptake when a small dose of fructose is acutely infused via the portal system. Glucagon, commonly elevated during inflammatory stress, is a potent inhibitor of glucose uptake by the liver during TPN. The aim was to determine if continuous fructose infusion could overcome the glucagon-mediated decrease in hepatic glucose uptake. Studies were performed in conscious, insulin-treated, chronically catheterized, pancreatectomized dogs that adapted to TPN for 33 hours. They were then assigned to 1 of 4 groups: TPN (C), TPN + fructose (4.4 μmol kg(-1) min(-1); F), TPN + glucagon (0.2 pmol kg(-1) min(-1); GGN), or TPN + fructose and glucagon (F + GGN) for an additional 63 hours (33-96 hours). Insulin, fructose, and glucagon were infused into the portal vein. During that period, all animals received a fixed insulin infusion of 0.4 mU·kg(-1)·min(-1) (33-96 hours); and the glucose infusion rates were adjusted to maintain euglycemia (6.6 mmol/L). Continuous fructose infusion was unable to further enhance net hepatic glucose uptake (in micromoles per kilogram per minute) (31.1 ± 2.8 vs 36.1 ± 5.0; C vs F), nor was it able to overcome glucagon-mediated decrease in net hepatic glucose uptake (10.0 ± 4.4 vs 12.2 ± 3.9; GGN vs F + GGN). In summary, continuous fructose infusion cannot augment liver glucose uptake during TPN; nor can it overcome the inhibitory effects of glucagon.
Copyright © 2011 Elsevier Inc. All rights reserved.
1 Communities
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19 MeSH Terms
Glucagon-mediated impairments in hepatic and peripheral tissue nutrient disposal are not aggravated by increased lipid availability.
Chen SS, Santomango TS, Williams PE, Lacy DB, McGuinness OP
(2009) Am J Physiol Endocrinol Metab 296: E1172-8
MeSH Terms: Animals, Blood Glucose, Blood Pressure, Body Weight, Dogs, Fatty Acids, Nonesterified, Female, Glucagon, Glucokinase, Glucose, Glucose-6-Phosphatase, Glycogen Synthase, Heart Rate, Insulin, Lactic Acid, Lipids, Liver, Male, Organ Size, Parenteral Nutrition, Total, Phosphorylases
Show Abstract · Added December 10, 2013
Glucose, fat, and glucagon availability are increased in diabetes. The normal response of the liver to chronic increases in glucose availability is to adapt to become a marked consumer of glucose. Yet this fails to occur in diabetes. The aim was to determine whether increased glucagon and lipid interact to impair the adaptation to increased glucose availability. Chronically catheterized well controlled depancreatized conscious dogs (n = 21) received 3 days of continuous parenteral nutrition (TPN) that was either high in glucose [C; 75% nonprotein calories (NPC)] or in lipid (HL; 75% NPC) in the presence or absence of a low dose (one-third basal) chronic intraportal infusion of glucagon (GN; 0.25 ng.kg(-1).min(-1)). During the 3 days of TPN, all groups received the same insulin algorithm; the total amount of glucose infused (GIR) was varied to maintain isoglycemia ( approximately 120 mg/dl). On day 3 of TPN, hepatic metabolism was assessed. Glucose and insulin levels were similar in all groups. GIR was decreased in HL and C + GN ( approximately 30%) and was further decreased in HL + GN (55%). Net hepatic glucose uptake was decreased approximately 15% in C + GN, and HL and was decreased approximately 50% in HL + GN. Lipid alone or combined with glucagon decreased glucose uptake by peripheral tissues. Despite impairing whole body glucose utilization, HL did not limit whole body energy disposal. In contrast, glucagon suppressed whole body energy disposal irrespective of the diet composition. In summary, failure to appropriately suppress glucagon secretion adds to the dietary fat-induced impairment in both hepatic and peripheral glucose disposal. In addition, unlike increasing the percentage of calories as fat, inappropriate glucagon secretion in the absence of compensatory hyperinsulinemia limits whole body nutrient disposition.
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21 MeSH Terms
Route-dependent effect of nutritional support on liver glucose uptake.
Chen SS, Torres-Sanchez CJ, Hosein N, Zhang Y, Lacy DB, Chang C, McGuinness OP
(2005) Am J Physiol Regul Integr Comp Physiol 289: R1319-27
MeSH Terms: Alanine, Animals, Blood Glucose, Dogs, Enteral Nutrition, Female, Glucose, Hepatic Artery, Insulin, Kinetics, Lactic Acid, Liver, Nutritional Support, Parenteral Nutrition, Total, Portal Vein, Regional Blood Flow, Time Factors
Show Abstract · Added December 10, 2013
The liver is a major site of glucose disposal during chronic (5 day) total parenteral (TPN) and enteral (TEN) nutrition. Net hepatic glucose uptake (NHGU) is dependent on the route of delivery when only glucose is delivered acutely; however, the hepatic response to chronic TPN and TEN is very similar. We aimed to determine whether the route of nutrient delivery altered the acute (first 8 h) response of the liver and whether chronic enteral delivery of glucose alone could augment the adaptive response to TPN. Chronically catheterized conscious dogs received either TPN or TEN containing glucose, Intralipid, and Travasol for either 8 h or 5 days. Another group received TPN for 5 days, but approximately 50% of the glucose in the nutrition was given via the enteral route (TPN+EG). Hepatic metabolism was assessed with tracer and arteriovenous difference techniques. In the presence of similar arterial plasma glucose levels (approximately 6 mM), NHGU and net hepatic lactate release increased approximately twofold between 8 h and 5 days in TPN and TEN. NHGU (26 +/- 1 vs. 23 +/- 3 micromol.kg(-1).min(-1)) and net hepatic lactate release (44 +/- 1 vs. 34 +/- 6 micromol.kg(-1).min(-1)) in TPN+EG were similar to results for TPN, despite lower insulin levels (96 +/- 6 vs. 58 +/- 16 pM, TPN vs. TPN+EG). TEN does not acutely enhance NHGU or disposition above that seen with TPN. However, partial delivery of enteral glucose is effective in decreasing the insulin requirement during chronic TPN.
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17 MeSH Terms
Time course of the hepatic adaptation to TPN: interaction with glycogen depletion.
Chen SS, Torres-Sanchez CJ, Hosein N, Zhang Y, Lacy DB, McGuinness OP
(2005) Am J Physiol Endocrinol Metab 288: E163-70
MeSH Terms: Adaptation, Physiological, Animals, Blood Glucose, Dogs, Female, Glucagon, Glycogen, Hindlimb, Insulin, Intestinal Mucosa, Liver, Liver Circulation, Parenteral Nutrition, Total
Show Abstract · Added December 10, 2013
In response to chronic (5 days) TPN, the liver becomes a major site of glucose disposal, removing approximately 45% (4.5 mg.kg(-1).min(-1)) of exogenous glucose. Moreover, approximately 70% of glucose is not stored but released as lactate. We aimed to determine in chronically catheterized conscious dogs the time course of adaptation to TPN and the glycogen depletion impact on early time course. After an 18-h (n = 5) fast, TPN was infused into the inferior vena cava for 8 (n = 5) or 24 h (n = 6). A third group, of 42-h-fasted animals (n = 6), was infused with TPN for 8 h. TPN was infused at a rate designed to match the dog's calculated basal energy and nitrogen requirements. NHGU (-2.3 +/- 0.1 to 2.2 +/- 0.7 to 3.9 +/- 0.6 vs. -1.7 +/- 0.3 to 1.1 +/- 0.5 to 2.9 +/- 0.4 mg.kg(-1).min(-1), basal to 4 to 8 h, 18 vs. 42 h) and net hepatic lactate release (0.7 +/- 0.3 to 0.6 +/- 0.1 to 1.4 +/- 0.2 vs. -0.6 +/- 0.1 to 0.1 +/- 0.1 to 0.8 +/- 0.1 mg.kg(-1).min(-1), basal to 4 to 8 h) increased progressively. Net hepatic glycogen repletion and tracer determined that glycogen syntheses were similar. After 24 h of TPN, NHGU (5.4 +/- 0.6 mg.kg(-1).min(-1)) and net hepatic lactate release (2.6 +/- 0.4 mg.kg(-1).min(-1)) increased further. In summary, 1) most hepatic adaptation to TPN occurs within 24 h after initiation of TPN, and 2) prior glycogen depletion does not augment hepatic adaptation rate.
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13 MeSH Terms
Role of nutrition for cardiovascular risk reduction in chronic kidney disease patients.
Ikizler TA
(2004) Adv Chronic Kidney Dis 11: 162-71
MeSH Terms: Cardiovascular Diseases, Dietary Supplements, Humans, Inflammation, Kidney Failure, Chronic, Malnutrition, Nutritional Support, Oxidative Stress, Parenteral Nutrition, Total, Risk Factors
Show Abstract · Added September 29, 2014
Cardiovascular disease (CVD) is the major cause of death in end-stage renal disease (ESRD) patients. Uremic malnutrition and chronic inflammation are important comorbid conditions, closely associated with CVD risk in ESRD patients. A pathophysiologic link between uremic malnutrition, chronic inflammation, and atherosclerosis has been proposed in this patient population. Uremic malnutrition can result from chronic inflammation and can accelerate the progression of cardiovascular disease. Chronic inflammation can also directly predispose ESRD patients to a proatherogenic state. Both uremic malnutrition and chronic inflammation are also associated with increased oxidative stress, a condition proposed as a unifying concept of CVD in uremia. Although a single common etiology has not been identified in this complex process, nutritional, anti-inflammatory, and antioxidant interventions can provide potential treatment options to improve the high mortality and morbidity in ESRD patients.
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10 MeSH Terms
Impact of infection on glucose-dependent liver glucose uptake during TPN: interaction with insulin.
Chen SS, Donmoyer CM, Pearson DA, Poole A, Zhang Y, Lacy DB, McGuinness OP
(2004) Am J Physiol Endocrinol Metab 286: E286-95
MeSH Terms: Animals, Blood Glucose, Dogs, Drug Interactions, Escherichia coli Infections, Female, Glucagon, Glucose, Hemodynamics, Hindlimb, Insulin, Intestines, Kinetics, Liver, Parenteral Nutrition, Total
Show Abstract · Added December 10, 2013
Chronic total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU). This adaptive increase is impaired by an infection despite accompanying hyperinsulinemia. In the nonadapted state, NHGU is dependent on the prevailing glucose levels. Our aims were to determine whether the adaptation to TPN alters the glucose dependence of NHGU, whether infection impairs this dependence, and whether insulin modulates the glucose dependence of NHGU during infection. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, dogs received either a bacterial fibrin clot to induce a nonlethal infection (INF, n = 9) or a sterile fibrin clot (Sham, n = 6). Forty-two hours after clot implantation, somatostatin was infused. In Sham, insulin and glucagon were infused to match the level seen in Sham (9 +/- 1 microU/ml and 23 +/- 4 pg/ml, respectively). In infected animals, either insulin and glucagon were infused to match the levels seen in infection (25 +/- 2 microU/ml and 101 +/- 15 pg/ml; INF-HI; n = 5) or insulin was replaced to match the lower levels seen in Sham (13 +/- 2 microU/ml), whereas glucagon was kept elevated (97 +/- 9 pg/ml; INF-LO; n = 4). Then a four-step (90 min each) hyperglycemic (120, 150, 200, or 250 mg/dl) clamp was performed. NHGU increased at each glucose step in Sham (from 3.6 +/- 0.6 to 5.4 +/- 0.7 to 8.9 +/- 0.9 to 12.1 +/- 1.1 mg.kg(-1).min(-1)); the slope of the relationship between glucose levels and NHGU (i.e., glucose dependence) was higher than that seen in nonadapted animals. Infection impaired glucose-dependent NHGU in both INF-HI (1.3 +/- 0.4 to 2.9 +/- 0.5 to 5.5 +/- 1.0 to 7.7 +/- 1.6 mg.kg(-1).min(-1)) and INF-LO (0.5 +/- 0.7 to 2.2 +/- 0.6 to 4.2 +/- 1.0 to 5.8 +/- 0.8 mg.kg(-1).min(-1)). In summary, TPN augments glucose-dependent NHGU, the presence of infection decreases glucose-dependent NHGU, and the accompanying hyperinsulinemia associated with infection does not sustain the glucose dependence of NHGU.
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15 MeSH Terms
Effects of fructose on hepatic glucose metabolism.
McGuinness OP, Cherrington AD
(2003) Curr Opin Clin Nutr Metab Care 6: 441-8
MeSH Terms: Area Under Curve, Dose-Response Relationship, Drug, Fructose, Glucokinase, Glucose, Humans, Insulin Resistance, Liver, Liver Glycogen, Parenteral Nutrition, Total
Show Abstract · Added December 10, 2013
PURPOSE OF REVIEW - The liver plays an important role in glucose tolerance. A number of studies have suggested fructose improves glucose tolerance especially in insulin resistant settings. This review summarizes the recent work suggesting that fructose enhances glucose tolerance by augmenting liver glucose uptake. This increase may be mediated by the translocation and activation of hepatic glucokinase.
RECENT FINDINGS - Catalytic quantities of fructose (<10% of total carbohydrate flux) enhance liver glucose uptake in a dose dependent manner. The primary fate of the glucose is glycogen synthesis. The ability of fructose to augment liver glucose uptake is not impaired by the presence of marked insulin resistance such as in type 2 diabetes or infection. In addition, it is able to further enhance liver glucose uptake in the normal adapted setting of total parenteral nutrition and reverse the infected-induced decrease in liver glucose uptake. Studies also demonstrate that the beneficial effects of fructose on liver glucose uptake during chronic nutritional support do not persist.
SUMMARY - Fructose is a potent acute regulator of liver glucose uptake and glycogen synthesis. Inclusion of catalytic quantities of fructose in a carbohydrate meal improves glucose tolerance. This improvement is primarily mediated by the activation of hepatic glucokinase and consequent facilitation of liver glucose uptake. The improvement in glucose tolerance is most evident in insulin resistant settings (e.g. Type 2 diabetes and infection). The beneficial effect of fructose on hepatic glucose disposal, however, does not persist if fructose is given continuously such as in total parenteral nutrition.
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10 MeSH Terms
Infection impairs insulin-dependent hepatic glucose uptake during total parenteral nutrition.
Donmoyer CM, Chen SS, Lacy DB, Pearson DA, Poole A, Zhang Y, McGuinness OP
(2003) Am J Physiol Endocrinol Metab 284: E574-82
MeSH Terms: Animals, Dogs, Dose-Response Relationship, Drug, Escherichia coli Infections, Female, Glucose, Hindlimb, Hormones, Insulin, Intestinal Mucosa, Liver, Parenteral Nutrition, Total
Show Abstract · Added December 10, 2013
Total parenteral nutrition (TPN) markedly augments net hepatic glucose uptake (NHGU) and hepatic glycolysis in the presence of mild hyperglycemia and hyperinsulinemia. This increase is impaired by an infection. We determined whether the adaptation to TPN alters the responsiveness of the liver to insulin and whether infection impairs that response. Chronically catheterized dogs received TPN for 5 days. On day 3 of TPN, either a nonlethal hypermetabolic infection was induced (INF, n = 5) or a sham surgery was performed (SHAM, n = 5). Forty-two hours after clot implantation, somatostatin and glucagon (34 +/- 3 vs. 84 +/- 11 pg/ml in artery, SHAM vs. INF) were infused, and a three-step (120 min each) isoglycemic (approximately 120 mg/dl) hyperinsulinemic (approximately 12, 25, and 50 microU/ml) clamp was performed to simulate levels seen in normal, infected, and exogenous insulin treatment states. In SHAM, NHGU (3.5 +/- 0.2 to 4.2 +/- 0.4 to 4.6 +/- 0.5 mg x kg(-1) x min(-1)) modestly increased. In INF, NHGU was consistently lower at each insulin step (1.1 +/- 0.5 to 2.6 +/- 0.5 to 2.8 +/- 0.7 mg x kg(-1) x min(-1)). Although NHGU increased from the first to the second step in INF, it did not increase further with the highest dose of insulin. Despite increases in NHGU, net hepatic lactate release did not increase in SHAM and fell in INF. In summary, in the TPN-adapted state, liver glucose uptake is unresponsive to increases in insulin above the basal level. Although the infection-induced increase in insulin sustains NHGU, further increments in insulin enhance neither NHGU nor glycolysis.
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12 MeSH Terms
Impact of chronic fructose infusion on hepatic metabolism during TPN administration.
Donmoyer CM, Lacy DB, Zhang Y, Chen SS, McGuinness OP
(2002) Am J Physiol Endocrinol Metab 283: E1151-8
MeSH Terms: Alanine, Animals, Blood Glucose, Catheterization, Dogs, Escherichia coli Infections, Fatty Acids, Nonesterified, Fructose, Glucagon, Glucose, Hemodynamics, Hepatic Artery, Hormones, Infusions, Intravenous, Insulin, Lactic Acid, Liver, Parenteral Nutrition, Total, Peritonitis, Portal Vein, Time, Vena Cava, Inferior
Show Abstract · Added December 10, 2013
During chronic total parenteral nutrition (TPN), net hepatic glucose uptake (NHGU) is markedly elevated. However, NHGU is reduced by the presence of an infection. We recently demonstrated that a small, acute (3-h) intraportal fructose infusion can correct the infection-induced impairment in NHGU. The aim of this study was to determine whether the addition of fructose to the TPN persistently enhances NHGU in the presence of an infection. TPN was infused continuously into the inferior vena cava of chronically catheterized dogs for 5 days. On day 3, a bacterial clot was implanted in the peritoneal cavity, and either saline (CON, n = 5) or fructose (+FRUC, 1.0 mg. kg(-1). min(-1), n = 6) infusion was included with the TPN. Forty-two hours after the infection was induced, hepatic glucose metabolism was assessed in conscious dogs with arteriovenous and tracer methods. Arterial plasma glucose concentration was lower with chronic fructose infusion (120 +/- 4 vs. 131 +/- 3 mg/dl, +FRUC vs. CON, P < 0.05); however, NHGU was not enhanced (2.2 +/- 0.5 vs. 2.8 +/- 0.4 mg. kg(-1). min(-1)). Acute removal of the fructose infusion dramatically decreased NHGU (2.2 +/- 0.5 to -0.2 +/- 0.5 mg. kg(-1). min(-1)), and net hepatic lactate release also fell (1.6 +/- 0.3 to 0.5 +/- 0.3 mg. kg(-1). min(-1)). This led to an increase in the arterial plasma glucose (Delta13 +/- 3 mg/dl, P < 0.05) and insulin (Delta5 +/- 2 micro U/ml) concentrations and to a decrease in glucagon (Delta-11 +/- 3 pg/ml) concentration. In conclusion, the addition of chronic fructose infusion to TPN during infection does not lead to a persistent augmentation of NHGU.
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22 MeSH Terms