5. Carbohydrates - ESPEN

1 5. CarbohydratesMETHODSL iterature SearchMedline search, Pub-Med : publications from 1983 to February of publications: papers, meta-analysesand Words: children, PN, Glucose, carbohydrate ,energy-resource, : English and are the main source of energy in nutri-tion and usually provide 40 60% of the energy supply inwestern diets. The majority of the carbohydrate derivedfrom a normal diet reaches the body s peripheral tissuesas glucose. Glucose is utilised by all cells and serves asmetabolic fuel for muscle, liver, heart, kidneys and gutand as the obligate energy source for brain, renal medullaand erythrocytes. Glucose is the main carbohydrate uti-lised during foetal life; about 7 g/kg per day (approxi-mately 5 mg/kg per minute) of glucose crosses theplacenta in the last trimester of major source of non-protein calories in paren-teral nutrition (PN) is D-Glucose (dextrose), which is pro-vided in the monohydrate form for intravenous usually contributes most of the osmolality ofthe PN considering the consequences of excessive glucoseintake during PN, and by taking into account the rate ofglucose production and oxidation, it is possible to esta-blish recommendations.

2 Energy provision during PNincludes the use of intravenous fat emulsions (IVFE) (seeLipids chapter). IVFE provide a concentrated source ofcalories with a low osmotic load ( kcal/ml for a 20%emulsion, compared to about kcal/ml for a 20% dex-trose solution). The optimal glucose/lipid ratio remainsto be defined. Glucose tolerance may be influenced bycyclical PN, metabolic status, acute illness and alwaysrequires careful of Overfeeding with GlucoseIn the past, PN for adults, children and infants pro-vided most of the energy as glucose, although it wasnot precisely known how much of the intravenously-administered glucose was glucose is administered in excess of the amountthat can be directly oxidized for energy production andglycogen, the excess is directed to lipogenesis thus pro-moting fat deposition (1,2).

3 Restoration of fat stores maybe a nutritional goal in patients with severe malnutrition,however excessive fat deposition may be the situation, this conversion into lipids ac-counts, in part, for the increase in energy expenditureobserved with high rates of glucose infusion (3).Excessive glucose intake is thought to increase CO2production and minute ventilation but few relevant dataare available to support the clinical relevance (4 6). Totalenergy delivery as well as amino acid intake also con-tribute to increased CO2 production and minute ventila-tion (5,6).Excessive glucose intake may also impair liver func-tion especially by inducing steatosis, while its contribu-tion to the development of cholestasis is not clearlyestablished (7 9).

4 Studies in normal adult volunteerssuggest that high carbohydrate feeding leads to an in-crease in total VLDL triglyceride secretion rate from denovo synthesis, primarily due to stimulation of the secre-tion of preformed fatty acids (FA) (10). These resultsimply that the liver derives it s energy from carbohydrateoxidation rather than from FA oxidation, while FA takenup by the liver are channelled into VLDL triglycerides(10). Hepatic steatosis results when export of the VLDL triglycerides does not keep pace with triglyceride pro-duction (10,11). PN may be associated with insulin re-sistance, due to both the substrate infusion and theunderlying disease (12,13).

5 Protein metabolism is influenced by the composition ofenergy intake in patients on PN (14 17). Lipid emulsionallows the energy input to be diversified, with a reductionin the consequences of excessive glucose supply. In adults,as well as in paediatric patients, the use of IVFE and/or thereduced glucose intake was shown to improve net nitrogenbalance (14 17).PN is associated with an increased risk of infectiouscomplications compared with enteral feeding or no nutri-tional support. The most recent and largest meta-analysisof 27 studies in 1828 adult surgical patients confirmedthat enteral feeding does carry a lower infective riskthan PN, but at the cost of a non-significant trend to-wards increased complications.

6 Overall, enteral feedingdid not reduce mortality compared to PN (18). However,Journal of Pediatric Gastroenterology and Nutrition41:S28 S32 November 2005 ESPGHAN. Reprinted with to prescribe PN for malnourished patients whoare unable to tolerate enteral feeds triples their risk ofdeath (19).Animal data suggests that hyperglycaemia might bea risk factor for infection. Hyperglycaemia in an animalmodel reduces the ability of lung macrophages to fightinfection (20). Animal data suggests that infection re-duces non-hepatic glucose utilisation and causes hyper-insulinism (21). High blood glucose levels in adult ICUpatients are associated with increased infectious-relatedmortality (22).

7 Rate of Endogenous Glucose Productionand Rate of Glucose OxidationThe efficiency with which glucose is used to meetenergy needs should guide its relative contribution to PNregimens. Exogenous glucose delivered in excess of therate of glucose oxidation may enter non-oxidative path-ways and is unlikely to improve energy majority of quantitative estimates of productionand oxidation of glucose have been performed using sta-ble isotopic tracers and indirect calorimetry in newborns,while only few studies are available for infants and chil-dren. Basal rate of glucose production (RGP) varies from2 mg/kg per min in adults, to 8 mg/kg per min in pre-term infants (or from 3 g/kg per day to g/kg perday) (23 26).

8 The RGP is maximal during the post natalperiod and decreases gradually with provides a significant amount ofglucose, and is responsible for about 31% rate of glucoseappearance in healthy full term newborns (23). A clinicaltrial of 20 preterm infants on PN (25) showed that theseinfants maintain normoglycaemia by glucose producedvia gluconeogenesis as a result of glycerol delivery fromfat metabolism. This suggests that not all the glucose hasto be provided exogenously (25).During PN, the rate of parenteral glucose deliverymust be kept constant without exceeding the maximumrate of glucose oxidation (RGO), which differssignificantly among patients according to their age andclinical status.

9 During high rates of glucose infusion,there is a complete suppression of endogenous pro-duction of glucose, accompanied by hyperinsulinism anda respiratory quotient equal to A linear relationshipwas shown in newborns between glucose intake andglucose utilization, measured by indirect calorimetry andglucose oxidation measured by stable isotopic tracers (24).In appropriate for gestational age-preterm infants, theRGO does not exceed 6 to 8 mg/kg per min ( g/kg perday) after birth (27,28) while in term surgical infantsor infants on long-term PN, the maximal RGO is about12 mg/kg per min (18 g/kg per day) (29,30). A study incritically burned children, demonstrated the maximalRGO to be 5 mg/kg per min, which is below caloricrequirements (31).

10 The clinical approach is probably toexercise restraint in the delivery of glucose in criticallyill children. While estimations of caloric requirementfor children often include a component to support growth,this may not be a reasonable goal in a child receivingacute care for severe injury or illness. Except for preterminfants, one could consider that maximal RGO is con-tinuously decreasing from birth to adulthood taking intoaccount the brain to total body weight ratio and the brainglucose glucose intake should be adapted to age andclinical situation premature babies, infants andchildren, critically ill patients and severe Excessive glucose intake may be responsible 1 Excessive glucose intake causes increased lipo-genesis and fat tissue deposition together withsubsequent liver steatosis and enhanced produc-tion of VLDL triglycerides by the 2-3 Excessive glucose intake causes increased CO2production and minute 3 Excessive glucose intake causes impaired 2-3 High blood glucose levels have been shown, inadult ICU patients.