Dextrose Energy Metabolism -
Simple sugars can raise blood sugar levels very quickly, and they often lack nutritional value. Examples of other simple sugars include glucose , fructose, and galactose. Products that are typically made of simple sugars include refined sugar, white pasta, and honey. Dextrose is used to make several intravenous IV preparations or mixtures, which are available only at a hospital or medical facility.
Dextrose is also available as an oral gel or in oral tablet form over the counter from pharmacies. Each dextrose concentration has its own unique uses. Dextrose is used in various concentrations for different purposes.
For example, a doctor may prescribe dextrose in an IV solution when someone is dehydrated and has low blood sugar. Dextrose IV solutions can also be combined with many drugs, for IV administration. Dextrose is a carbohydrate. Solutions containing dextrose provide calories and may be given intravenously in combination with amino acids and fats.
High-concentration dextrose injections are only given by professionals. These injections are administered to people whose blood sugar may be very low and who cannot swallow dextrose tablets, foods, or drinks. If your potassium levels are too high hyperkalemia , sometimes doctors also give dextrose injections of 50 percent, followed by insulin intravenously.
This may be done in the hospital setting. When cells take in extra glucose, they also take in potassium. The dextrose is given to prevent hypoglycemia, while the insulin is treating the elevated potassium. People with diabetes or hypoglycemia chronically low blood sugar may carry dextrose gel or tablets in case their blood sugar gets too low.
Examples of low blood sugar symptoms include weakness, confusion, sweating, and elevated heart rate. A medical professional should not give dextrose to people with certain kinds of medical conditions.
This is because the dextrose could potentially cause too-high blood sugar or fluid shifts in the body that lead to swelling or fluid buildup in the lungs.
If you are diabetic and your doctor prescribes dextrose oral gel or tablets, these should only be used when you have a low blood sugar reaction. Your doctor or diabetes educator should teach you how to spot the signs of low blood sugar and when to use the tablets.
If you need to have the gel or tablets on hand, you should keep them with you at all times. Your doctor should also explain to other family members when to use the gel or tablets, in case others need to give them to you.
If you have an allergy to corn, you could have an allergic reaction to IV dextrose. Talk to your doctor before using it. You can check your blood sugar with home tests. They involve testing blood from a finger prick on a blood strip. If you do find that you or someone else is having a negative reaction due to low blood sugar, the dextrose tablets should be taken immediately.
According to the Joslin Diabetes Center , four glucose tablets are equal to 15 grams of carbs and can be taken in the case of low blood sugar levels unless otherwise advised by your doctor.
Chew the tablets thoroughly before swallowing. No water is needed. Your symptoms should improve within 20 minutes. The dextrose gel often comes in single-serving tubes. If your blood sugar is still too low after an additional 10 minutes, contact your doctor. Dextrose can be used in children similarly to how it is used in adults, as a medical intervention for hypoglycemia.
In cases of severe pediatric hypoglycemia, children will often be given dextrose intravenously. Prompt and early treatment in children and infants with hypoglycemia is essential, as untreated hypoglycemia can result in neurological damage.
In the case of neonatal hypoglycemia, which can be caused by several disorders such as metabolism defects or hyperinsulinism, infants can have small amounts of dextrose gel added to their diet to help them maintain healthy blood sugar levels. Consult your doctor for how much dextrose to add to their diet.
Infants that were born prematurely are at risk for hypoglycemia, and may be given dextrose via an IV. Dextrose is naturally calorie-dense and easy for the body to break down for energy. Because of this, dextrose powder is available and sometimes used as a nutritional supplement by bodybuilders who are looking to increase weight and muscle.
Dextrose should be carefully given to people who have diabetes, because they might not be able to process dextrose as quickly as would someone without the condition. If you need to use dextrose, your blood sugar could increase too much afterward. You should test your blood sugar after using dextrose tablets, as directed by your doctor or diabetes educator.
You may need to adjust your insulin to lower your blood sugar. If you are given IV fluids with dextrose in the hospital, a nurse will check your blood sugar.
If the blood sugar tests too high, the dose of your IV fluids may be adjusted or even stopped, until your blood sugar reaches a safer level. You could also be given insulin, to help reduce your blood sugar.
It is safe to use long term on an as-needed basis. Dextrose does not come without risks, however, and even those without diabetes should carefully monitor their blood sugar when taking it.
Always consult a doctor before stopping treatment for diabetes, or if you test your blood sugar and it is high. If you have glucose gel or tablets in your home, keep them away from children. Large amounts taken by small children could be especially dangerous. Statistical analyses for this study were generated using SAS software version 9.
As shown in Fig. Seventeen subjects were excluded after randomization due to reasons described in Fig. As shown in Table 1 , there were no significant differences in birth weight, GA, Apgar scores, and acuity scores SNAPPE-II between the three groups.
There were no significant differences in baseline pain scores between the three intervention groups Table 2. There were also no significant differences in pain scores in response to heel lance between the three groups Table 2.
Oral dextrose with and without facilitated tucking did not increase plasma markers of ATP metabolism and oxidative stress Table 2. The difference may be due to the metabolism of the fructose moiety of sucrose. Although fructose and dextrose d-glucose have identical chemical formulas, their chemical structure is dissimilar, resulting in distinctions in absorption and metabolism.
Unlike fructose, the metabolism of glucose is highly regulated and dependent on cellular energy demand. If the cellular need for energy is modest, glucose influx is lessened through a reduction in the density of glucose transporters GLUT2 at the plasma membrane, and glucose is diverted away from glycolysis through allosteric inhibition of phosphofructokinase-1 [ 10 ].
This biochemical reaction has been documented in the hepatocytes of children and adults [ 22 ]. It was also shown in premature neonates, where a single dose of oral sucrose given before a clinically required heel lance increased plasma markers of increased ATP degradation [ 5 , 6 ].
These findings suggested that administration of oral sucrose may increase ATP utilization due to the biochemical cost of metabolizing fructose. Our current data suggest that the administration of oral dextrose does not have this effect on ATP utilization.
More recently, the effect of fructose on glucose metabolism was investigated in adipocytes from human Simpson-Golabi-Behmel syndrome [ 23 ]. Glucose metabolism was also shown to be diverted away from glycogenesis, gluconeogenesis, ribose-phosphate synthesis, and nucleotide synthesis [ 23 ].
Instead, glucose was metabolized to lactate and diverted to serine oxidation glycine cleavage pathway SOGC , a pathway utilized for lipogenesis and storage [ 23 ]. The diversion of glucose to the SOGC pathway resulted in lower ATP synthesis due to diminished mitochondrial energy metabolism [ 23 ].
It will be important to determine if this effect occurs in other cell types since fructose is also taken up and metabolized by skeletal muscle cells and renal cortical cells [ 24 , 25 , 26 ]. This finding is different from that previously observed using sucrose.
Formation of ROS may be due to fructose-induced hyperuricemia. While uric acid is documented to be an antioxidant, it can also act as a potent prooxidant molecule [ 25 ]. However, ROS can also be formed when accessible carbonyls of aldehydes or ketones interact with basic amino groups of proteins, or with free hydroxyls found in lipids [ 27 ].
At normal pH and temperature, glucose molecules are found in the stable 6-member glucopyranose ring form, limiting aldehyde exposure, and reducing ROS generation [ 27 ].
However, fructose forms a 5-member fructofuranose ring with two axial hydroxymethyl groups, exposing reactive ketone moiety [ 27 ]. This fructose-generated ROS can lead to cellular damage, especially in the liver, as has been demonstrated in cultured hepatocytes [ 28 ] and in animal models [ 29 ].
Heel lance was documented to result in moderate pain, with pain scores ranging from 8. This is especially important because the long-term effects of repeated administration of sweet solutions like sucrose and dextrose, specifically on organs such as the brain, liver, kidneys, and skeletal muscle, are still unclear.
A study by Johnston et al. In addition, a recent study in neonatal mice showed that repeated exposure to sucrose led to significantly smaller white matter volumes corpus callosum, stria terminalis, and fimbria as well as a significantly smaller hippocampus and cerebellum [ 32 ]. Mice pups that received ten daily doses of sucrose, with nonpainful handling, had significantly poorer short-term memory in adulthood [ 33 ].
Moreover, the effect of sucrose or dextrose on the gastrointestinal system, starting with the mouth, has not been investigated. Does the administration of sweet solutions for pain alter the oral and intestinal microbiome of the premature infant? Because hospitalized neonates are exposed to 7—17 painful procedures per day [ 1 ], leading to potential administration of repeated doses of oral sucrose or dextrose per day, it is important to examine the effect of oral sucrose or oral dextrose on the development of the gastrointestinal microbiome.
This reduces the applicability of findings to critically ill preterm neonates, considered to have SNAPPE-II scores of 37 and above [ 34 ]. An appropriately effective analgesic for critically ill preterm neonates is still not known. Effects of prolonged repeated doses of dextrose on ATP metabolism, oxidative stress, and pain relief are unknown.
In addition, effects of sweet solutions on other biochemical markers, such as markers of inflammation, are not known. Long-term cellular and organ effects of sweet solutions given during the neonatal period are not yet well understood in humans.
Further studies are required to investigate these ubiquitously administered analgesics. Cruz MD, Fernandes AM, Oliveira CR.
Epidemiology of painful procedures performed in neonates: a systematic review of observational studies. Eur J Pain. Article CAS Google Scholar.
Slater L, Asmerom Y, Boskovic DS, Bahjri K, Plank MS, Angeles KR, et al. Procedural pain and oxidative stress in premature neonates. J Pain. Kristoffersen L, Malahleha M, Duze Z, Tegnander E, Kapongo N, Stoen R, et al.
Randomised controlled trial showed that neonates received better pain relief from a higher dose of sucrose during venepuncture. Acta Paediatr. Stevens B, Yamada J, Ohlsson A, Haliburton S, Shorkey A. Sucrose for analgesia in newborn infants undergoing painful procedures. Cochrane Database Syst Rev.
Google Scholar. Asmerom Y, Slater L, Boskovic DS, Bahjri K, Holden MS, Phillips R, et al. Oral sucrose for heel lance increases adenosine triphosphate use and oxidative stress in preterm neonates. J Pediatr. Angeles DM, Asmerom Y, Boskovic DS, Slater L, Bacot-Carter S, Bahjri K, et al.
Oral sucrose for heel lance enhances adenosine triphosphate use in preterm neonates with respiratory distress. SAGE Open Med. Article Google Scholar. Dilen B, Elseviers M. Oral glucose solution as pain relief in newborns: results of a clinical trial. Bueno M, Yamada J, Harrison D, Khan S, Ohlsson A, Adams-Webber T, et al.
A systematic review and meta-analyses of nonsucrose sweet solutions for pain relief in neonates. Pain Res Manag. Mayes PA. Intermediary metabolism of fructose.
Am J Clin Nutr. Liemburg-Apers DC, Imamura H, Forkink M, Nooteboom M, Swarts HG, Brock R, et al. Quantitative glucose and ATP sensing in mammalian cells. Pharm Res. Sundaram B, Shrivastava S, Pandian JS, Singh VP.
Facilitated tucking on pain in pre-term newborns during neonatal intensive care: a single blinded randomized controlled cross-over pilot trial. J Pediatr Rehabil Med.
Obeidat H, Kahalaf I, Callister LC, Froelicher ES. Use of facilitated tucking for nonpharmacological pain management in preterm infants: a systematic review. J Perinat Neonatal Nurs. Reuter S, Moser C, Baack M. Respiratory distress in the newborn. Pediatr Rev. quiz Gibbins S, Stevens BJ, Yamada J, Dionne K, Campbell-Yeo M, Lee G, et al.
Validation of the premature infant pain profile-revised PIPP-R. Early Hum Dev. Freire NB, Garcia JB, Lamy ZC. Evaluation of analgesic effect of skin-to-skin contact compared to oral glucose in preterm neonates. Skogsdal Y, Eriksson M, Schollin J.
Analgesia in newborns given oral glucose. Gradin M, Eriksson M, Holmqvist G, Holstein A, Schollin J. Pain reduction at venipuncture in newborns: oral glucose compared with local anesthetic cream. Plank MS, Calderon TC, Asmerom Y, Boskovic DS, Angeles DM. Biochemical measurement of neonatal hypoxia.
J Vis Exp. Gruber J, Tang SY, Jenner AM, Mudway I, Blomberg A, Behndig A, et al. Allantoin in human plasma, serum, and nasal-lining fluids as a biomarker of oxidative stress: avoiding artifacts and establishing real in vivo concentrations. Antioxid Redox Signal.
Pavitt DV, de Fonseka S, Al-Khalaf N, Cam JM, Reaveley DA. Assay of serum allantoin in humans by gas chromatography-mass spectrometry. Clin Chim Acta. Perheentupa J, Raivio K. Fructose-induced hyperuricaemia.
Mosca A, Nobili V, De Vito R, Crudele A, Scorletti E, Villani A, et al. Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents.
J Hepatol. Varma V, Boros LG, Nolen GT, Chang CW, Wabitsch M, Beger RD, et al. Fructose alters intermediary metabolism of glucose in human adipocytes and diverts glucose to serine oxidation in the one-carbon cycle energy producing pathway.
Jaiswal N, Maurya CK, Arha D, Avisetti DR, Prathapan A, Raj PS, et al. Fructose induces mitochondrial dysfunction and triggers apoptosis in skeletal muscle cells by provoking oxidative stress.
Cirillo P, Gersch MS, Mu W, Scherer PM, Kim KM, Gesualdo L, et al. Ketohexokinase-dependent metabolism of fructose induces proinflammatory mediators in proximal tubular cells.
J Am Soc Nephrol. Andres-Hernando A, Li N, Cicerchi C, Inaba S, Chen W, Roncal-Jimenez C, et al. Protective role of fructokinase blockade in the pathogenesis of acute kidney injury in mice. Nat Commun. Lustig RH. Adv Nutr. Fructose and carbonyl metabolites as endogenous toxins.
Chem Biol Interact. Pickens MK, Yan JS, Ng RK, Ogata H, Grenert JP, Beysen C, et al. Dietary sucrose is essential to the development of liver injury in the methionine-choline-deficient model of steatohepatitis.
J Lipid Res. Gibbins S, Stevens B, Hodnett E, Pinelli J, Ohlsson A, Darlington G. Efficacy and safety of sucrose for procedural pain relief in preterm and term neonates.
Nurs Res. Johnston CC, Filion F, Snider L, Majnemer A, Limperopoulos C, Walker CD, et al. Tremblay S, Ranger M, Chau CMY, Ellegood J, Lerch JP, Holsti L, et al.
Repeated exposure to sucrose for procedural pain in mouse pups leads to long-term widespread brain alterations. Ranger M, Tremblay S, Chau CMY, Holsti L, Grunau RE, Goldowitz D.
Adverse behavioral changes in adult mice following neonatal repeated exposure to pain and sucrose. Front Psychol. Harsha SS, Archana BR. SNAPPE-II Score for Neonatal Acute Physiology with Perinatal Extension-II in predicting mortality and morbidity in NICU.
J Clin Diagn Res. PubMed PubMed Central Google Scholar. Download references. We thank Yayesh Asmerom, MS, for performing all the purine and allantoin measurements and Desiree Wallace, PharmD, for providing the study drug and assisting with the randomization of subjects.
Department of Basic Sciences, School of Medicine, Loma Linda University, Loma Linda, CA, USA. Danilyn M. Angeles, Danilo S. Boskovic, John C. Department of Pediatrics, School of Medicine, Loma Linda University, Loma Linda, CA, USA. Angeles, Raylene M.
We strongly recommend that Calorie intake and metabolism boosting foods Vegan quinoa recipes the Myth vs reality in nutrition at Dexhrose 2 Carbohydrate loading and pre-competition meals Metabopism before you depart on your activity. Dextro Energy Tablets provide Metabolizm energy if the body Calorie intake and metabolism boosting foods an extra boost to maintain performance during training, Enetgy and other periods of high energy output. The tablets immediately increases performance ability as the dextrose, in handy dose form, provides immediate energy in performance peaks. Dextrose is a monosaccharide which does not need to be digested. It enters the bloodstream immediately and provides the muscles and brain cells with immediate energy. Dextrose is, therefore, an easily and quickly available source of energy. Additional vitamins: the Dextrose Tablets also include three vitamins — vitamins B1, B6 and C and the mineral magnesium.Dextrose Energy Metabolism -
After a carbohydrate-rich meal, blood glucose concentration rises sharply and a massive amount of glucose is taken up by hepatocytes by means of GLUT2. This type of transporter has very low affinity for glucose and is effective only when glucose concentration is high.
Thus, during the fed state the liver responds directly to blood glucose levels by increasing its rate of glucose uptake. In addition to being the main source of energy, glucose is utilized in other pathways, such as glycogen and lipid synthesis by hepatocytes. The whole picture becomes far more complex when we consider how hormones influence our energy metabolism.
Fluctuations in blood levels of glucose trigger secretion of the hormones insulin and glucagon. How do such hormones influence the use of fuel molecules by the various tissues? Demands by one cell type can be met by the consumption of its own reserves and by the uptake of fuel molecules released in the bloodstream by other cells.
Energy use is tightly regulated so that the energy demands of all cells are met simultaneously. Elevated levels of glucose stimulate pancreatic β-cells to release insulin into the bloodstream.
Virtually all cells respond to insulin; thus, during the fed state cell metabolism is coordinated by insulin signaling. Figure 3: Blood glucose concentration after carbohydrate-rich and carbohydrate-poor meals.
An extraordinary example is how insulin signaling rapidly stimulates glucose uptake in skeletal muscle and adipose tissue and is accomplished by the activity of GLUT4. In the absence of insulin, these transporters are located inside vesicles and thus do not contribute to glucose uptake in skeletal muscle and adipose tissue.
Insulin, however, induces the movement of these transporters to the plasma membrane, increasing glucose uptake and consumption. As different tissues continue to use glucose, the blood glucose concentration tends to reach the pre-meal concentration Figure 3.
This, in turn, decreases the stimulus for insulin synthesis and increases the stimulus for the release of glucagon, another hormone secreted by the α-pancreatic cells. Therefore, during fasting, cell metabolism is coordinated by glucagon signaling and the lack of insulin signaling.
As a consequence, GLUT4 stays inside vesicles, and glucose uptake by both skeletal muscle cells and adipocytes is reduced. Now, with the low availability of glucose and the signals from glucagon, those cells increase their use of fatty acids as fuel molecules.
Therefore, the use of fatty acids during fasting clearly contributes to the maintenance of adequate blood glucose concentration to meet the demands of cells that exclusively or primarily rely on glucose as a fuel.
But, mentioned above, glucose is used at an apparently high rate by the brain and constantly by red blood cells. And, under physiological conditions, blood glucose is maintained at a constant level, even during fasting.
How, then, is that delicate balance achieved? The liver is a very active organ that performs different vital functions. In Greek mythology, Prometheus steals fire from Zeus and gives it to mortals. As a punishment, Zeus has part of Prometheus's liver fed to an eagle every day. Since the liver grows back, it is eaten repeatedly.
This story illustrates the high proliferative rate of liver cells and the vital role of this organ for human life. One of its most important functions is the maintenance of blood glucose. The liver releases glucose by degrading its glycogen stores. This reserve is not large, and during overnight fasting glycogen reserves fall severely.
However, only the liver supplies the blood with glucose since it has an enzyme that make it possible for glucose molecules to be transported across cell membranes.
Since glycogen stores are limited and are reduced within hours of fasting, and blood glucose concentration is kept within narrow limits under most physiological conditions, another mechanism must exist to supply blood glucose. Indeed, glucose can be synthesized from amino acid molecules.
This process is called de novo synthesis of glucose, or gluconeogenesis. Amino acids, while being degraded, generate several intermediates that are used by the liver to synthesize glucose Figure 2.
Alanine and glutamine are the two amino acids whose main function is to contribute to glucose synthesis by the liver. The kidneys also possess the enzymes necessary for gluconeogenesis and, during prolonged fasting, contribute to some extent to the supply of blood glucose.
Furthermore, since de novo glucose synthesis comes from amino acid degradation and the depletion of protein stores can be life-threatening, this process must be regulated. Insulin, glucagon, and another hormone, glucocorticoid, play important roles in controlling the rate of protein degradation and, therefore, the rate of glucose production by the liver.
Alterations in factors that control food intake and regulate energy metabolism are related to well-known pathological conditions such as obesity, type 2 diabetes and the metabolic syndrome , and some types of cancer. In addition, many effects and regulatory actions of well-known hormones such as insulin are still poorly understood.
The consideration of adipose tissue as a dynamic and active tissue, for instance, raises several important issues regarding body weight and the control of food intake. These factors point to the importance of further studies to expand our understanding of energy metabolism, thereby improving our quality of life and achieving a comprehensive view of how the human body functions.
Cahill, G. Fuel metabolism in starvation. Annual Review of Nutrition 26 , 1—22 Iyer, A. Inflammatory lipid mediators in adipocyte function and obesity. Nature Reviews Endocrinology 6 , 71—82 Kaelin, W. Kodde, I. Metabolic and genetic regulation of cardiac energy substrate preference.
Kresge, N. Otto Fritz Meyerhof and the elucidation of the glycolytic pathway. Journal of Biological Chemisry , e3 Kroemer, G.
Tumor cell metabolism: Cancer's Achilles' heel. Cancer Cell 13 , — Vander Heiden, M. Understanding the Warburg effect: The metabolic requirements of cell proliferation Science 22 , — van der Vusse, G. Critical steps in cellular fatty acid uptake and utilization. Molecular and Cellular Biochemistry , 9—15 What Is a Cell?
Eukaryotic Cells. Cell Energy and Cell Functions. Photosynthetic Cells. Cell Metabolism. The Two Empires and Three Domains of Life in the Postgenomic Age. Why Are Cells Powered by Proton Gradients? The Origin of Mitochondria.
Mitochondrial Fusion and Division. Beyond Prokaryotes and Eukaryotes : Planctomycetes and Cell Organization. The Origin of Plastids.
The Apicoplast: An Organelle with a Green Past. The Origins of Viruses. Discovery of the Giant Mimivirus. Volvox, Chlamydomonas, and the Evolution of Multicellularity. Yeast Fermentation and the Making of Beer and Wine. Dynamic Adaptation of Nutrient Utilization in Humans. Nutrient Utilization in Humans: Metabolism Pathways.
An Evolutionary Perspective on Amino Acids. Fatty Acid Molecules: A Role in Cell Signaling. Mitochondria and the Immune Response. Stem Cells in Plants and Animals.
G-Protein-Coupled Receptors, Pancreatic Islets, and Diabetes. Promising Biofuel Resources: Lignocellulose and Algae. The Discovery of Lysosomes and Autophagy.
The Mystery of Vitamin C. The Sliding Filament Theory of Muscle Contraction. Dynamic Adaptation of Nutrient Utilization in Humans By: Tatiana El Bacha, Ph.
Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro , Mauricio R. Luz, Ph. Da Poian, Ph. Instituto de Bioquimica Medica, Universidade Federal do Rio de Janeiro © Nature Education. Citation: El Bacha, T. Nature Education 3 9 Food in, energy out? Aa Aa Aa. Energy Metabolism and ATP Synthesis in Human Cells.
Different Cell Types Require Different Fuel Molecules. The Type of Fuel Molecule Changes according to Cell Function and Physiological Context. Hormones Regulate Cell Metabolism. The Liver Supplies Blood Glucose. References and Recommended Reading Cahill, G. Annual Review of Nutrition 26 , 1—22 Iyer, A.
Nature Reviews Endocrinology 6 , 71—82 Kaelin, W. Journal of Biological Chemisry , e3 Kroemer, G. Cancer Cell 13 , — Vander Heiden, M. Understanding the Warburg effect: The metabolic requirements of cell proliferation Science 22 , — van der Vusse, G.
Article History Close. Share Cancel. Revoke Cancel. The separation was performed using an Agilent —G capillary column Helium was used as the carrier gas at a flow rate of 1. This temperature was maintained until the end of the run.
Allantoin was quantified using selected ion monitoring mode with the The ion abundance ratios The research technician that performed allantoin analysis was blinded to group assignment. Categorical variables were compared with intervention groups using a χ 2 test and continuous variables using a t -test.
Repeated-measures ANOVA was utilized to evaluate the effects of interventions on plasma purines and allantoin concentrations over time, with main effects of intervention group, time, and intervention group by time interactions.
Separate models were fit for each outcome. The intervention effect was defined as a significant interaction effect between intervention group and time. Correlations between purines, allantoin, and biobehavioral markers i.
Statistical analyses for this study were generated using SAS software version 9. As shown in Fig. Seventeen subjects were excluded after randomization due to reasons described in Fig. As shown in Table 1 , there were no significant differences in birth weight, GA, Apgar scores, and acuity scores SNAPPE-II between the three groups.
There were no significant differences in baseline pain scores between the three intervention groups Table 2. There were also no significant differences in pain scores in response to heel lance between the three groups Table 2. Oral dextrose with and without facilitated tucking did not increase plasma markers of ATP metabolism and oxidative stress Table 2.
The difference may be due to the metabolism of the fructose moiety of sucrose. Although fructose and dextrose d-glucose have identical chemical formulas, their chemical structure is dissimilar, resulting in distinctions in absorption and metabolism.
Unlike fructose, the metabolism of glucose is highly regulated and dependent on cellular energy demand. If the cellular need for energy is modest, glucose influx is lessened through a reduction in the density of glucose transporters GLUT2 at the plasma membrane, and glucose is diverted away from glycolysis through allosteric inhibition of phosphofructokinase-1 [ 10 ].
This biochemical reaction has been documented in the hepatocytes of children and adults [ 22 ]. It was also shown in premature neonates, where a single dose of oral sucrose given before a clinically required heel lance increased plasma markers of increased ATP degradation [ 5 , 6 ].
These findings suggested that administration of oral sucrose may increase ATP utilization due to the biochemical cost of metabolizing fructose.
Our current data suggest that the administration of oral dextrose does not have this effect on ATP utilization. More recently, the effect of fructose on glucose metabolism was investigated in adipocytes from human Simpson-Golabi-Behmel syndrome [ 23 ].
Glucose metabolism was also shown to be diverted away from glycogenesis, gluconeogenesis, ribose-phosphate synthesis, and nucleotide synthesis [ 23 ]. Instead, glucose was metabolized to lactate and diverted to serine oxidation glycine cleavage pathway SOGC , a pathway utilized for lipogenesis and storage [ 23 ].
The diversion of glucose to the SOGC pathway resulted in lower ATP synthesis due to diminished mitochondrial energy metabolism [ 23 ].
It will be important to determine if this effect occurs in other cell types since fructose is also taken up and metabolized by skeletal muscle cells and renal cortical cells [ 24 , 25 , 26 ].
This finding is different from that previously observed using sucrose. Formation of ROS may be due to fructose-induced hyperuricemia. While uric acid is documented to be an antioxidant, it can also act as a potent prooxidant molecule [ 25 ].
However, ROS can also be formed when accessible carbonyls of aldehydes or ketones interact with basic amino groups of proteins, or with free hydroxyls found in lipids [ 27 ]. At normal pH and temperature, glucose molecules are found in the stable 6-member glucopyranose ring form, limiting aldehyde exposure, and reducing ROS generation [ 27 ].
However, fructose forms a 5-member fructofuranose ring with two axial hydroxymethyl groups, exposing reactive ketone moiety [ 27 ]. This fructose-generated ROS can lead to cellular damage, especially in the liver, as has been demonstrated in cultured hepatocytes [ 28 ] and in animal models [ 29 ].
Heel lance was documented to result in moderate pain, with pain scores ranging from 8. This is especially important because the long-term effects of repeated administration of sweet solutions like sucrose and dextrose, specifically on organs such as the brain, liver, kidneys, and skeletal muscle, are still unclear.
A study by Johnston et al. In addition, a recent study in neonatal mice showed that repeated exposure to sucrose led to significantly smaller white matter volumes corpus callosum, stria terminalis, and fimbria as well as a significantly smaller hippocampus and cerebellum [ 32 ].
Mice pups that received ten daily doses of sucrose, with nonpainful handling, had significantly poorer short-term memory in adulthood [ 33 ]. Moreover, the effect of sucrose or dextrose on the gastrointestinal system, starting with the mouth, has not been investigated.
Does the administration of sweet solutions for pain alter the oral and intestinal microbiome of the premature infant? Because hospitalized neonates are exposed to 7—17 painful procedures per day [ 1 ], leading to potential administration of repeated doses of oral sucrose or dextrose per day, it is important to examine the effect of oral sucrose or oral dextrose on the development of the gastrointestinal microbiome.
This reduces the applicability of findings to critically ill preterm neonates, considered to have SNAPPE-II scores of 37 and above [ 34 ]. An appropriately effective analgesic for critically ill preterm neonates is still not known. Effects of prolonged repeated doses of dextrose on ATP metabolism, oxidative stress, and pain relief are unknown.
In addition, effects of sweet solutions on other biochemical markers, such as markers of inflammation, are not known. Long-term cellular and organ effects of sweet solutions given during the neonatal period are not yet well understood in humans. Further studies are required to investigate these ubiquitously administered analgesics.
Cruz MD, Fernandes AM, Oliveira CR. Epidemiology of painful procedures performed in neonates: a systematic review of observational studies. Eur J Pain. Article CAS Google Scholar. Slater L, Asmerom Y, Boskovic DS, Bahjri K, Plank MS, Angeles KR, et al.
Procedural pain and oxidative stress in premature neonates. J Pain. Kristoffersen L, Malahleha M, Duze Z, Tegnander E, Kapongo N, Stoen R, et al. Randomised controlled trial showed that neonates received better pain relief from a higher dose of sucrose during venepuncture. Acta Paediatr. Stevens B, Yamada J, Ohlsson A, Haliburton S, Shorkey A.
Sucrose for analgesia in newborn infants undergoing painful procedures. Cochrane Database Syst Rev. Google Scholar. Asmerom Y, Slater L, Boskovic DS, Bahjri K, Holden MS, Phillips R, et al.
Oral sucrose for heel lance increases adenosine triphosphate use and oxidative stress in preterm neonates. J Pediatr. Angeles DM, Asmerom Y, Boskovic DS, Slater L, Bacot-Carter S, Bahjri K, et al.
Oral sucrose for heel lance enhances adenosine triphosphate use in preterm neonates with respiratory distress. SAGE Open Med. Article Google Scholar. Dilen B, Elseviers M. Oral glucose solution as pain relief in newborns: results of a clinical trial.
Bueno M, Yamada J, Harrison D, Khan S, Ohlsson A, Adams-Webber T, et al. A systematic review and meta-analyses of nonsucrose sweet solutions for pain relief in neonates. Pain Res Manag. Mayes PA. Intermediary metabolism of fructose.
Am J Clin Nutr. Liemburg-Apers DC, Imamura H, Forkink M, Nooteboom M, Swarts HG, Brock R, et al. Quantitative glucose and ATP sensing in mammalian cells. Pharm Res. Sundaram B, Shrivastava S, Pandian JS, Singh VP. Facilitated tucking on pain in pre-term newborns during neonatal intensive care: a single blinded randomized controlled cross-over pilot trial.
J Pediatr Rehabil Med. Obeidat H, Kahalaf I, Callister LC, Froelicher ES. Use of facilitated tucking for nonpharmacological pain management in preterm infants: a systematic review. J Perinat Neonatal Nurs. Reuter S, Moser C, Baack M.
Respiratory distress in the newborn. Pediatr Rev. quiz Gibbins S, Stevens BJ, Yamada J, Dionne K, Campbell-Yeo M, Lee G, et al. Validation of the premature infant pain profile-revised PIPP-R.
Early Hum Dev. Freire NB, Garcia JB, Lamy ZC. Evaluation of analgesic effect of skin-to-skin contact compared to oral glucose in preterm neonates. Skogsdal Y, Eriksson M, Schollin J. Analgesia in newborns given oral glucose.
Gradin M, Eriksson M, Holmqvist G, Holstein A, Schollin J. Pain reduction at venipuncture in newborns: oral glucose compared with local anesthetic cream. Plank MS, Calderon TC, Asmerom Y, Boskovic DS, Angeles DM.
Biochemical measurement of neonatal hypoxia. J Vis Exp. Gruber J, Tang SY, Jenner AM, Mudway I, Blomberg A, Behndig A, et al. Allantoin in human plasma, serum, and nasal-lining fluids as a biomarker of oxidative stress: avoiding artifacts and establishing real in vivo concentrations.
Antioxid Redox Signal. Pavitt DV, de Fonseka S, Al-Khalaf N, Cam JM, Reaveley DA. Assay of serum allantoin in humans by gas chromatography-mass spectrometry. Clin Chim Acta. Perheentupa J, Raivio K. Fructose-induced hyperuricaemia. Mosca A, Nobili V, De Vito R, Crudele A, Scorletti E, Villani A, et al.
Serum uric acid concentrations and fructose consumption are independently associated with NASH in children and adolescents. J Hepatol. Varma V, Boros LG, Nolen GT, Chang CW, Wabitsch M, Beger RD, et al. Fructose alters intermediary metabolism of glucose in human adipocytes and diverts glucose to serine oxidation in the one-carbon cycle energy producing pathway.
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