Content uploaded by Linda Nebeling
Author content
All content in this area was uploaded by Linda Nebeling
Content may be subject to copyright.
A preview of the PDF is not available
Effects of a Ketogenic Diet on Tumor Metabolism and Nutritional Status in Pediatric Oncology Patients: Two Case Reports
Abstract
Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient's overall nutritional status.
Case report.
University Hospitals of Cleveland.
Two female pediatric patients with advanced stage malignant Astrocytoma tumors.
Patients were followed as outpatients for 8 weeks. Ketosis was maintained by consuming a 60% medium chain triglyceride oil-based diet.
Tumor glucose metabolism was assessed by Positron Emission Tomography (PET), comparing [Fluorine-18] 2-deoxy-2-fluoro-D-glucose (FDG) uptake at the tumor site before and following the trial period.
Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression.
While this diet does not replace conventional antineoplastic treatments, these preliminary results suggest a potential for clinical application which merits further research.
... During the research, one of the patients experienced a substantial improvement in her clinical condition, which prompted her to decide to extend the KD by an additional year. She was not afflicted by any further progression of the disease during this time frame [57], which encompasses the period in question. ...
... As emerged from the first study, conducted on pediatric patients, food intake, quantified by dietary history, even improved during the ketogenic diet phase, satisfying the nutritional and energy needs of the enrolled subjects. This demonstrated that the ketogenic diet does not necessarily affect the nutritional status of the subjects [57] Moreover, regarding the quality of life, Martin-McGill et al. found an improvement on the part of the subjects involved through the administration of validated questionnaires [67]. An important argument about quality of life in this particular disease has been conducted by Sargaço et al. [12]: the level of quality of life of each patient is strictly related to factors other than KD, such as the stage of the disease, general well-being, symptoms of the disease and of adverse events coming from chemoradiotherapy, and the patient's response to therapy. ...
Recent scientific research has shown that the ketogenic diet may have potential benefits in a variety of medical fields, which has led to the diet receiving a substantial amount of attention. Clinical and experimental research on brain tumors has shown that the ketogenic diet has a satisfactory safety profile. This safety profile has been established in a variety of applications, including the management of obesity and the treatment of drug-resistant epileptic cases. However, in human studies, the impact of ketogenic therapy on the growth of tumors and the life expectancy of patients has not provided results that are well characterized. Consequently, our purpose is to improve the comprehension of these features by succinctly presenting the developments and conclusions that have been gained from the most recent study that pertains to this non-pharmacological technique. According to the findings of our study, patients with brain tumors who stick to a ketogenic diet are more likely to experience improved survival rates. However, it is required to conduct additional research on humans in order to more accurately define the anti-tumor efficiency of this diet as well as the underlying processes that support the therapeutic effects of this dieting regimen.
... The ketogenic diet (KD), also known as ketogenic metabolic therapy (KMT), is defined by the inclusion of fat-rich foods with the exclusion of carbohydrate-rich foods. Together, this diet alteration was the initial attempt to alleviate the potential burden of hyperglycemia for malignant brain cancer (107). Due to the lack of sugars in the diet, the intent was to induce ketone body use for energy rather than glucose, which would mitigate the impact of the Warburg effect. ...
... flurodeoxyglucose showed a significant reduction in glucose uptake (107). ...
The study of the relationship between cancer and diabetes mellitus (DM) has been under investigation for many decades. Particularly in the field of neurology and neurosurgery, increasing emphasis has been put on the examination of comorbid DM in patients with cranial tumors. Namely, as the most common and invasive type of malignant adult brain tumor, glioblastoma (GBS) has been the focus of said research. Several mechanisms have been described in the attempt to elucidate the underlying association between DM and GBS, with the metabolic phenomenon known as the Warburg effect and its consequential downstream effects serving as the resounding culprits in recent literature. Since the effect seen in cancers like GBS exploits an upregulated form of aerobic glycolysis, the role of a sequela of DM, known as hyperglycemia, will be investigated. In particular, in the treatment of GBS, surgical resection and subsequent chemotherapy and/or radiotherapy are used in conjunction with corticosteroid therapy, the latter of which has been linked to hyperglycemia. Unsurprisingly, comorbid DM patients are significantly susceptible to this disposition. Further, this fact is reflected in recent literature that demonstrates the impact of hyperglycemia on cancer advancement and patient outcomes in several preclinical and clinical studies. Thus, this review will aim to underline the significance of diabetes and glycemic control via standard-of-care treatments such as metformin administration, as well as to describe emerging treatments such as the signaling modulation of insulin-like growth factor and the employment of the ketogenic diet.
... Practically, three variables can be obtained as a result of the implementation of this diet: having an antitumor effect and helping to improve the quality of life of patients, having adverse effects although in clinical trials there are no records of serious adverse effects, or having no significant effect on tumor growth (Weber et al., 2020). Some of the reports described in recent articles documented the case of 2 pediatric female patients with malignant astrocytoma already in the advanced stages of the disease, KD was introduced into the diet of both children for 2 months, imaging studies were performed, it was documented that 7 days after the implementation of the diet, blood glucose levels decreased while ketone bodies were elevated and an improvement in mood and quality of life was observed (Nebeling et al., 1995). ...
... Delayed tumor growth compared to the SD group. Nebeling et al., (1995). ...
This book contains seven chapters that present research on the ketogenic diet and its roles in neuroscience and cancer. Chapter one highlights the roles of the ketogenic diet in neuroprotection and biochemical processes involved in the control of epilepsy. Chapter two reviews the use of the ketogenic diet, a low-carb, high-fat regimen, as an adjuvant treatment for neurological diseases such as Parkinson’s disease. Chapter three discusses how the antioxidant properties of the ketogenic diet might benefit patients by potentially ameliorating the harmful consequences of Alzheimer’s disease. Chapter four examines abnormalities in the different molecular components of the GABAergic system in neuropsychiatric disorders as well as the beneficial effects the ketogenic diet on them. Chapters five and six discuss the ketogenic diet’s role in cancer prevention and neuroglia. Chapter 7 presents the effect of the ketogenic diet on NKCC1 cotransporter regional expression.
... CNS tumours have aberrant cancer metabolism, which could be harnessed clinically in a number of ways. Firstly, it potentially offers a novel means to treat cancers [for example by the ketogenic diet (6,7), or by therapeutic arginine depletion through consuming arginase to deplete extracellular arginine, to counter auxotrophism (8,9)] ( Figure 1). Secondly, it offers a potential means to monitor the presence of the cancer during and following treatment (i.e. ...
Central nervous system (CNS) tumours are the most common cancer cause of death in under 40s in the UK, largely because they persist and recur and sometimes metastasise during treatment. Therefore, longitudinal monitoring of patients during and following treatment must be undertaken to understand the course of the disease and alter treatment plans reactively. This monitoring must be specific, sensitive, rapid, low cost, simple, and accepted by the patient. Cerebrospinal fluid (CSF) examination obtained following lumbar puncture, already a routine part of treatment in paediatric cases, could be better utilised with improved biomarkers. In this review, we discuss the potential for metabolites in the CSF to be used as biomarkers of CNS tumour remission, progression, response to drugs, recurrence and metastasis. We confer the clinical benefits and risks of this approach and conclude that there are many potential advantages over other tests and the required instrumentation is already present in UK hospitals. On the other hand, the approach needs more research investment to find more metabolite biomarkers, better understand their relation to the tumour, and validate those biomarkers in a standardised assay in order for the assay to become a clinical reality.
... Ketogenic metabolic therapy consists of a high-fat and low-carbohydrate diet aimed at reducing glucose levels and facilitating a physiological state of systemic ketosis. Thus far, studies have included small sample sizes without enough statistical power to characterize the efficacy of the ketogenic diet sufficiently [73,74]. Furthermore, survival endpoints were not directly examined to evaluate the causal or additive efficacy of dietary interventions. ...
Opinion Statement
As the peak incidence of isocitrate dehydrogenase (IDH)-mutant gliomas is amongst young adults, there is a need to balance tumor control with long term side effects of therapy. Following initial clinical presentation and acquisition of contrasted diagnostic imaging, tissue diagnosis is essential in suspected diffuse glioma. Depending on the location and extent of disease, maximal surgical resection is preferred both for histologic diagnosis and initial therapy. Partial resection or biopsy alone is considered when the tumor cannot be completely resected or if there are clinical reservations regarding a more significant operation. The classification of diffuse glioma has evolved over time, with histopathology and molecular marker status guiding discussions of prognosis and postoperative management. In patients with IDH-mutant grade 2 glioma and low-risk features, observation with active surveillance is generally recommended following a gross total resection. For those with high-risk features, which historically included age > 40 years or subtotal resection, adjuvant chemotherapy and radiation therapy are generally recommended, however decisions for adjuvant therapy pose challenges as many of the landmark historical trials guiding adjuvant therapy were performed prior to the molecularly defined era. This is an area where multiple clinical trials are ongoing and hold promise to inform treatment paradigms, including recent data on the use of IDH-mutant inhibitors in grade 2 tumors with recurrent or residual disease. For IDH-mutant grade 3 and 4 glioma, adjuvant chemotherapy and radiation are recommended for all patients after initial resection.
... Furukawa et al. (2018) administered chemotherapy in combination with the modified ketogenic diet for one year in 10 patients with colon cancer and found the ketogenic diet exhibited a response rate of 60% and control of disease by 70% in cancer patient. Nebeling et al. (1995) demonstrated a 21.8% decrease in tumor standardized uptake value. Additionally, the ketogenic diet has demonstrated a high level of safety and tolerability, as well as an improvement in overall quality of life (Kim 2017). ...
Mixed invasive ductal and lobular carcinoma (Mi-DLC) is a subtype of breast cancer having both ductal and lobular morphology. The coexistence of both morphologies together is not sufficiently addressed in earlier research, so the metastatic behavior of Mi-DLC is not known to healthcare professionals. We introduce the mathematical model to analyze the metastatic behavior of Mi-DLC for controlling the proliferation of tumors. Breast cancer is highly sensitive to estrogen receptors. We incorporate estrogen in the competition among the population of healthy cells, lobular cells, ductal cells, and immune cells. The ketogenic diet sensitizes cancer cells and alters their metabolism. We obtain the increase in the ketogenic diet with the use of anticancer drugs in humans, resulting in a stable cancer-free equilibrium state. We find that the immune response of humans is incapable of fighting the disease when the initial volume of Mi-DLC is high and the ketogenic diet rate is low in the body. The model has four cancer invasion equilibriums: lobular cancer invasion, ductal cancer invasion, mixed ductal and lobular invasion, and dead equilibrium state. We obtain all four cancer invasion equilibriums are stable when we consider the low rate of the ketogenic diet in the body. We calculate that with the proper use of anticancer drugs and a ketogenic diet in humans, the Mi-DLC moves to its dormant stage, and the co-existing equilibrium is stable. The numerical simulation supports the mathematical analysis of the model and establish that the 10% increase in ketogenic diet rate leads to the inhibition of both lobular and ductal tumor cells by 60% and 70%, respectively. The model represents the ketogenic diet with all the other therapies together as the promising adjuvant to inhibit the growth of tumors. The model is helpful in finding the metastatic behavior of Mi-DLC to control the proliferation of tumor cells effectively.
The aim of the present study is to assess if 2-[18F]FDG uptake can be enhanced by subjecting human ADK-LPA derived cell lines and murine models carrying ADK-LPA to a low-glucose intake dietary regimen so to potentially ameliorate the CT/PET sensitivity in human patients.
A dietary regimen envisaging a low glucose uptake (ketogenic diet) and a normal diet were applied to a human ADK-LPA derived cell line (NCI-H358) and to other two lung carcinoma cell lines (A549 and NCI-H1299) for comparison purposes. Cells were afterwards incubated with 2-[18F]FDG. Moreover, the correspondent regimens were enforced on murine models carrying ADK-LPA xenografts to evaluate the influence of the diet on the 2-[18F]FDG biodistribution and visualization upon injection.
As expected, when incubated with glucose-rich medium, NCI-H358 (ADK-LPA) cells have a really low [18F]FDG uptake (up to 4-fold less) compared to A549 and NCI- H1299 cells. On the other hand, when a glucose-depleted medium is used, a significantly enhanced uptake in NCI-H358 cells respect to the other two lines (up to 10-fold higher after 5 days) was obtained. In the PET/CT images, tumors are clearly better visualized in mice subjected to ketogenic diet respect to control group already after 3 days.
The study attested how 2-[18F]FDG uptake in a low glucose dependent tumor, usually not detected by PET/CT, can be controlled in vitro and in murine models by a dietary regimen. The outputs of this study open the way to a possible method to improve the [18F]FDG-PET/CT performances in the detection of ADK-LPA thus laying the foundations of a possible future application in humans.
Plant dietary lipids remain one of the most intriguing and complex classes of biological molecules. Among them, medium-chain triglycerides (MCTs) have garnered recognition for their unique physico-chemical properties and potential health benefits. Despite their classification as saturated fats, they stand apart from other saturated fatty acids due to their distinctive characteristics, positioning them as a valuable component in nutrition. While traditional dietary fats primarily contain long-chain triglycerides (LCTs), MCTs consist of medium-chain fatty acids (MCFAs), naturally found in coconut and palm oils. The structural dissimilarity grants MCTs advantageous attributes, encompassing rapid digestion and absorption, providing a swift source of energy. Importantly, MCT oil derived from coconuts surpasses traditional coconut oil in efficiency and speed of energy conversion due to its higher concentration of readily metabolizable MCTs, making it a superior choice in human nutrition. This comprehensive study delves deeply into the potential of coconut-derived MCT oil, illuminating its chemical constituents, production from coconut oil, distinctive physical and chemical properties, and metabolic characteristics. Additionally, it highlights a range of potential biological activities of the oil, including its efficacy in managing gastrointestinal disorders and promising roles in anticancer, neuroprotective, and antimicrobial effects. The report also discusses the extensive applications of MCT oil across diverse industrial and technological sectors, as well as its utilization in structured lipids, oleogels, and as a carrier for capsaicin. Addressing safety concerns and providing dosage guidelines, this paper emphasizes MCT oil as an alternative to coconut oil in various applications, offering a holistic perspective on its benefits.
Due to rapid research expansion on dietary factors and development of cancer prevention guidelines, the field of dietary pattern and its relationship to cancer risk has gained more focus. Numerous epidemiology studies have reported associations between Gastric Cancer (GC) and both data-driven posteriori dietary pattern and priori dietary pattern defined by predetermined dietary indexes. As dietary patterns have evolved, a series of patterns based on biological markers has advanced, offering deeper insights into the relationship between diet and the risk of cancer. Although researches on dietary patterns and cancer risk are booming, there is limited body of literature focusing specifically on GC. In this study, we compare the similarities and differences among the specific components of dietary patterns and indices, summarize current state of knowledge regarding dietary patterns related to GC and illustrate their potential mechanisms for GC prevention. In conclusion, we offer suggestions for future research based on the emerging themes within this rapidly evolving field.
We describe an automated kinetic assay for acetoacetate in blood. Acetoacetate is enzymatically reduced to D-beta-hydroxybutyrate and the reaction is monitored for 60 s with a reaction-rate analyzer. This technique allows low concentrations of acetoacetate to be measured with good precision and overcomes many of the problems associated with other automated techniques. Our studies on the stability of acetoacetate emphasize the need for care in handling specimens. The use of a reaction-rate analyzer, an item of equipment common to most laboratories, allows for rapid handling of samples in small or large batches, depending on the needs of the laboratory.
In 1919, glucose intolerance became the earliest recognized metabolic abnormality in cancer patients. Prior to the development of severe malnutrition, colon, gastric, sarcoma, endometrial, prostate, localized head, neck, and lung cancer patients had many of the metabolic abnormalities of type II (noninsulin dependent) diabetes mellitus. These metabolic abnormalities include glucose intolerance, an increase in both hepatic glucose production (HGP) and glucose recycling, and insulin resistance. In a study of over 600 cancer patients, a diabetic pattern of glucose tolerance test was noted in over one-third of the patients. An increased rate of HGP, commonly seen in diabetics, has been noted in almost all types of cancer patients studied to date. Etiology of the increased glucose production in the cancer patient is not known, but abnormalities in the counter regulatory hormones, especially growth hormone, may contribute to the development of abnormal glucose metabolism. A second possible stimulus for the increase in HGP could be the glucose needs of the tumor. Abnormally high glucose utilization rates in small amounts of tumor tissue have recently been described. This suggests that small tumors may have large needs for glucose calories. An increase in anaerobic glycolysis in the tumor tissue can increase lactate production in the tumor-bearing human, thus supplying substrate to the liver to increase glucose production rates. In this paper, the nature of abnormal glucose metabolism in cancer patients is described.
Using data from over 10 000 men, women, and children who participated in the Lipid Research Clinics prevalence studies, we have examined the formula adopted by Friedewald et al1 for estimating plasma or serum concentrations of low-density lipoprotein cholesterol (LDL-C) when (for economy, or in the absence of an ultracentrifuge) only fasting total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), and triglyceride (TG) concentrations are measured in milligrams per liter, ie, LDL-C=TC—(HDL-C+0.20XTG). Values for LDL-C obtained by use of the Friedewald formula were compared with values derived from the Lipid Research Clinics ultracentrifugal procedure for LDL-C, which was used as a reference. Participants who were pregnant, who had not fasted, or whose plasma contained chylomicrons or floating 0-lipoproteins were excluded. We concluded that a better estimator for LDL-C was provided by the equation LDL-C-TC—(HDL-C+0.16XTG), since it produced an error (relative to the reference method) of lesser magnitude than the previous formula. The expression 0.16XTG (0.37XTG when measurements are reported in millimoles per liter) also produced a more accurate estimate of very low-density lipoprotein cholesterol relative to values obtained by the standard Lipid Research Clinics procedure for this component. The proposed formula is more precise for plasmas or sera with a TG concentration within the normal range.
(JAMA 1986;256:2372-2377)
• Positron emission tomographic scanning with fludeoxyglucose F 18 (18F-fluorodeoxyglucose) was used to study acute changes in gliomas after chemotherapy. In six experimental subjects, scans were obtained before and at days 1, 7, and 30 after treatment. Five control patients with gliomas who did not undergo chemotherapy had two scans, 1 month apart. Ratios were calculated between peak tumor regional cerebral metabolic rate for glucose and contralateral white matter. The percent change in ratios relative to each patient's baseline scan was calculated. Ratios in three stable controls remained unchanged over the study interval; in two controls it increased 155% and 36% and both died of tumor progression. In experimental subjects, ratios increased 20% to 100% 24 hours after chemotherapy and then decreased until at 28 days they varied between 22% above and 35% below baseline. The increased fludeoxyglucose F 18 uptake at 24 hours could be from uncoupling oxidative phosphorylation or shunting glucose to ribose phosphates for salvage nucleoside synthesis.
Tracer techniques and quantitative autoradiographic and tissue counting models for measurement of metabolic rates were combined with positron computed tomography (PCT) and (F-18)2-fluoro-2-deoxy-D-glucose (FDG) for the measurement of local cerebral metabolic rate for glucose (LCMRGlc) in humans. A three-compartment model, which incorporates hydrolysis of FDG-6-PO4 to FDG, was developed for the measure of kinetic constants and calculation of LCMRGlc. Our model is an extension of that developed by Sokoloff et al. Although small, hydrolysis of FDG-6-PO4 was found to be significant. A PCT system, the ECAT, was used to determine the rate constants, lumped constant, and stability of the model in human beings. The data indicate that cerebral FDG-6-PO4 in humans increases for about 90 minutes, plateaus, and then slowly decreases. After 10 minutes, cerebral blood FDG activity levels were found to be a minor fraction of tissue activity. Precursor pool turnover rate, distribution volumes, and red blood cell-plasma concentration ratios were determined. Reproducibility (precision) of LCMRGlc measurements (approximate 2 cm2 regions) was +/- 5.5% over a 5-hour period. The replacement of arterial blood sampling with venous sampling was validated.
Since the CNS can normally utilize ketone bodies, including acetoacetate, the authors sought to establish if this ability was enhanced in tumors of the nervous system. In contrast to expectations, it was found that the CoA transferase activity of the nervous system tumors was either equal to or less than that of the normal human white matter. When compared on a protein basis, astrocytomas and fibrillary astrocytomas both demonstrated significantly reduced activity. The seven glioblastoma multiforme tumors analyzed exhibited a wide range of activities (53-180 nmol/min/mg protein), but as a whole appeared to be reduced in terms of activity/mg protein. Schwannomas, also non-neuronal tumors, had very reduced CoA transferase activity, as did the craniopharyngiomas. The meningiomas were more heterogeneous in nature, having a range of activities of 46-442 nmol of acetoacetate formed/min/mg protein. The same was true of the metastatic tumors (activity range, 13.3-244 umol/min/mg protein. The two melanomas analyzed had activities comparable to that of the normal white matter. All of the tumors have been compared to white matter because the primary tumors of the nervous system studied were of white matter origin, not grey.
Metabolic effects of a new ketogenic regimen in which ketonemia is induced by feeding of medium chain triglycerides (MCT) are described, and comparisons are made with effects of the standard high fat ketogenic diet. Eighteen children maintained on the MCT diet for 3 months to 4 years failed to show elevations of serum cholesterol and had only a slight rise in serum total fatty acids, in contrast to the marked hyperlipidemia observed in children on the standard high fat diet. Long term use of the MCT diet did not affect pH of venous blood. Blood glucose fell below 50 mg/100 ml in one-third of the children, the lowest levels being reached 2--3 weeks after the start of the diet. Plasma D(--)-beta-hydroxybutyrate (BHB) and acetoacetate rose gradually after institution of diet therapy, maximum levels being reached after about 1 month. Higher levels of BHB and acetoacetate were achieved in children under the age of 10 years (BHB = 4.3 mM +/- 0.6 SEM, acetoacetate = 1.8 mM +/- 0.3 SEM) than in 10--18 year olds (BHB = 1.6 mM +/- 0.2 SEM, acetoacetate = 0.57 mM +/- 0.08 SEM). Plasma BHB and acetoacetate levels in children maintained on a 3:1 high fat diet were similar to those in children on a 60% MCT diet. Plasma levels of BHB showed a significant correlation with anticonvulsant effect (P less than 0.02). Both the ketonemia and the anticonvulsant action were reversed rapidly by intravenous infusion of glucose.
To evaluate the possible role of altered glucose metabolism in malignant cachexia, metabolic parameters including total glucose turnover, glucose oxidation, and Cori cycle activity were measured in fourteen patients with metastatic carcinoma. Eight patients with progressive weight loss (PWL) were compared to 6 without (controls). Cori cycle activity was significantly increased (p less than 0.02) in PWL patients, 90 mg/kg/hr (range, 22 to 193) compared to 18 mg/kg/hr (range, 13 to 24) in controls. Total glucose turnover was moderately increased in PWL patients, 196 mg/kg/hr compared to 110 mg/kg/hr in controls. Glucose oxidation was 62 mg/kg/hr versus 48 mg/kg/hr, and total caloric expenditure was 36 kcal/sq m/hr compared to 33 Kcal/sq m/hr. PWL patients were metabolically heterogenous and mean values are skewed by four patients with increased glucose turnover, oxidation, and markedly high recycling rates that were equivalent to total endogenous glucose turnover of a normal subject. Total caloric expenditure was greatest in three of the four patients with a marked increase in Cori cycle activity. Energy loss associated with a high rate of gluconeogenesis from lactate has been suggested as an explanation for increased energy expenditure in some cancer patients, thus contributing to mechanisms that promote weight loss.
The combination of FDG and PET has demonstrated clinical utility in the evaluation of patients with brain tumors. At the time of diagnosis, FDG PET provides information concerning the degree of malignancy and patient prognosis. After therapy, FDG PET is able to assess persistence of tumor, determine degree of malignancy, monitor progression, differentiate recurrence from necrosis, and assess prognosis. Other studies using PET provide information that may be clinically useful. Determination of tumor blood flow and permeability of the blood-brain barrier may help in the selection of appropriate therapy. Amino acid imaging using 11C-methionine is being evaluated in patients with brain tumors and provides different information than FDG imaging.
The utilization and distribution of radioactively labeled lipid emulsions were evaluated in Sprague-Dawley rats. Animals received one of three lipid emulsions. Group 1 received [14C]medium-chain-triglyceride (MCT) lipid emulsion, group 2 received a 75%:25% (vol:vol) admixture of [14C]MCT: unlabeled long-chain-triglyceride (LCT) lipid emulsion, and group 3 received only [14C]LCT. The radioactive dose appearing in expired carbon dioxide and various body tissues was monitored over a 24-h period. Results indicate that MCT is oxidized more rapidly and completely than in LCT; approximately 90% of the MCT is converted to carbon dioxide with in 24 h compared with 45% for LCT. When MCT and LCT are administered together, the metabolism of MCT is slowed but remains more rapid than that of LCT. Removal of MCT from the blood was more rapid than was removal of LCT, and tissue radioactivity was lower.