Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat

Crozier, Gayle; Bois-Joyeux, Brigitte; Chanez, Marc; Girard, Jean; Péret, J

doi:10.1016/0026-0495(87)90122-3

Cited by 76 publications

(45 citation statements)

References 44 publications

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“…Feeding of an MCT-containing formula for 4 d promotes a mild ketosis in preterm infants (27). These ketone bodies will be quickly utilized peripherally, especially after a period of adaptation (28). Because the conversion to ketones is a rapid process (29), most of the excreted I3CO2 due to the oxidation of ketone bodies derived from MCT will also contribute to the 13C enrichment in expired air, thus being included in our calculation.…”

Section: Resultsmentioning

confidence: 99%

Quantisation of Oxidation of Medium-Chain Triglycerides in Preterm Infants1

1989

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ABSTRACT. Medium-chain triglycerides, with a chain length of eight and 10 carbon atoms, form up to 50% of the total fat content in some preterm infant formulas. In 20 small preterm infants (birthwt: 1153 f 227 g; mean 2 SD) fed a special formula containing 40% MCT, a primed constant oral infusion study of l-'3C-potassium octanoate was conducted to quantify the oxidation of MCT. A plateau in 13C enrichment in breath COz was reached in all patients within 1-3 h. Simultaneously, substrate utilization was measured using a closed system indirect calorimeter. No significant difference was found between appropriate for gestational age (n = 8) and small for gestational age (n = 12) infants in the percentage of the administered tracer that was oxidized (44.9 f 9

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Section: Resultsmentioning

confidence: 99%

Quantisation of Oxidation of Medium-Chain Triglycerides in Preterm Infants1

1989

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“…Due to its concerted induction with glucose-6-phosphate dehydrogenase and 6-phospho-gluconate dehydrogenase, two NADPH producing enzymes important for fatty acid synthesis, ME-1 is also considered a lipogenic enzyme [1][2][3][4][5][6]. Indeed, higher levels of liver ME-1 activity have been associated with obese mouse and rat models [7,8].…”

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confidence: 99%

“…Liver and adipose activity of ME-1 is induced by a high carbohydrate/low-fat diet, and down-regulated by a highfat diet [2,[4][5][6]. Due to its concerted induction with glucose-6-phosphate dehydrogenase and 6-phospho-gluconate dehydrogenase, two NADPH producing enzymes important for fatty acid synthesis, ME-1 is also considered a lipogenic enzyme [1][2][3][4][5][6].…”

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confidence: 99%

Deficiency in Cytosolic Malic Enzyme Does Not Increase Acetaminophen‐Induced Hepato‐Toxicity

Mumick

Nizner

et al. 2008

Basic Clin Pharma Tox

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Cytosolic malic enzyme (ME-1) is a nicotinamide adenine dinucleotide phosphate (NADP)-dependent enzyme that generates NADPH. The activity of this enzyme, the reversible oxidative decarboxylation of malate to yield pyruvate, links glycolytic pathway to citric acid cycle. The high level of ME-1 expression in liver, and its involvement in NADPH production, suggests reduced ME-1 activity might compromise hepatic production of reduced glutathione (GSH) by the NADPH-dependent enzyme glutathione reductase, and hence affect xenobiotic detoxification. The role of ME-1 in liver detoxification was evaluated in Mod1 deficient mice ( mod1 -/-) by evaluating their sensitivity to acetaminophen-induced liver injury. The results show that mod1 -/-mice are not more sensitive to acetaminophen hepato-toxicity. Although GSH levels were initially depleted more in the mod1 -/-liver than in wild-type controls, the GSH levels recovered quickly. In conclusion, our data indicate that ME-1 deficiency does not adversely affect GSH-dependent detoxification.

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“…In these cases. the observed increase in metabolic rate has been ascribed either to ketogenesis (4). obligatory oxidation (5.…”

Section: Discussionmentioning

confidence: 99%

“…1 ) (4) Glucose production was calculated by subtracting the glucose intake (calculated from the individual intakes of the continuously fed formula) from the rate of glucose appearance obtained by isotope dilution, Ra true. Glucose intake was calculated from the glucose part of lactose plus the glucose within the glucose polymers.…”

Section: Ra Truementioning

confidence: 99%

Decreased Glucose Oxidation in Preterm Infants Fed a Formula Containing Medium-Chain Triglycerides

et al. 1993

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ABSTRACT. Several formulas for preterm infants contain Abbreviations medium-chain triglycerides (MCT) to enhance fat absorption. Although fat absorption with MCT was slightly MCT, medium-chain triglyceride higher in several studies in preterm infants, a beneficial LCT, long-chain triglyceride Ra, rate of appearance effect on growth has only been reported in one publication. We hypothesized that when part of the fat blend of preterm formula is substituted by MCT oil, this might lead to a different metabolic pattern in which, due to the preferential oxidation of MCT, an increase in lipogenesis from glucoseThe fat blend of several special formulas for preterm infants could lead to an increase in metabolic rate. To study the consists of 30% to 50% MCT to enhance fat absorption. In impact of MCT on glucose metabolism, 18 preterm infants several studies in which MCT-containing fat blends were used in were randomized to receive either an M a or an L a preterm infants, increased fat absorption without improved formula containing 38-and 6%-by-weight medium-chain weight gain was reported (1-3); thus, one might expect that fatty acids, respectively, in their fat blend. ~t 4 wk of age, infants fed an MCT-containing formula either have an increased the metabolic rate, substrate utilization, glucose kinetics, energy expenditure or lay down relatively more fat Per g new and oxidation were measured by indirect respiratory calo-tissue, resulting in a higher energy cost of growth. We hypotherimetry in with a constant-rate oral infusion sized that an increased energy expenditure, which has been o f [~-~3~~g l u c o s e . ~h~ fitrue" rate ofappearance of glucose described before in animals and human adults during overfeeding ( R~ true^) was measured from the dilution of the with MCT (4-7), explains the lack of increase in growth rate at formly labeled (m + 6) species of infused tracer, whereas the higher energy absorption in preterrn infants fed MCT forrate of appearance of glucose (Ra mulas. We further speculated that an increased metabolic rate was measured from the dilution of infused tracer C (car-might result from an increased lipogenesis with ongoing fat bon). The latter was measured by an on-line combustion oxidation, as MCT feeding is known to be associated with increased lipogenesis. In a previous study (8). using the same lnethod using a gas ratio mass methods as in the present article, we showed a higher metabolic At a carbohydrate intake of 8'4 rate in parenterally fed infants receiving only glucose as their min-', total utilization of carbohydrate was equal in both nonprotein energy source with infants receiving glugroups at 7.6 m g kg-'.min-'. glucoseoxidation, cose and lipids. Moreover, we showed strong evidence that the as measured by the appearance of 1 3 ' in breath '02 was higher metabolic rate was due to the conversion of glucose into lower in the MCT group (4.5 ' 0.83 versus fat, resulting in a lower food efficiency. To elucidate the mech-5.7 Oh7 mg. kg-' ' min-ly MCT versus LCT). anism of the apparently lower ...

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Metabolic effects induced by long-term feeding of medium-chain triglycerides in the rat

Cited by 76 publications

References 44 publications

Quantisation of Oxidation of Medium-Chain Triglycerides in Preterm Infants1

Quantisation of Oxidation of Medium-Chain Triglycerides in Preterm Infants1

Deficiency in Cytosolic Malic Enzyme Does Not Increase Acetaminophen‐Induced Hepato‐Toxicity

Decreased Glucose Oxidation in Preterm Infants Fed a Formula Containing Medium-Chain Triglycerides

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