Effects of medium- and long-chain fatty acids on whole body leucine and glucose kinetics in man

Keller, Ulrich; Turkalj, Igor; Laager, R.; Bloesch, D.; Bilz, Stefan

doi:10.1053/meta.2002.32806

Cited by 14 publications

(14 citation statements)

References 32 publications

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“…Some factors are known to influence BCKD complex activity and BCAAs oxidation. In normal subjects, insulin suppresses leucine (KIC) oxidation and this effect is blunted in diabetes mellitus (Tessari et al 1986;Keller et al 2002). The administration of long-chain fatty acids, unlike medium-chain triglycerides, also decreases leucine oxidation compared with controls (Keller et al 2002).…”

Section: Leucinementioning

confidence: 99%

“…In normal subjects, insulin suppresses leucine (KIC) oxidation and this effect is blunted in diabetes mellitus (Tessari et al 1986;Keller et al 2002). The administration of long-chain fatty acids, unlike medium-chain triglycerides, also decreases leucine oxidation compared with controls (Keller et al 2002). In contrast, leucine oxidation is activated in healthy subjects by glucagon, (Pacy et al 1990) glucocorticosteroid therapy (Zimmerman et al 1989), and ammonium chloride-induced metabolic acidosis (Reaich et al 1992;Straumann et al 1992).…”

Section: Leucinementioning

confidence: 99%

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Insulin resistance and the metabolism of branched-chain amino acids in humans

Adeva¹,

et al. 2011

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Peripheral resistance to insulin action is the major mechanism causing the metabolic syndrome and eventually type 2 diabetes mellitus. The metabolic derangement associated with insulin resistance is extensive and not restricted to carbohydrates. The branched-chain amino acids (BCAAs) are particularly responsive to the inhibitory insulin action on amino acid release by skeletal muscle and their metabolism is profoundly altered in conditions featuring insulin resistance, insulin deficiency, or both. Obesity, the metabolic syndrome and diabetes mellitus display a gradual increase in the plasma concentration of BCAAs, from the obesity-related low-grade insulin-resistant state to the severe deficiency of insulin action in diabetes ketoacidosis. Obesity-associated hyperinsulinemia succeeds in maintaining near-normal or slightly elevated plasma concentration of BCAAs, despite the insulin-resistant state. The low circulating levels of insulin and/or the deeper insulin resistance occurring in diabetes mellitus are associated with more marked elevation in the plasma concentration of BCAAs. In diabetes ketoacidosis, the increase in plasma BCAAs is striking, returning to normal when adequate metabolic control is achieved. The metabolism of BCAAs is also disturbed in other situations typically featuring insulin resistance, including kidney and liver dysfunction. However, notwithstanding the insulin-resistant state, the plasma level of BCAAs in these conditions is lower than in healthy subjects, suggesting that these organs are involved in maintaining BCAAs blood concentration. The pathogenesis of the decreased BCAAs plasma level in kidney and liver dysfunction is unclear, but a decreased afflux of these amino acids into the blood stream has been observed.

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Section: Leucinementioning

confidence: 99%

Section: Leucinementioning

confidence: 99%

Insulin resistance and the metabolism of branched-chain amino acids in humans

Adeva¹,

et al. 2011

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“…Therefore, medium-and long-chain triacyglycerols (MLCT) were developed to overcome these weaknesses. In recent years, there have been a considerable number of papers published on MLCT Keller et al 2002;Matsuo et al 2001a).…”

Section: Introductionmentioning

confidence: 99%

Modeling and Optimization of Lipozyme RM IM-Catalyzed Esterification of Medium- and Long-Chain Triacyglycerols (MLCT) Using Response Surface Methodology

Arifin

Soo-Peng

Long

et al. 2010

Food Bioprocess Technol

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Optimization conditions of Lipozyme RM IM lipase esterification of capric and stearic acids with glycerol for the production of medium-and long-chain triacyglycerols (MLCT) fat suitable for food applications such as margarine and shortening were investigated. Response surface methodology (RSM) was applied to model and optimize the reaction conditions, namely, the reaction time (8-24 h), enzyme load (5-15 wt.%), and fatty acids/ glycerol ratio (3:1-4:1) and represented by Ti, En, and Sb, respectively. Best-fitting models were successfully established for both MLCT yield (R 2 =0.9507) and residual FFA (R 2 =0.9315) established by multiple regressions with backward elimination. Optimal reaction conditions were 13.6-14.0 h for reaction time, 7.9-8.0 wt.% for enzyme load, and 3:1 for fatty acids/glycerol molar ratio. Chi-square test showed that there were no significant (P>0.05) differences between the observed and predicted values of both models. Refined MLCT fat blend had sufficient solid fat at room temperature and made it suitable to use as a hard stock in shortening and margarine production.

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“…In studies in healthy humans, exogenously infused fatty acids have been shown to result in a decrease in the rate of protein breakdown by the skeletal muscle, evidenced by a decrease in the rate of net release of amino acids across the limb (4), and by a decrease in the rate of appearance of essential amino acids leucine and phenylalanine as measured by isotopic tracer methods (5,6). Although the mechanism of the observed effect of fatty acids on protein breakdown has not been identified, it does not appear to be related to hepatic oxidation of fatty acids and consequent increase in ketone levels.…”

mentioning

confidence: 99%

Fatty Acids, Insulin Resistance, and Protein Metabolism

Kalhan

2009

The Journal of Clinical Endocrinology & Metabolism

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A ccretion and maintenance of lean body mass, because of its fundamental role in health and disease, continues to be an area of intense investigation. By using sophisticated tracer isotopic methods, organ balance techniques, and molecular analysis of tissue samples in humans and animal models, a detailed analysis of the signaling pathway and metabolic fluxes has been possible. Despite these, understanding the regulatory mechanism of nitrogen/protein accretion and maintenance of lean body mass in vivo continues to be challenging. This is particularly difficult because of the adaptation of metabolism to various modifying influences, and because of the multiple levels of regulation in vivo. Yet, by careful studies, a number of investigators have systematically examined the influence of diverse modifiers on the physiology of protein synthesis and breakdown in humans in vivo.In this issue of JCEM, Katsanos et al. have examined, in healthy humans, the impact of elevated plasma fatty acids levels, induced by iv infusion of intralipid and heparin, on the responsiveness of the skeletal muscle protein synthesis and balance to an enterally administered essential amino acid mixture. By using isotopic tracers in combination with arteriovenous balance measurements across the leg and by quantifying tracer incorporation into muscle proteins, Katsanos et al. (1) have presented a detailed analysis of protein kinetics in the skeletal muscle. As anticipated, increase in plasma free fatty acids resulted in the development of insulin resistance (2). Their data show that in the basal state, in the presence of elevated plasma fatty acids levels and insulin resistance, there was a decrease in the rate of appearance of phenylalanine across the leg, suggesting a lower rate of protein breakdown. The rate of disappearance of phenylalanine was not affected, resulting in an improved or less negative amino acid balance. Essential amino acid administration resulted in no change in protein breakdown and caused an increase in phenylalanine rate of disappearance (increase in protein synthesis) and an increase in the fractional rate of protein synthesis. Of significance, fatty acids and/or fatty acid-induced insulin resistance did not impact the rate of protein synthesis by skeletal muscle in response to the amino acid load.Fatty acids are critical oxidative substrates that are mobilized during fasting and result in sparing of glucose and amino acids. Elevated fatty acid levels during fasting are associated with decreased glucose uptake by skeletal muscle, decreased protein breakdown, and a lower rate of protein oxidation and urea synthesis (3). The cause and effect relating fatty acids to changes in fasting metabolism has been examined in a large number of studies. These studies have been done either during fasting when there is a spontaneous increase in plasma fatty acid concentration or by infusing intralipid with heparin, resulting in an increase in the plasma fatty acid levels in the high physiological range. Fatty acids could impact glucose an...

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Effects of medium- and long-chain fatty acids on whole body leucine and glucose kinetics in man

Cited by 14 publications

References 32 publications

Insulin resistance and the metabolism of branched-chain amino acids in humans

Insulin resistance and the metabolism of branched-chain amino acids in humans

Modeling and Optimization of Lipozyme RM IM-Catalyzed Esterification of Medium- and Long-Chain Triacyglycerols (MLCT) Using Response Surface Methodology

Fatty Acids, Insulin Resistance, and Protein Metabolism

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