Is the glutamine story over?

Smedberg, Marie; Wernerman, Jan

doi:10.1186/s13054-016-1531-y

Cited by 33 publications

(33 citation statements)

References 43 publications

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“…Glutamine, but not glutamate, is found to be decreased in plasma of PA and MMA patients which has been attributed to shortage of α‐ketoglutarate . Glutamine supplementation is controversial in critically ill patients, given the associated high rate of adverse outcomes that raised the hypothesis that low glutamine levels are an adaptive response . Therefore, glutamate supplementation, which was for example demonstrated to improve postischaemic heart function in rats, might be a better option to consider.…”

Section: Therapy Targets and Treatment Strategiesmentioning

confidence: 99%

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Haijes

Hasselt

Jans

et al. 2019

J of Inher Metab Disea

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Despite realizing increased survival rates for propionic acidemia (PA) and methylmalonic acidemia (MMA) patients, the current therapeutic regimen is inadequate for preventing or treating the devastating complications that still can occur. The elucidation of pathophysiology of these complications allows us to evaluate and rethink treatment strategies. In this review we display and discuss potential therapy targets and we give a systematic overview on current, experimental and unexplored treatment strategies in order to provide insight in what we have to offer PA and MMA patients, now and in the future. Evidence on the effectiveness of treatment strategies is often scarce, since none were tested in randomized clinical trials. This raises concerns, since even the current consensus on best practice treatment for PA and MMA is not without controversy. To attain substantial improvements in overall outcome, gene, mRNA or enzyme replacement therapy is most promising since permanent reduction of toxic metabolites allows for a less strict therapeutic regime. Hereby, both mitochondrial‐associated and therapy induced complications can theoretically be prevented. However, the road from bench to bedside is long, as it is challenging to design a drug that is delivered to the mitochondria of all tissues that require enzymatic activity, including the brain, without inducing any off‐target effects. To improve survival rate and quality of life of PA and MMA patients, there is a need for systematic (re‐)evaluation of accepted and potential treatment strategies, so that we can better determine who will benefit when and how from which treatment strategy.

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Section: Therapy Targets and Treatment Strategiesmentioning

confidence: 99%

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Haijes

Hasselt

Jans

et al. 2019

J of Inher Metab Disea

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“…Als Konsequenz wurde das Therapieziel formuliert, die Glutaminspiegel im Plasma kritisch Kranker auf den Wert gesunder Probanden anzuheben und damit das Behandlungsergebnis zu verbessern. Die Richtigkeit dieser Zielsetzung wurde bisher aber nie systematisch untersucht [55] und wird durch die inzwischen vorliegenden negativen Studien [56][57][58] infrage gestellt. In den Augen kritischer Beobachter ist das Konzept von Glutamin als konditionell essenzieller Aminosäure und die daraus abgeleitete Indikation zur Supplementierung bei kritisch Kranken Intensivpatienten nicht mehr haltbar [55].…”

Section: Merke Der Stoffwechsel Der Dünndarmmukosa Ist Dieunclassified

“…Die Richtigkeit dieser Zielsetzung wurde bisher aber nie systematisch untersucht [55] und wird durch die inzwischen vorliegenden negativen Studien [56][57][58] infrage gestellt. In den Augen kritischer Beobachter ist das Konzept von Glutamin als konditionell essenzieller Aminosäure und die daraus abgeleitete Indikation zur Supplementierung bei kritisch Kranken Intensivpatienten nicht mehr haltbar [55]. Möglicherweise handelt es sich bei dem Absinken der Glutaminspiegel kritisch Kranker eher um einen adaptiven Prozess als um einen Mangel [59].…”

Section: Merke Der Stoffwechsel Der Dünndarmmukosa Ist Dieunclassified

Glutamin in der Ernährungstherapie – Welche Indikation bleibt?

Plauth¹

2020

Aktuel Ernahrungsmed

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Glutamine, a non-essential amino acid, is an indispensable substrate for all rapidly dividing cells. Enteral feeding solutions contain glutamine at approximately 5?6?g per liter while conventional amino acid solutions for parenteral nutrition do not contain any glutamine for pharmaceutical reasons. In critically ill patients, an association between subnormal plasma levels of glutamine and increased morbidity and mortality was noted and led to the concept of glutamine as a conditionally essential amino acid. Accordingly, supplementing glutamine, particularly in total parenteral nutrition, was expected to improve clinical outcome. The initial enthusiasm for this therapeutic concept, however, has waned and given way for a sobering view questioning the concept of glutamine as a conditionally essential amino acid and the resulting indication to supplement. Currently, the supplementation of glutamine can be considered only in critically ill patients without multi-organ failure who need to be managed on total parenteral nutrition exclusively for more than five days.

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“…Alimentary proteins contain universally a smallest proportion of EAA and a largest of NEAA, and, as said, arginine and glutamine/glutamic acid, are preferred substrates and precursors of urea synthesis and most abundant in alimentary foods [23]. Certainly arginine and glutamine availability may become limited in plasma of patients with hyper-catabolic conditions and insufficient supply of nitrogen sources, but in front of health problems deriving by introduction of each of those amino acids [24], [25], [26] on the contrary, increasing supply of EAA as therapy, that is increasing EAA input as naturally occurring metabolic precursors of the NEAA arginine and glutamine/glutamic acid, is a solution that has never been fully explored. But, when supplementation with EAA has been done in small series of critically ill, results were exceptionally good [27].…”

Section: Thinking To Some Solutionmentioning

confidence: 99%

Where the Pendulum of Knowledge Stands Now: Is Circulating Albumin a Marker of Inflammation or of Malnutrition? How to Manage Hypoalbuminemia by Nutrition?

Dioguardi¹

2018

JNB

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Low plasma albumin levels have been historically associated with insufficient nutritional nitrogen support. Recently, linked to the poor response of actual therapies and available supplements to manage this alteration, the role of this alteration has been attributed to the vast ensemble of modifications referred generally as consequent to inflammation. On the contrary, as recently it has been reported that life based on introduction of mainly essential amino acids is possible, and life span is improved when compared to standard diets, it is possible to hypothesize that by normal foods or by actually most widely diffused supplements insufficient amounts of essential amino acids to match with real needs of hypoalbuminemic patients are not provided. Peculiarly, some non essential amino acids provided in excess by diets may mislead clinicians by suggesting achievement of sufficient nitrogen intake if urea syntheses is used as reference of sufficient nutrition, while syntheses of liver proteins is not sufficiently implemented. Studies suitable to understand if some innovative therapy would be efficient in implementing albumin syntheses and thus prognosis in hypoalbuminemic patients are necessary.

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Is the glutamine story over?

Cited by 33 publications

References 43 publications

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Pathophysiology of propionic and methylmalonic acidemias. Part 2: Treatment strategies

Glutamin in der Ernährungstherapie – Welche Indikation bleibt?

Where the Pendulum of Knowledge Stands Now: Is Circulating Albumin a Marker of Inflammation or of Malnutrition? How to Manage Hypoalbuminemia by Nutrition?

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