Aggressive Nutritional Support Does Not Prevent Protein Loss Despite Fat Gain in Septic Intensive Care Patients

Streat, Stephen; Beddoe, A H; Hill, Graham L.

doi:10.1097/00005373-198703000-00006

Cited by 433 publications

(175 citation statements)

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“…Several studies in other catabolic states have suggested that the normal anabolic response is inhibited or completely blocked by mediators of inflammation. Thus, for example, severely-septic intensive care patients fail to accrue lean tissue, even when supplied with a more-than-adequate input of amino acids and energy (Streat et al 1987). By contrast, in HIV-infected patients, we found a quantitatively similar change in protein metabolism, as reflected by leucine kinetics, as we found in healthy controls (Fig.…”

Section: Protein Metabolism and Anabolic Blocksupporting

confidence: 61%

Metabolic abnormalities and wasting in human immunodeficiency virus infection

Macallan

1998

Proc. Nutr. Soc.

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Section: Protein Metabolism and Anabolic Blocksupporting

confidence: 61%

Metabolic abnormalities and wasting in human immunodeficiency virus infection

Macallan

1998

Proc. Nutr. Soc.

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“…If onset of recovery does not follow within several days of intensive medical care, critical illness often becomes prolonged and intensive care must be continued for weeks or even months. At this stage, and in contrast to the early phase of severe illnesses, patients no longer ef®ciently use fatty acids as metabolic substrates (1). They store fat with feeding, both in adipose tissue and as fatty in®ltrates in vital organs such as the pancreas and the liver, but they continue to lose large amounts of protein from skeletal muscle and from organs, which causes impairment of vital functions, weakness and delayed or hampered recovery (2).…”

Section: Introductionmentioning

confidence: 99%

Novel insights into the neuroendocrinology of critical illness

Berghe

2000

European Journal of Endocrinology

226

104

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An unexplained hallmark of prolonged critical illness is the fact that food does not prevent or reverse protein wasting, while fat is paradoxically accrued. This`wasting syndrome' often persists after the underlying disease has been resolved and thus perpetuates intensive care dependency. Although the crucial role of an intact hypothalamus±pituitary axis for homeostasis during stress is well recognized, the differences between the neuroendocrine changes observed in acute and prolonged critical illness were only recently described. Novel insights in this area are reviewed here.The initial endocrine stress response consists primarily of a peripheral inactivation of anabolic pathways while pituitary activity is essentially ampli®ed or maintained. These responses presumably provide the metabolic substrates and host defense required for survival and to delay anabolism, and thus should be considered as adaptive and bene®cial. Persistence of this acute stress response throughout the course of critical illness was hitherto assumed. This assumption has now been invalidated, since a uniformly reduced pulsatile secretion of ACTH, TSH, LH, prolactin (PRL) and GH has been observed in protracted critical illness, causing diminished stimulation of several target organs. Impaired pulsatile secretion of anterior pituitary hormones in the chronic phase of critical illness seems to have a hypothalamic rather than a pituitary origin, as administration of relevant releasing factors evoked immediate and pronounced pituitary hormone release. A reduced availability of TRH, one of the endogenous ligands of the GH-releasing peptide (GHRP) receptor (such as the recently discovered ghrelin) and, in very long-stay critically ill men, also of GHRH, appear to be involved. This hypothesis was further explored by investigating the effects of continuous i.v. infusion of GHRH, GHRP, TRH and their combinations for several days. Pulsatile secretion of GH, TSH and PRL was re-ampli®ed by relevant combinations of releasing factors which also substantially increased circulating levels of IGF-I, GH-dependent binding proteins, thyroxine and tri-iodothyronine (T3) while avoiding a rise in reverse T3. Active feedback-inhibition loops prevented overstimulation of target organs and metabolic improvement was noted with the combined infusion of GHRP and TRH. Whether this novel endocrine strategy will also enhance clinical recovery from critical illness remains to be explored.

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“…4,5 It is not clear how this closely integrated system would respond to the introduction of lipid energy via an intravenous route, when many of the normal regulatory features would presumably be absent. However, patients fed intravenously with lipid-based feeding regimens, may show accumulation of body fat, despite protein catabolism, 6 so there must be mechanisms by which the regulation of fat balance is maintained. We therefore hypothesised that during intravenous infusion of a lipid emulsion, changes in adipose tissue metabolism would occur which would resemble those observed in the postprandial state, in the sense that net fat mobilization would be spared.…”

Section: Introductionmentioning

confidence: 99%

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

Samra¹,

Giles²,

Summers³

et al. 1998

Int J Obes

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OBJECTIVE: To test the hypothesis that intravenous infusion of lipid would bring about changes in adipose tissue metabolism, which would tend to spare net fat mobilization, and to attempt to identify the mediators of such responses. DESIGN: The triacylglycerol (TG) emulsion, Intralipid, was infused and metablic changes in subcutaneous adipose tissue and forearm muscle were assessed by measurements of arterio-venous differences. SUBJECTS: Six normal male subjects aged 21 ± 37 y, with body mass index (BMI) 23.0 ± 25.9 kgam 2 . RESULTS: Plasma TG and non-esteri®ed fatty acid (NEFA) concentrations rose during infusion as expected. The rise in systemic plasma NEFA concentration occurred despite decreased NEFA release from adipose tissue. Intralipid infusion resulted in a suppression of intracellular lipolysis in adipose tissue, by mechanisms which are not clear. Plasma leptin concentrations, measured in a search for the regulator of lipolysis, showed consistent leptin release from adipose tissue which did not change signi®cantly with time. CONCLUSION: The suppression of intracellular lipolysis in adipose tissue during Intralipid infusion is a new observation and may re¯ect a novel mechanism for regulation of fat storage.

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Aggressive Nutritional Support Does Not Prevent Protein Loss Despite Fat Gain in Septic Intensive Care Patients

Cited by 433 publications

References 0 publications

Metabolic abnormalities and wasting in human immunodeficiency virus infection

Metabolic abnormalities and wasting in human immunodeficiency virus infection

Novel insights into the neuroendocrinology of critical illness

Peripheral fat metabolism during infusion of an exogeneous triacylglycerol emulsion

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