Metabolic Adaptations for Energy Production During Trauma and Sepsis

Ryan, N. Thomas

doi:10.1016/s0039-6109(16)41032-7

Cited by 98 publications

(22 citation statements)

References 63 publications

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“…The catabolic rate after a major operation is well-known to be increased, resulting in a loss of lean body mass, which consequently causes a reduction in body weight [26]. Thus, the reduced loss and the more rapid recovery of body weight after the operation is believed to indicate a lower catabolic rate and enhanced recovery in the ASC-treated group.…”

Section: Discussionmentioning

confidence: 99%

Adipose-tissue-derived Stem Cells Enhance the Healing of Ischemic Colonic Anastomoses: An Experimental Study in Rats

Yoo

Shin

et al. 2012

J Korean Soc Coloproctol

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PurposeThis experimental study verified the effect of adipose-tissue-derived stem cells (ASCs) on the healing of ischemic colonic anastomoses in rats.MethodsASCs were isolated from the subcutaneous fat tissue of rats and identified as mesenchymal stem cells by identification of different potentials. An animal model of colonic ischemic anastomosis was induced by modifying Nagahata's method. Sixty male Sprague-Dawley rats (10-week-old, 370 ± 50 g) were divided into two groups (n = 30 each): a control group in which the anastomosis was sutured in a single layer with 6-0 polypropylene without any treatment and an ASCtreated group (ASC group) in which the anastomosis was sutured as in the control group, but then ASCs were locally transplanted into the bowel wall around the anastomosis. The rats were sacrificed on postoperative day 7. Healing of the anastomoses was assessed by measuring loss of body weight, wound infection, anastomotic leakage, mortality, adhesion formation, ileus, anastomotic stricture, anastomotic bursting pressure, histopathological features, and microvascular density.ResultsNo differences in wound infection, anastomotic leakage, or mortality between the two groups were observed. The ASC group had significantly more favorable anastomotic healing, including less body weight lost, less ileus, and fewer ulcers and strictures, than the control group. ASCs augmented bursting pressure and collagen deposition. The histopathological features were significantly more favorable in the ASC group, and microvascular density was significantly higher than it was in the control group.ConclusionLocally-transplanted ASCs enhanced healing of ischemic colonic anastomoses by increasing angiogenesis. ASCs could be a novel strategy for accelerating healing of colonic ischemic risk anastomoses.

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Section: Discussionmentioning

confidence: 99%

Adipose-tissue-derived Stem Cells Enhance the Healing of Ischemic Colonic Anastomoses: An Experimental Study in Rats

Yoo

Shin

et al. 2012

J Korean Soc Coloproctol

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“…These responses could be explained at least in part by the changes in hormone concentrations. Glucagon significantly increased, and it is well established that glucagon is the predominant stimulator ofthe accelerated rate ofglucose production in sepsis (35,36). On the other hand, adrenergic activity has been shown to be the most important stimulator of lipolysis (36), and thus in the absence of a change in catecholamine concentration, a stimulation of lipolysis would not have been expected.…”

Section: Discussionmentioning

confidence: 99%

Short-term effects of tumor necrosis factor on energy and substrate metabolism in dogs.

Sakurai¹,

Zhang²,

Wolfe³

1993

J. Clin. Invest.

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In vivo short-term effects of recombinant human TNF-a on lipolysis, FFA flux, fat oxidation, triglyceride-fatty acid cycling, and glucose kinetics were evaluated with stable isotopic tracers and indirect calorimetry along with monitoring of hemodynamic parameters in fasted dogs. High-dose TNF infusion ( 10 ,gg/kg) caused a fall in mean arterial pressure (P < 0.01), pulmonary arterial pressure (P < 0.001), and cardiac index (CI) (P < 0.05). The rate of appearance of glycerol (Ra glycerol) and the rate of appearance of FFA (Ra FFA) were decreased by 20% (P < 0.05) and by 42% (P < 0.01), respectively. Total fat oxidation fell by 23% (P < 0.05). In contrast, TNF infusion significantly increased glucose production by 13% (P < 0.05) and metabolic clearance rate of glucose by 25% (P < 0.01). However, TNF infusion did not change energy expenditure. Low-dose TNF infusion (3.5 ;tg/kg) caused changes similar in all respects, except magnitude, to the highdose effects. There was a significant correlation between percent change of CI (ACI) and percent change of rate of appearance of palmitate (Ra palmitate; ARa palmitate) (P < 0.0001, r = 0.69), Ra FFA (ARa FFA) (P < 0.0001, r = 0.60), and Ra glycerol (ARa glycerol) (P < 0.0329, r = 0.36). The correlation between ACI and ARa palmitate was greater than the correlation between ACI and ARa glycerol (P = 0.028). We conclude that the acute response to TNF causes a shift towards carbohydrate as an energy substrate in a dose-dependent manner by both decreasing the availability of FFAs and increasing glucose production. (J. Clin. Invest. 1993.91:2437-2445

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“…'4C]leucine by isolated muscles from septic man (3) and rabbit (15) was shown to be increased. The mechanism responsible for the apparent increase in BCAA catabolism is not known.…”

Section: Introductionmentioning

confidence: 97%

Administration of endotoxin, tumor necrosis factor, or interleukin 1 to rats activates skeletal muscle branched-chain alpha-keto acid dehydrogenase.

Nawabi¹,

Block²,

Chakrabarti³

et al. 1990

J. Clin. Invest.

111

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Protein catabolic states (i.e., sepsis and trauma) are thought to be associated with accelerated oxidation of branched-chain amino acids (BCAA). Branched-chain a-keto acid dehydrogenase (BCKAD), the rate-limiting enzyme for BCAA oxidation by muscle, is regulated by phosphorylation/dephosphorylation. Skeletal muscle BCKAD was only 2-4% active in control rats. Intravenous injection of Salmonella enteritidis endotoxin (0.25-10 mg/kg) did not change total BCKAI) activity, but increased the percent active enzyme in muscle three-to fourfold in 4-6 h. Identical results were observed in adrenalectomized rats pretreated with one dose of a-methylprednisolone (2.5 mg/kg i.p.) 30-60 min before saline or endotoxin injection, indicating that endotoxin's effect was not mediated by hypersecretion of adrenal hormones. Cortisone pretreatment of normal rats (100 mg/kg per d) for 2 d prevented endotoxin-induced activation of muscle BCKAD, suggesting that endogenous secretion products mediated BCKAD activation by endotoxin. Human recombinant tumor necrosis factor-a and/or IL-1ft or a (50 jig/kg) increased muscle BCKAD activation two-to fourfold in normal rats 4-6 h after intravenous injection. We conclude that cytokine-mediated activation of muscle BCKAD may contribute to accelerated BCAA oxidation in

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Metabolic Adaptations for Energy Production During Trauma and Sepsis

Cited by 98 publications

References 63 publications

Adipose-tissue-derived Stem Cells Enhance the Healing of Ischemic Colonic Anastomoses: An Experimental Study in Rats

Adipose-tissue-derived Stem Cells Enhance the Healing of Ischemic Colonic Anastomoses: An Experimental Study in Rats

Short-term effects of tumor necrosis factor on energy and substrate metabolism in dogs.

Administration of endotoxin, tumor necrosis factor, or interleukin 1 to rats activates skeletal muscle branched-chain alpha-keto acid dehydrogenase.

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