Increased intestinal protein synthesis during sepsis and following the administration of tumour necrosis factor <i>α</i> or interleukin-1 <i>α</i>

Allmen, Daniel von; Hasselgren, Per-Olof; Higashiguchi, Takashi; Frederick, Janice A.; Zamir, Oded; Fischer, Josef E.

doi:10.1042/bj2860585

Cited by 32 publications

(18 citation statements)

References 34 publications

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“…has been shown that an acutely induced systemic inflammation results in increased protein catabolism and altered protein synthesis (24,33), showing the importance of inflammation in protein metabolism. Furthermore, chronic inflammation induced by DSS treatment in rats resulted in a stimulation of protein synthesis in various splanchnic organs, i.e., the spleen and intestine, whereas muscle protein turnover was reduced (24).…”

Section: Discussionmentioning

confidence: 99%

Mice with experimental colitis show an altered metabolism with decreased metabolic rate

Melgar¹,

Bjursell²,

Gerdin³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Melgarn S, Bjursell M, Gerdin AK, Svensson L, Michaëlsson E, and Bohlooly-Y M. Mice with experimental colitis show an altered metabolism with decreased metabolic rate. Am J Physiol Gastrointest Liver Physiol 292: G165-G172, 2007. First published July 13, 2006; doi:10.1152/ajpgi.00152.2006.-Patients with inflammatory bowel disease (IBD) suffer from body weight loss, malnutrition, and several other metabolic alterations affecting their quality of life. The aim of this study was to investigate the metabolic changes that may occur during acute and chronic colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Clinical symptoms and inflammatory markers revealed the presence of an ongoing inflammatory response in the DSS-treated mice. Mice with acute inflammation had decreased body weight, respiratory exchange ratios (RER), food intake, and body fat content. Mice with chronic inflammation had decreased nutrient uptake, body fat content, locomotor activity, metabolic rates, and bone mineral density. Despite this, the body weight, food and water intake, lean mass, and RER of these mice returned to values similar to those in healthy controls. Thus, murine experimental colitis is associated with significant metabolic alterations similar to IBD patients. Our data show that the metabolic responses during acute and chronic inflammation are different, although the metabolic rate is reduced in both phases. These observations suggest compensatory metabolic alterations in chronic colitis resulting in a healthy appearance despite gross colon pathology. dual-energy X-ray absorptiometry; dextran sulfate sodium; colon inflammation; respiratory exchange ratio INFLAMMATORY BOWEL DISEASE (IBD) in humans consists of two main chronic diseases: ulcerative colitis (UC) and Crohn's disease (CD). Patients with CD can be affected anywhere along the gastrointestinal tract, with the majority being affected in the ileum or in the ileocolonic area. The inflammatory response can extend through all layers of the intestinal wall (28). In contrast, patients with UC are affected in the large intestine, where the inflammation starts in the rectum and spreads upward. The inflammatory response is usually confined to the mucosal layer (28). UC and CD are chronic diseases, and IBD patients have an affected quality of life, suffering from wasting and malnutrition, hypoalbuminemia, anemia, and various vitamin and mineral deficiencies (12). As a consequence, the body composition of an adult IBD patient is altered, e.g., with a reduction in bone mineral density (BMD), which implies that there is a high prevalence of osteopenia and osteoporosis in these patients (20). Nutritional impairment occurs in up to 60% of UC patients and in up to 75% of CD patients (6). It has been suggested that factors contributing to weight loss in CD patients are suppression of food intake secondary to anorexia and pain associated with eating (26, 29). Furthermore, an increased metabolic rate and a reduction in body fat mass may contribute to the decreased body weigh...

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Section: Discussionmentioning

confidence: 99%

Mice with experimental colitis show an altered metabolism with decreased metabolic rate

Melgar¹,

Bjursell²,

Gerdin³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Animals from each group received a bolus intravenous injection of L-[ l-'3C]valine (150 pmo1/100 g body weight, 30 atom% excess, 0.5 m1/100 g body weight) (~-[l-'~C]valine, 99 atom% from Mass Trace, Woburn, MA, U.S.A.). In each group, one animal was killed by decapitation after anaesthesia with sodium pentobarbital (6 mg/100 g body weight) at 4,8,12,16,20,24,28,36,44 and 52min after the tracer injection. Times from 4 to 24 min were used for the determination of liver and intestine protein synthesis rates, in order to take into account the synthesis of exported proteins.…”

Section: Measurement Of Protein Synthesismentioning

confidence: 99%

Sustained Modifications of Protein Metabolism in Various Tissues in a Rat Model of Long-Lasting Sepsis

Breuillé

Arnal²,

Rambourdin³

et al. 1998

Clinical Science

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1. Sepsis was induced in rats by an intravenous injection of live bacteria. Infected and pair-fed animals were studied before the infection, in an acute septic phase (day 2 post-infection), in a chronic septic phase (day 6) and in a late septic phase (day 10). Protein synthesis rates were measured in vivo after administration of a flooding dose of L[1-13C]valine. 2. During the acute phase, muscle protein loss associated with infection resulted from both a decrease in protein synthesis and an increase in proteolysis. During the chronic phase and the late phase, the increase of proteolysis in infected rats as compared with pair-fed animals persisted, worsening muscle atrophy. Skin protein synthesis rates were not significantly modified by infection. However, skin protein content decreased 6 and 10 days after infection, suggesting an increased proteolysis in response to sepsis. 3. Protein synthesis in liver of infected rats was twice that of pair-fed animals. Liver protein synthesis remained elevated in infected rats compared with pair-fed animals until day 10. Hypoalbuminaemia and high plasma concentrations of fibrinogen were evident at all periods studied. alpha 2-Macroglobulin and alpha 1-acid glycoprotein reached peak concentrations during the acute phase (concentrations increased 50 times in infected rats). On day 10, the levels of these proteins were still about 12-fold higher. 4. Protein synthesis rates were significantly increased in the digestive tract and lung of infected rats compared with pair-fed groups on days 2 and 6, but were similar in the two groups on day 10 post-infection. The fractional protein synthesis rate was increased 3-fold over the entire experimental period in the spleen. 5. The results show that sepsis stimulates protein synthesis in various tissues over a long time, and that skin, like muscle, can provide amino acids to the rest of the body.

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“…Previous studies suggest that the enterocyte and intestinal mucosa participate in the inflammatory and metabolic responses to sepsis and endotoxaemia [1][2][3][4]. For example, we recently found evidence that the acute-phase protein complement component C3 is produced in the mucosa of the small intestine after injection of endotoxin in mice [5], and in cultured Caco-2 cells (a human intestinal epithelial cell line) following treatment with interleukin-1β (IL-1β) described in cells subjected to hyperthermia [14].…”

Section: Introductionmentioning

confidence: 99%

Stress response decreases the interleukin-1β-induced production of complement component C3 in human intestinal epithelial cells

Moon

Pritts

Parikh³

et al. 1999

Clinical Science

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Interleukin-1beta (IL-1beta) increases the production of complement component C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various cell types. We tested the hypothesis that the heat-shock response regulates IL-1beta-induced C3 production in the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10-500 microM) for 1 h or subjected to hyperthermia (43 degrees C) for 1-4 h, and allowed to recover for 1 h. The cells were then treated with IL-1beta (0.5 ng/ml) for up to 24 h, whereafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analysis. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot analysis. Treatment of the cells with sodium arsenite or subjecting them to hyperthermia induced the expression of hsp72. The IL-1beta-induced expression of C3 mRNA and C3 production were down-regulated by hyperthermia and sodium arsenite in a dose-dependent fashion. The results suggest that the stress response induced by hyperthermia or sodium arsenite decreases IL-1beta-induced C3 production in human enterocytes.

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Increased intestinal protein synthesis during sepsis and following the administration of tumour necrosis factor α or interleukin-1 α

Cited by 32 publications

References 34 publications

Mice with experimental colitis show an altered metabolism with decreased metabolic rate

Mice with experimental colitis show an altered metabolism with decreased metabolic rate

Sustained Modifications of Protein Metabolism in Various Tissues in a Rat Model of Long-Lasting Sepsis

Stress response decreases the interleukin-1β-induced production of complement component C3 in human intestinal epithelial cells

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