Trial reportCritical care (London, England)2013
Critical illness induces nutrient-independent adipogenesis and accumulation of alternatively activated tissue macrophages.
Trial report in Critical care (London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Novel Adipokines in Critical Illness and Sepsis: Chemerin, Vaspin, and Omentin-1: A Comprehensive Evidence-Based Review.Biomedicines · 2026Review
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Clinical Outcomes of Hypocaloric/Hyperproteic vs Normocaloric Enteral Feeding in the Acute Phase of Critical Illness among Patients Admitted in the Intensive Care Unit: A Systematic Review with Meta-analysis.Indian journal of critical care medicine : peer-reviewed, official publication of Indian Society of Critical Care Medicine · 2024Article
- Development of muscle weakness in a mouse model of critical illness: does fibroblast growth factor 21 play a role?Skeletal muscle · 2023Article
- Shared biological mechanisms of depression and obesity: focus on adipokines and lipokines.Aging · 2023Review
- Skeletal Muscle Myokine Expression in Critical Illness, Association With Outcome and Impact of Therapeutic Interventions.Journal of the Endocrine Society · 2023Article
- Pseudomonas aeruginosa-derived pyocyanin reduces adipocyte differentiation, body weight, and fat mass as mechanisms contributing to septic cachexia.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2019Article
- Adipose tissue protects against sepsis-induced muscle weakness in mice: from lipolysis to ketones.Critical care (London, England) · 2019Article
- Proliferation and differentiation of adipose tissue in prolonged lean and obese critically ill patients.Intensive care medicine experimental · 2017Article
- The Role of Autophagy in Critical Illness-induced Liver Damage.Scientific reports · 2017Article
- Late Therapeutic Intervention with Antibiotics and Fluid Resuscitation Allows for a Prolonged Disease Course with High Survival in a Severe Murine Model of Sepsis.Shock (Augusta, Ga.) · 2017Article
- Inability to replete white adipose tissue during recovery phase of sepsis is associated with increased autophagy, apoptosis, and proteasome activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2017Article
- Premorbid obesity, but not nutrition, prevents critical illness-induced muscle wasting and weakness.Journal of cachexia, sarcopenia and muscle · 2017Article
- Adipose tissue alterations in critical illness: a paradox as to patient outcomes.Critical care (London, England) · 2013Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionWe previously reported that in artificially-fed critically ill patients, adipose tissue reveals an increase in small adipocytes and accumulation of M2-macrophages. We hypothesized that nutrient-independent factors of critical illness explain these findings, and that the M2-macrophage accumulation may not be limited to adipose tissue.
methodsIn a long-term cecal ligation and puncture (CLP) mouse model of sepsis, we compared the effect of parenteral nutrition (CLP-fed, n = 13) with nutrient restriction (CLP-restricted, n = 11) on body composition, adipocyte size and macrophage accumulation in adipose tissue, liver and lungs. Fed healthy mice (n = 11) were studied as controls. In a human study, in vivo adipose tissue biopsies were studied from ICU patients (n = 40) enrolled in a randomized control trial which compared early initiation of parenteral nutrition (PN) versus tolerating nutrient restriction during the first week of ICU stay. Adipose tissue morphology was compared with healthy human controls (n = 13).
resultsIrrespective of nutritional intake, critically ill mice lost weight, fat and fat-free mass. Adipocyte number, proliferation marker Proliferating Cell Nuclear Antigen (PCNA) and adipogenic markers PPARγ and CCAAT/enhancer binding protein-β (C/EBPβ) increased with illness, irrespective of nutritional intake. M2-macrophage accumulation was observed in adipose tissue, liver and lungs of critically ill mice. Macrophage M2-markers correlated with CCL2 expression. In adipose tissue biopsies of critically ill patients, increased adipogenic markers and M2 macrophage accumulation were present irrespective of nutritional intake.
conclusionsAdipogenesis and accumulation of tissue M2-macrophages are hallmarks of prolonged critical illness, irrespective of nutritional management. During critical illness, M2-macrophages accumulate not only in adipose tissue, but also in the liver and lungs.
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