Table 3 |
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The energy appeal reaction |
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Known reaction |
Physiological meaning in transient inflammatory episodes |
Pathophysiological problem in chronic inflammatory diseases |
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Fatigue |
Stop of energy expenditure for brain and muscles, stop of courtship and foraging behavior |
Depressive symptoms/longstanding fatigue (sickness behavior) |
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Anorexia |
Stop of energy expenditure for gut function |
Reduced or stopped uptake of energy-rich substrates |
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Malnutrition |
Stop of energy expenditure for gut function |
Reduced or stopped uptake of vitamins and trace elementsa |
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Muscle breakdown |
Stop of energy expenditure for muscles, and redirection of muscle proteins to gluconeogenesis |
Cachexia |
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Increased muscle relative to fat breakdown |
Stop of energy expenditure for muscles, and redirection of muscle proteins to gluconeogenesis |
Cachectic obesity |
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Insulin (insulin-like growth factor-1) resistance in liver, muscle, and fat tissue |
Redirection of glucose and free fatty acids to immune cells, which do not become insulin (insulin-like growth factor-1) resistant |
Insulin resistance as part of the metabolic syndrome |
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Appearance of a proinflammatory form of HDL cholesterol |
Acute-phase reaction of lipid metabolism leading to higher delivery of cholesterol and other lipids to macrophages |
Dyslipidemia as part of the metabolic syndrome |
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Alterations of steroid hormone axes |
Cytokine/leptin-driven hypoandrogenemia supports muscle breakdown and protein delivery for gluconeogenesis and support of an activated immune system (alanine, glutamine) |
Cortisol-to-androgen preponderance in chronic inflammation is catabolic and gluconeogenetic |
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Elevated sympathetic tone and local sympathetic nerve fiber loss, decreased parasympathetic tone |
Cytokine-driven increase of sympathetic nervous system activity increases gluconeogenesis and lipolysis. The parallel loss of sympathetic nerve fibers in inflamed tissue supports local inflammation and local lipolysis |
Hypertension as part of the metabolic syndrome |
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Increase of body water |
Cytokine-driven activation of the water retention system due to systemic water loss during inflammation |
Hypertension as part of the metabolic syndrome |
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Inflammation-related anemia |
Stop of energy expenditure for brain and muscle activity |
Anemia |
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Inflammation-related provision of calcium and phosphorus |
High calcium and phosphorus are mandatory for energy-consuming reactions (think of ATP) |
Local and general osteopenia |
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Data taken from [2,90]. HDL, high-density lipoprotein. aHypovitaminosis D and others, deficiency in zinc, iron, copper, magnesium, and similar. |
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Spies et al. Arthritis Research & Therapy 2012 14:216 doi:10.1186/ar3885 |
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