Central nervous system mechanisms contributing to the cachexia–anorexia syndrome

Plata‐Salamán, Carlos R.

doi:10.1016/s0899-9007(00)00413-5

Cited by 231 publications

(139 citation statements)

References 37 publications

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“…Loss of taste/aversion and loss of appetite may be symptoms of the cancer anorexia-cachexia syndrome [12,21]. This syndrome is the result of a multifactorial process involving cytokines, hormones and neuropeptides [15,21,22].…”

Section: Discussionmentioning

confidence: 99%

Critical weight loss in head and neck cancer—prevalence and risk factors at diagnosis: an explorative study

Jager‐Wittenaar

Dijkstra

Vissink

et al. 2007

Support Care Cancer

164

132

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Goals of work Critical weight loss (≥5% in 1 month or ≥10% in 6 months) is a common phenomenon in head and neck cancer patients. It is unknown which complaints are most strongly related to critical weight loss in head and neck cancer patients at the time of diagnosis. The aim of this explorative study was to assess the prevalence of critical weight loss and to analyze risk factors for critical weight loss in head and neck cancer patients before treatment. Materials and methods Critical weight loss and factors reducing dietary intake were assessed in 447 patients referred to an ear, nose and throat clinic at the time of diagnosis. Main results In total, data of 407 patients were analyzed. Critical weight loss was present in 19% of the patients. Patients with cancer in the hypopharynx, oropharynx/oral cavity and supraglottic larynx had the highest risk for critical weight loss. Loss of appetite, dysphagia/passage difficulties and loss of taste/aversion were significantly (p<0.05) associated with critical weight loss. Conclusions Already before treatment, critical weight loss is a considerable problem in head and neck cancer patients. Critical weight loss is frequently observed in patients with cancer in the hypopharynx, oropharynx/oral cavity and supraglottic larynx.

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Section: Discussionmentioning

confidence: 99%

Critical weight loss in head and neck cancer—prevalence and risk factors at diagnosis: an explorative study

Jager‐Wittenaar

Dijkstra

Vissink

et al. 2007

Support Care Cancer

164

132

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“…In patients with OGC, a number of primary and secondary causes of reduced dietary intake are at work simultaneously, including dysphagia (McKernan et al, 2008), early satiety (Davis et al, 2006), chronic nausea (McKernan et al, 2008), alterations in circulating neuroendocrine hormones (e.g., ghrelin (Isomoto et al, 2005) and leptin (Huang et al, 2005;Zhao et al, 2007)), hypogeusia/hyposmia (Plata-Salaman, 2000), and cytokine-induced central anorexia (Plata-Salaman, 2001;Turrin et al, 2004). Assuming that MIC-1 may be a modulator of appetite in humans, the complex constellation of additional factors also controlling food intake may explain why plasma MIC-1 concentrations did not correlate with nutritional status in this study.…”

Section: Crp (Mg Lmentioning

confidence: 99%

Plasma MIC-1 correlates with systemic inflammation but is not an independent determinant of nutritional status or survival in oesophago-gastric cancer

et al. 2010

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BACKGROUND: Macrophage inhibitory cytokine-1(MIC-1) is a potential modulator of systemic inflammation and nutritional depletion, both of which are adverse prognostic factors in oesophago-gastric cancer (OGC). METHODS: Plasma MIC-1, systemic inflammation (defined as plasma C-reactive protein (CRP) of X10 mg l -1 or modified Glasgow prognostic score (mGPS) of X1), and nutritional status were assessed in newly diagnosed OGC patients (n ¼ 293). Healthy volunteers (n ¼ 35) served as controls. RESULTS: MIC-1 was elevated in patients (median ¼ 1371 pg ml -1 ; range 141 -39 053) when compared with controls (median ¼ 377 pg ml -1 ; range 141 -3786; Po0.001). Patients with gastric tumours (median ¼ 1592 pg ml -1 ; range 141 -12 643) showed higher MIC-1 concentrations than patients with junctional (median ¼ 1337 pg ml -1 ; range 383 -39 053) and oesophageal tumours (median ¼ 1180 pg ml -1 ; range 258 -31 184; P ¼ 0.015). Patients showed a median weight loss of 6.4% (range 0.0 -33.4%), and 42% of patients had an mGPS of X1 or plasma CRP of X10 mg l -1 (median ¼ 9 mg l -1 ; range 1 -200). MIC-1 correlated positively with disease stage (r 2 ¼ 0.217; Po0.001), age (r 2 ¼ 0.332; Po0.001), CRP (r 2 ¼ 0.314; Po0.001), and mGPS (r 2 ¼ 0.336; Po0.001), and negatively with Karnofsky Performance Score (r 2 ¼ À0.269; Po0.001). However, although MIC-1 correlated weakly with dietary intake (r 2 ¼ 0.157; P ¼ 0.031), it did not correlate with weight loss, BMI, or anthropometry. Patients with MIC-1 levels in the upper quartile showed reduced survival (median ¼ 204 days; 95% CI 157 -251) when compared with patients with MIC-1 levels in the lower three quartiles (median ¼ 316 days; 95% CI 259 -373; P ¼ 0.036), but MIC-1 was not an independent prognostic indicator. CONCLUSIONS: There is no independent link between plasma MIC-1 levels and depleted nutritional status or survival in OGC.

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“…In IL-6 knockout mice, a central injection of IL-6 caused a significant increase in energy expenditure, which was not mediated by peripheral injection (1). In humans, high cytokine levels (including IL-6) and cytokine brain synthesis were found to increase resting energy expenditure and induce cachexia (7). Additionally, a subcutaneous injection of IL-6 increased resting metabolic rate and hypothalamic-pituitary-adrenal axis activity in a dose-dependent fashion, suggesting that hypothalamic corticotrophin-releasing hormone may mediate both of these actions in humans (8).…”

Section: Diabetes Vol 52 February 2003mentioning

confidence: 99%

The C-174G Promoter Polymorphism of the IL-6 Gene Affects Energy Expenditure and Insulin Sensitivity

Kubaszek

Pihlajamäki

Punnonen³

et al. 2003

Diabetes

131

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1Interleukin-6 (IL-6) is a pleiotropic cytokine expressed in many tissues. IL-6 null mice show low energy expenditure, but the effect of the variants of the IL-6 gene on energy expenditure has not been previously studied in humans. Therefore, we investigated the effect of the C-174G promoter polymorphism of the IL-6 gene on energy expenditure, measured by indirect calorimetry in healthy Finnish subjects (n ‫؍‬ 124). We also measured insulin sensitivity by the hyperinsulinemic-euglycemic clamp. Subjects with the C-174C genotype of the IL-6 gene had significantly lower energy expenditure than subjects with the G-174C or G-174G genotypes both in fasting (CC 13. 68 ; P ‫؍‬ 0.016). The rates of both oxidative (P ‫؍‬ 0.013) and nonoxidative (P ‫؍‬ 0.016) glucose disposal were significantly affected by the IL-6 promoter polymorphism. In conclusion, the C-174C promoter polymorphism of the IL-6 gene influences energy expenditure and insulin sensitivity in healthy normoglycemic subjects. Whether this polymorphism is a risk factor for obesity or type 2 diabetes can be estimated only in prospective population-based studies. Diabetes 52:558 -561, 2003 I nterleukin-6 (IL-6) is a multifunctional cytokine expressed in many tissues, including adipose tissue, skeletal muscle and hypothalamus, which are involved in the regulation of body energy balance. In IL-6 null mice, the lack of circulating IL-6 was associated with obesity and low energy expenditure (1). Moreover, IL-6 -deficient mice exhibited high leptin levels and leptin insensitivity, and did not lose weight or decrease food intake after leptin treatment. The promoter of the IL-6 gene is dynamically regulated at many sites, including the multiple response element (Ϫ173 to 145), which responds to interleukin-1, tumor necrosis factor-␣, and other factors (2). The recently described C-174G promoter polymorphism of the IL-6 gene has been found to influence transcriptional regulation (2,3) and plasma IL-6 levels in patients with systemic-onset juvenile chronic arthritis and in patients with primary Sjö gren's syndrome (3,4). Moreover, the C-164G polymorphism has been found to be associated with insulin resistance measured by a frequently sampled intravenous glucose tolerance test in one previous study (5).In humans, the effect of the C-174G promoter polymorphism of the IL-6 gene on energy expenditure has not been previously studied. Therefore, we investigated the effect of this polymorphism on energy expenditure and insulin sensitivity during fasting and during the euglycemic-hyperinsulinemic clamp in 124 healthy normoglycemic subjects.The frequency of the CC genotype was 30%, the CG genotype 44%, and the GG genotype 26% in our study subjects. Age, BMI and waist-to-hip ratio, systolic and diastolic blood pressure, fasting plasma glucose and insulin levels, and IL-6 concentration (n ϭ 72) did not differ among the genotypes (Table 1).Fasting energy expenditure was 8% lower in subjects with the CC genotype than in subjects with the CG or GG genotypes (13.68 Ϯ 1.98, 14.73 Ϯ 1.57...

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Central nervous system mechanisms contributing to the cachexia–anorexia syndrome

Cited by 231 publications

References 37 publications

Critical weight loss in head and neck cancer—prevalence and risk factors at diagnosis: an explorative study

Critical weight loss in head and neck cancer—prevalence and risk factors at diagnosis: an explorative study

Plasma MIC-1 correlates with systemic inflammation but is not an independent determinant of nutritional status or survival in oesophago-gastric cancer

The C-174G Promoter Polymorphism of the IL-6 Gene Affects Energy Expenditure and Insulin Sensitivity

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