Cytokines and feeding

Plata‐Salamán, Carlos R.

doi:10.1038/sj.ijo.0801911

Cited by 136 publications

(56 citation statements)

References 27 publications

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“…Data in Experiment 1 indicate that the ICV injection of LPS decreases feed intake 4 h post injection in FD 3 chicks which was in agreement with previous reports in rat (Langhans et al 1989), goldfish (Volkoff and Peter 2004), mammals (Inui 2001(Inui , 2002Plata-Salaman 2001), and chicken (Johnson et al 1993;Zendehdel et al 2012d). Previous as well as recent studies proved the hypophagic effect of peripheral and central injection of LPS.…”

Section: Discussionsupporting

confidence: 92%

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The role of cyclooxygenase inhibitors in lipopolysaccharide-induced hypophagia in chicken

Zendehdel¹,

Baghbanzadeh²,

Yeganeh³

et al. 2015

CZECH J ANIM SCI

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Previous studies showed that cyclooxygenase 1 (COX) enzyme has an important role in lipopolysaccharide (LPS)-induced hypophagia in mammals but the effect of COX on LPS-induced hypophagia has not been studied in avian species. The current study was designed to investigate the effects of Indomethacin, a non-selective cyclooxygenase inhibitor, Aspirin (irreversible cyclooxygenase inhibitor), Piroxicam (a selective COX-1 inhibitor), and Celecoxib (a selective COX-2 inhibitor) on LPS-induced hypophagia in 3-h fooddeprived (FD 3 ) cockerels. One hundred and sixty ROSS 308 chickens were randomly divided into 5 experiments and 4 treatment groups (8 replicates in each group of experiments). Guide cannula was surgically implanted into the lateral ventricle of chickens. In Experiment 1, birds received LPS (5, 10, and 20 ng) intracerebroventricularly (ICV). In Experiment 2, chickens were intraperitoneally (i.p.) injected with Indomethacin (5 mg/kg) prior to LPS injection (20 ng; ICV). In Experiment 3, birds were i.p. injected with Aspirin (50 mg/kg) followed by LPS injection (20 ng; ICV). In Experiment 4, chickens were given LPS (20 ng; ICV) after Piroxicam injection (10 mg/kg; i.p.). In Experiment 5, chickens were injected with Celecoxib (10 mg/kg; i.p.) prior to LPS injection (20 ng; ICV). Cumulative feed intake was determined until 8 h post-injection. According to the results, LPS significantly decreased feed intake at 4 and 8 h post injection in birds (P ≤ 0.05). Furthermore, LPS-induced hypophagia was attenuated by pre-injection with Indomethacin, Aspirin, and Celecoxib (P ≤ 0.05). However, Piroxicam had no effect on LPS-induced hypophagia (P ≥ 0.05). These results suggest that presumably COX-2 mediates LPS-induced hypophagia in broilers.

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Section: Discussionsupporting

confidence: 92%

“…injection of LPS (125, 100, 75, and 50 μg/kg) suppressed feed retake in rat. The same results were reported on food intake after administration of LPS in mammals (Inui 2001;Plata-Salaman 2001;Inui 2002). …”

Section: Introductionsupporting

confidence: 82%

The role of cyclooxygenase inhibitors in lipopolysaccharide-induced hypophagia in chicken

Zendehdel¹,

Baghbanzadeh²,

Yeganeh³

et al. 2015

CZECH J ANIM SCI

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“…Conversely, weight loss and exercise decrease IL-18 levels (Bruun et al, 2007; Esposito et al, 2003; Leick et al, 2007; Madsen et al, 2009; Vilarrasa et al, 2007). Some adipocytokines whose levels increase with obesity (e.g, leptin) oppose positive energy balance in negative feedback fashion (Plata-Salaman, 2001; Wong and Pinkney, 2004). Perhaps reminiscent of obesity-related leptin resistance, leukocytes from patients with obesity or type 2 diabetes are resistant to IL-18 (Zilverschoon et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Interleukin-18 null mutation increases weight and food intake and reduces energy expenditure and lipid substrate utilization in high-fat diet fed mice

Zorrilla

Conti

2014

Brain, Behavior, and Immunity

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Objective The proinflammatory cytokine interleukin-18 (IL-18) putatively modulates food intake and energy metabolism, but the effects of IL-18 in high-fat diet fed animals are unknown. Whether IL-18 alters basal metabolic rate or metabolic processes of living is unknown. Here, we tested the hypothesis that IL-18 modulates weight gain, energy intake, whole-body energy expenditure, and utilization of lipid as a fuel substrate in high-fat diet fed mice. Methods Food intake, whole-body metabolism, and motor activity of IL-18 knockout mice were compared to those of wildtype littermates; anorectic effects of intracerebroventricular IL-18 administration were compared between IL-18 receptor knockout, IL-18/IL-18R knockout and wildtype mice. Results Chow-reared IL-18 knockout mice were overweight at 6 months of age and then gained excess weight on both low-fat and high-fat diets, ate more high-fat diet, and showed reduced whole-body energy expenditure and increased respiratory exchange ratios. Reductions in energy expenditure of IL-18 knockout mice were seen across fasting vs. feeding conditions, low- vs. high-fat diets, high vs. low levels of physical activity and times of day, suggesting actions on basal metabolic rate. The circadian amplitude of energy expenditure, but not respiratory exchange ratio, food intake, or motor activity, also was blunted in IL-18 knockout mice. Central IL-18 administration reduced high-fat diet intake in wildtype mice, but not in mice lacking the IL-18 receptor. Conclusion The loss-of-function results support the hypothesis that endogenous IL-18 suppresses appetite and promote energy expenditure and lipid fuel substrate utilization not only during sickness, but also in healthy adults consuming high-fat diets.

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“…Inflammation is often accompanied with anorexia, but the mechanisms underlying this phenomenon are poorly understood (Plata-Salaman 2001). One of the pathways could involve MCH neurons.…”

Section: Physiopathological Considerationsmentioning

confidence: 99%

Multiple actions of the chemokine stromal cell-derived factor-1α on neuronal activity

Guyon¹,

Nahon²

2007

Journal of Molecular Endocrinology

118

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The chemokine SDF-1a and its cognate receptor CXCR4 are expressed in several neuronal populations. This review focuses on our current knowledge about the actions of this chemokine on neuronal excitability, through CXCR4 or other yet unknown pathways. In various neuronal populations (CA1 neurons of the hippocampus, granular and Purkinje cells of the cerebellum, melanin-concentrating hormone neurons of the lateral hypothalamus, vasopressinergic neurons of the supraoptic and the paraventricular nucleus of the hypothalamus, and dopaminergic neurons of the substantia nigra), SDF-1a can modulate the activity of neurons by multiple regulatory pathways including and often combining: (i) modulation of voltage-dependent channels (sodium, potassium, and calcium), (ii) activation of the G-protein-activated inward rectifier potassium current, and (iii) increase in neurotransmitter release (gamma-amino butyric acid (GABA), glutamate, and dopamine), often through Ca-dependent mechanisms. The possible mechanisms underlying these effects and their consequences in terms of modulation of neuroendocrine systems and physiopathology are discussed.

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Cytokines and feeding

Cited by 136 publications

References 27 publications

The role of cyclooxygenase inhibitors in lipopolysaccharide-induced hypophagia in chicken

The role of cyclooxygenase inhibitors in lipopolysaccharide-induced hypophagia in chicken

Interleukin-18 null mutation increases weight and food intake and reduces energy expenditure and lipid substrate utilization in high-fat diet fed mice

Multiple actions of the chemokine stromal cell-derived factor-1α on neuronal activity

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