Signals generating anorexia during acute illness

Langhans, Wolfgang

doi:10.1017/s0029665107005587

Cited by 77 publications

(50 citation statements)

References 121 publications

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“…[4][5][6] It is well known that cytokines are able to inhibit appetite both in healthy conditions and in various diseases (cancer, sepsis, cardiac cachexia, chronic obstructive pulmonary disease). [18][19][20][21][22] Thus, it may be questioned why, in this study, the IL-6 levels of patients who had only anorexia did not differ from those of patients who complained fatigue alone or of patients who were both not-anorexic and fatigued. The answer to this question is difficult but some considerations may be helpful: (1) in a recent study we found a trend toward higher levels of CRP in patients with poor or very poor appetite with respect to patients with very good or good appetite, although the differences were not statistically significant; 8 (2) in this study, the median IL-6 levels in patients without anorexia and fatigue, with anorexia alone, and with fatigue alone were particularly low (all below 3 pg/mL); (3) our patients, unlike those of other studies, 4,5 received a Mediterranean diet and this may have contributed to low levels of IL-6;…”

Section: Discussionmentioning

confidence: 54%

Anorexia, fatigue, and plasma interleukin-6 levels in chronic hemodialysis patients

et al. 2010

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This study aimed at evaluating the possible relationship between anorexia and fatigue in hemodialysis (HD) patients and at measuring the plasma levels of interleukin-6 (IL-6) and C-reactive protein (CRP) in HD patients with or without anorexia and/or fatigue. The first question of the Hemodialysis Study Appetite questionnaire was used to assess the appetite of the HD patients and the vitality scale of the SF-36 to assess fatigue. The Charlson Comorbidity Index was assessed in each patient. Seventy-six HD patients were studied. Forty-four were males and 32 females. Thirty-two were classified as not-anorexic and not-fatigued, 12 as not-anorexic but fatigued, 6 as anorexic and not-fatigued, and 26 as anorexic and fatigued. Plasma IL-6 levels (pg/mL) were significantly higher in anorexic and fatigued patients (10.9 ± 11.9) than in not-anorexic and not-fatigued (1.6 ± 0.6) ( p < 0.001) and in anorexic but not-fatigued patients (1.8 ± 1.7) (p < 0.01). With respect to not-anorexic but fatigued patients (3.1 ± 1.5), the difference was not statistically significant (p = 0.058). The plasma CRP levels (mg/dL) also were significantly higher in anorexic and fatigued patients (9.2 ± 6.3) than in not-anorexic and not-fatigued patients (4.1 ± 4.5), in anorexic but not-fatigued patients (2.5 ± 1.6), and in not-anorexic but fatigued patients (4.1 ± 4.4) ( p = 0.001). The presence of both anorexia and fatigue in chronic HD patients is associated with significantly higher levels of plasma IL-6 and CRP and a higher frequency of comorbidities.

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Section: Discussionmentioning

confidence: 54%

Anorexia, fatigue, and plasma interleukin-6 levels in chronic hemodialysis patients

et al. 2010

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“…Like PPG neurons, serotonin neurons have been shown to be involved in the regulation of food intake (30,51), and both cell populations are activated by visceral malaise (48,52,80). Similarly, both cell populations have been implicated in thermoregulation (34,70).…”

Section: Medullary Projections Of Ppg Neuronsmentioning

confidence: 99%

PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation

Trapp

Cork

2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Within the brain, glucagon-like peptide-1 (GLP-1) affects central autonomic neurons, including those controlling the cardiovascular system, thermogenesis, and energy balance. Additionally, GLP-1 influences the mesolimbic reward system to modulate the rewarding properties of palatable food. GLP-1 is produced in the gut and by hindbrain preproglucagon (PPG) neurons, located mainly in the nucleus tractus solitarii (NTS) and medullary intermediate reticular nucleus. Transgenic mice expressing glucagon promoter-driven yellow fluorescent protein revealed that PPG neurons not only project to central autonomic control regions and mesolimbic reward centers, but also strongly innervate spinal autonomic neurons. Therefore, these brain stem PPG neurons could directly modulate sympathetic outflow through their spinal inputs to sympathetic preganglionic neurons. Electrical recordings from PPG neurons in vitro have revealed that they receive synaptic inputs from vagal afferents entering via the solitary tract. Vagal afferents convey satiation to the brain from signals like postprandial gastric distention or activation of peripheral GLP-1 receptors. CCK and leptin, short-and long-term satiety peptides, respectively, increased the electrical activity of PPG neurons, while ghrelin, an orexigenic peptide, had no effect. These findings indicate that satiation is a main driver of PPG neuronal activation. They also show that PPG neurons are in a prime position to respond to both immediate and long-term indicators of energy and feeding status, enabling regulation of both energy balance and general autonomic homeostasis. This review discusses the question of whether PPG neurons, rather than gut-derived GLP-1, are providing the physiological substrate for the effects elicited by central nervous system GLP-1 receptor activation. appetite; brain stem; glucagon-like peptide-1; hippocampus; neuroanatomy FOR TWO DECADES, IT HAS BEEN known that glucagon-like peptide (GLP-1) reduces food intake by acting within the central nervous system (95). That first study showed through the use of the GLP-1 receptor antagonist exendin-9 (Ex9) that endogenous GLP-1 has the ability to suppress food intake and that this effect is dependent on the feeding state of the animal. While unequivocally showing that GLP-1 has a physiological role in brain, the source of centrally acting GLP-1 remains less clear. Does postprandially released GLP-1 from the enteroendocrine L-cells reach the central nervous system (CNS) from the circulation, despite its short half-life in the blood, or does the small number of preproglucagon (PPG) neurons in the lower brain stem (37,58,65) provide sufficient GLP-1 for the plethora of brain regions that express its receptor? Although this question remains largely unanswered, it is clear that central GLP-1 is integral to many more processes linked to energy homeostasis than simply food intake. This review provides a detailed account of the different actions of GLP-1 in the brain, with a particular emphasis on the potential role of the PPG...

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“…Their neurons possess various membrane receptors for injuryassociated molecules such as cytokines, eicosanoids, and adenosine triphosphate. [12][13][14][15] They send partially overlapping axonal projections to the entire gray matter of forebrain and diencephalon, as well as many brainstem regions. 16,17 Serotonin, in addition to being a classic neurotransmitter, is known from an extensive literature to have positive developmental, neuroprotective, and regenerative effects.…”

Section: Introductionmentioning

confidence: 99%

Midbrain Raphe Stimulation Improves Behavioral and Anatomical Recovery from Fluid-Percussion Brain Injury

Gonzalez

Blaya

Alonso

et al. 2013

Journal of Neurotrauma

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The midbrain median raphe (MR) and dorsal raphe (DR) nuclei were tested for their capacity to regulate recovery from traumatic brain injury (TBI). An implanted, wireless self-powered stimulator delivered intermittent 8-Hz pulse trains for 7 days to the rat's MR or DR, beginning 4-6 h after a moderate parasagittal (right) fluid-percussion injury. MR stimulation was also examined with a higher frequency (24 Hz) or a delayed start (7 days after injury). Controls had sham injuries, inactive stimulators, or both. The stimulation caused no apparent acute responses or adverse long-term changes. In watermaze trials conducted 5 weeks post-injury, early 8-Hz MR and DR stimulation restored the rate of acquisition of reference memory for a hidden platform of fixed location. Short-term spatial working memory, for a variably located hidden platform, was restored only by early 8-Hz MR stimulation. All stimulation protocols reversed injury-induced asymmetry of spontaneous forelimb reaching movements tested 6 weeks post-injury. Post-mortem histological measurement at 8 weeks post-injury revealed volume losses in parietal-occipital cortex and decussating white matter (corpus callosum plus external capsule), but not hippocampus. The cortical losses were significantly reversed by early 8-Hz MR and DR stimulation, the white matter losses by all forms of MR stimulation. The generally most effective protocol, 8-Hz MR stimulation, was tested 3 days post-injury for its acute effect on forebrain cyclic adenosine monophosphate (cAMP), a key trophic signaling molecule. This procedure reversed injury-induced declines of cAMP levels in both cortex and hippocampus. In conclusion, midbrain raphe nuclei can enduringly enhance recovery from early disseminated TBI, possibly in part through increased signaling by cAMP in efferent targets. A neurosurgical treatment for TBI using interim electrical stimulation in raphe repair centers is suggested.

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Signals generating anorexia during acute illness

Cited by 77 publications

References 121 publications

Anorexia, fatigue, and plasma interleukin-6 levels in chronic hemodialysis patients

Anorexia, fatigue, and plasma interleukin-6 levels in chronic hemodialysis patients

PPG neurons of the lower brain stem and their role in brain GLP-1 receptor activation

Midbrain Raphe Stimulation Improves Behavioral and Anatomical Recovery from Fluid-Percussion Brain Injury

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