Interleukin-8 modulates feeding by direct action in the central nervous system

1993 ◽  
Vol 265 (4) ◽  
pp. R877-R882 ◽  
Author(s):  
C. R. Plata-Salaman ◽  
J. P. Borkoski
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Food Intake ◽  
Direct Action ◽  
Intraperitoneal Administration ◽  
Interleukin 8 ◽  
Short Term ◽  
Lipopolysaccharide Endotoxin ◽  
The Central Nervous System ◽  
Necrosis Factor

Interleukin-8 (IL-8) is released in response to infection, inflammation, and trauma. The most important stimuli for IL-8 release during these pathological processes are IL-1, tumor necrosis factor, and bacterial lipopolysaccharide (endotoxin), factors that have been shown to suppress feeding. In the present study, the participation of IL-8 on the central regulation of feeding was investigated. Intracerebroventricular (icv) microinfusion of recombinant human IL-8 (rhIL-8, 1.0-100 ng/rat) suppressed the short-term (2-h) food intake. The most effective dose of rhIL-8, 20 ng, decreased 2-h food intake by 25% and nighttime food intake by 23%. Intracerebroventricular microinfusion of anti-rhIL-8 antibody (200 and 500 ng) blocked the effect of 20 ng rhIL-8 on 2-h and nighttime food intakes. Computerized analysis of behavioral patterns for the 2-h period demonstrated a specific reduction of meal size (by 33%), whereas meal frequency and meal duration were not affected after the icv microinfusion of 20 ng rhIL-8. This short-term food intake suppression by icv rhIL-8 was accompanied by a small, but significant, increase in cerebrospinal fluid-brain and rectal temperatures. Intraperitoneal administration of rhIL-8 in doses equivalent to those administered centrally had no effect on food intake. The results suggest that IL-8 acts directly in the central nervous system to decrease feeding. This effect of IL-8 may contribute to the food intake suppression frequently accompanying pathological processes.

Brain Respiration and Glycolysis in Cardiazol Convulsions

1940 ◽  
Vol 86 (361) ◽  
pp. 276-280 ◽  
Author(s):  
Leslie Dundonald MacLeod ◽  
Max Reiss
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Direct Action ◽  
Reducing Power ◽  
Liver Glycogen ◽  
Potassium Ions ◽  
Blood Picture ◽  
The Central Nervous System ◽  
Respiratory Centre ◽  
Convulsant Effect

Since Hildebrandt (1926) described the convulsant effect of cardiazol injection, several studies have been carried out on the mechanism of such convulsions. Zung and Tremonti (1931) suggested a direct action on the respiratory centre when cardiazol is used as a stimulant; Kerr and Antaki (1937) found no effect on brain glycogen or phosphocreatine in cardiazol-induced convulsions; Hashimoto (1937) found differences in distribution of calcium and potassium ions in the central nervous system after cardiazol. Goodwin and Lloyd (1938) recorded a direct effect on brain potential changes as shown on oscillographic records. Leibel and Hall (1938) found a large (75 per cent.) diminution of cerebral blood-flow at the onset of cardiazol convulsions. Weigand (1938) found no effect on liver glycogen or vitamin A content, reducing power of suprarenal cortex or blood picture. Denyssen and Watterson (1938) and Watterson and Macdonald (1939) attribute the convulsions to action on the vasomotor centre and note the action of vasodilator drugs in inhibiting convulsions. Wortis (1938) quoted by Quastel (1939) found no effect on brain respiration.

Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake

2004 ◽  
Vol 286 (1) ◽  
pp. G7-G13 ◽  
Author(s):  
Stephen C. Woods
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Food Intake ◽  
Social Situation ◽  
Meal Size ◽  
Gi Tract ◽  
The Social ◽  
Adiposity Signals ◽  
The Central Nervous System

An overview is presented of those signals generated by the gastrointestinal (GI) tract during meals that interact with the central nervous system to create a sensation of fullness and satiety. Although dozens of enzymes, hormones, and other factors are secreted by the GI tract in response to food in the lumen, only a handful are able to influence food intake directly. Most of these cause meals to terminate and hence are called satiety signals, with CCK being the most investigated. Only one GI signal, ghrelin, that increases meal size has been identified. The administration of exogenous CCK or other satiety signals causes smaller meals to be consumed, whereas blocking the action of endogenous CCK or other satiety signals causes larger meals to be consumed. Satiety signals are relayed to the hindbrain, either indirectly via nerves such as the vagus from the GI tract or else directly via the blood. Most factors that influence how much food is eaten during individual meals act by changing the sensitivity to satiety signals. This includes adiposity signals as well as habits and learning, the social situation, and stressors.

Brain-blood permeability: TNF-α promotes escape of protein tracer from CSF to blood

2000 ◽  
Vol 279 (1) ◽  
pp. R148-R151 ◽  
Author(s):  
Jodi B. Dickstein ◽  
Harvey Moldofsky ◽  
John B. Hay
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Tumor Necrosis ◽  
Venous Blood ◽  
Protein Clearance ◽  
Tracer Recovery ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Necrosis Factor

The objective of this study was to determine the effect of tumor necrosis factor (TNF)-α on the efflux of protein from the central nervous system to blood based on assessing the clearance of radiolabeled albumin from the cerebrospinal fluid (CSF) to blood in rats. 125I-labeled human serum albumin (125I-HSA) was injected into a lateral ventricle, and venous blood was sampled hourly to determine the basal CSF protein clearance into the blood. After this, rats were intraventricularly infused with 10 μl TNF-α and 10 μl131I-HSA ( n = 6) or 10 μl saline and 10 μl 131I-HSA ( n = 6). Venous blood was sampled hourly for 3 h. 131I-HSA tracer recovery increased threefold in the venous blood and was significantly higher in the spleen, muscles, and skin in animals treated with TNF-α. No significant changes were observed in control animals treated with saline. The data suggest that TNF-α promotes the clearance of protein macromolecules from the CSF to the venous blood.

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