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W Langhans

Publications and source records attributed to W Langhans.

At least 19 recordsLinked to original sources
PubMed1992

[Effect of carbohydrate intake during a long distance run on work capacity and metabolism].

The present study addressed the effects of carbohydrate consumption during endurance exercise on performance, energy turnover, and metabolism. Well-trained endurance runners consumed a beverage with (cho[+]) or without (cho[-]) carbohydrates during a long-distance run (46.6 km). The respiratory quotient (RQ), plasma levels of carbohydrate and fat metabolites, and of hormones (insulin, glucagon) were measured before, several times during, and after the run. The mean running speed for the entire distance was 13.6 and 13.4 km/h with the cho[+] and cho[-] beverage, respectively. The decrease in speed that was observed towards the end of the run was somewhat more pronounced with consumption of the cho[-] beverage. The RQ decreased during the run almost linearly. This decrease was independent of the consumed beverage. The changes in plasma levels of lactate, free fatty acids (FFA), glycerol, D-3-hydroxybutyrate (DHB), glucagon and insulin that occurred during the run were not affected by intake of the cho[+] beverage. However, intake of the cho[+] beverage prevented the decrease in plasma glucose observed towards the end of the run under control conditions, and eliminated the steep postexercise increase in plasma DHB. The intake of the cho[+] beverage also caused a rapid decrease in plasma levels of FFA and glucagon after the run, and slightly increased plasma insulin. The results demonstrate that ingestion of a carbohydrate-containing beverage during a long-distance run affects metabolism only during the final phase of the run and during the subsequent recovery period. Moreover, carbohydrate consumption improves performance only during the final phase of a long-distance run.

3-Hydroxybutyric Acid↗
PubMed1992

Enhancement or loss of the hypophagic effect of interleukin-1 upon chronic administration.

To further characterize the effect of interleukin-1 on food intake, we tested whether a tolerance to the hypophagic effect of recombinant human interleukin-1 beta (rhIL-1 beta) develops with repeated injections or continuous infusion in rats. Daily intraperitoneal (IP) injections of rhIL-1 beta (25,000 LAF units/kg b.wt.) for 4 days did not result in tolerance to rhIL-1 beta's hypophagic effect. The hypophagic effect of the same dose of rhIL-1 beta actually increased if injections were given every second day, when the hypophagic effect of the preceding injection had subsided. A dose of rhIL-1 beta that usually did not affect food intake (5000 LAF units/kg b.wt.) reduced food intake if injected repeatedly. Continuous infusion of rhIL-1 beta (25,000 LAF units/kg b.wt/day) via IP-implanted osmotic minipumps caused a strong initial suppression of feeding followed by the development of tolerance to the hypophagic effect of the infused rhIL-1 beta. Nevertheless, hypophagia caused by a subsequent IP injection of rhIL-1 beta (25,000 LAF units/kg b.wt.) was enhanced. As specific antibodies to rhIL-1 beta could be detected in sera of only three of 11 rhIL-1 beta-infused rats, the observed tolerance was probably not due to a humoral immune response. The results demonstrate that, dependent on test conditions, chronic administration of rhIL-1 beta in the rat can lead to an enhancement or to a loss of its hypophagic effect. The reasons for this difference remain unclear.

Animals↗
PubMed1991

Mechanisms of vasopressin's anorectic effect.

The present experiments investigated the effect of vasopressin (VP) on food intake in rats under various conditions. VP (1.25-10 micrograms/kg body weight = b.wt.) injected intraperitoneally (IP) at the onset of the dark phase of the lighting cycle inhibited feeding in a dose-dependent manner. The suppression of feeding induced by VP was primarily due to a delayed onset of the first meal after injection and was reversed by a V1-receptor antagonist (7 micrograms/kg b.wt., IP), by the Ca(++)-channel blocker verapamil (5 mg/kg b.wt., IP) and by the alpha-adrenergic receptor antagonist phentolamine (500 micrograms/kg b.wt.), but not by dissection of the hepatic branch of the vagus. In further experiments VP inhibited gastric emptying. This effect was not reversed by phentolamine. VP had also an aversive effect, but this effect was weaker than that of LiCl and probably not involved in VP-induced hypophagia. The results suggest that VP reduces feeding through a V1-receptor-mediated activation of an alpha-adrenergic mechanism. The inhibition of gastric emptying or a possible stimulation of hepatic oxidative metabolism by VP seems to be not essential for VP's effect on feeding. The results are consistent with a role of VP in stress-induced anorexia in rats.

Animals↗
PubMed1991

Hepatic and intestinal handling of metabolites during feeding in rats.

Changes in hepatic vein, hepatic portal vein and aortal plasma levels of glucose, lactate, nonesterified fatty acids, and D-3-hydroxybutyrate as well as changes in hepatic glycogen and lactate levels were studied during feeding after 12 h of food deprivation in rats. Feeding caused an increase in portal vein lactate concentration and a transient net hepatic lactate uptake that led to hepatic lactate accumulation. As in previous experiments, feeding was associated with hepatic glycogenolysis and net hepatic glucose release, despite a profound increase in portal vein plasma glucose. Net hepatic uptake of nonesterified fatty acids and net hepatic release of D-3-hydroxybutyrate declined during feeding but did not cease, suggesting that hepatic fatty acid oxidation continued throughout feeding. A prandial net intestinal uptake from arterial blood was observed for nonesterified fatty acids and D-3-hydroxybutyrate, while a net intestinal release was found for glucose and lactate. The results are consistent with the idea that under the conditions tested, glucose, lactate and nonesterified fatty acids jointly activate a hepatic metabolic mechanism of satiety.

3-Hydroxybutyric Acid↗
PubMed1991

Changes in feeding behavior and plasma vasopressin concentration during water deprivation in goats.

To further characterize the suppression of feeding that normally accompanies water deprivation and to test whether vasopressin contributes to this hypophagia, food intake, meal patterns and plasma vasopressin concentrations were measured during 24 h or 72 h of water deprivation in pygmy goats. The effects of exogenous vasopressin and of a V1-receptor antagonist on feeding during water deprivation were also assessed. The hypophagia during water deprivation was primarily due to decreases in meal size. The plasma vasopressin concentration increased about 2.5-fold and 10-fold after 24 and 72 h of water deprivation, respectively. Plasma osmolality also increased (measured only after 72 h of water deprivation). Intraperitoneally (ip) injected vasopressin (1.5 micrograms/kg b. wt.) that previously reduced food intake in goats with ad lib, access to water (Meyer et al., 1989), failed to affect cumulative food intake in water deprived goats, but led to a transient increase in meal size. The V1-receptor antagonist (2.5 micrograms/kg b. wt., ip) did not affect cumulative food intake or meal patterns either. These findings indicate that endogenous vasopressin is not crucially involved in the hypophagia during water deprivation. The results are in line with the hypothesis that an abnormal prandial increase in the osmolality of the ruminal fluid is a major contributor to the hypophagia during water deprivation.

Animals↗
PubMed1991

Differential feeding responses to bacterial lipopolysaccharide and muramyl dipeptide.

The present study was designed to test whether a tolerance to the hypophagic effects of bacterial lipopolysaccharide (LPS) and muramyl dipeptide (MDP) develops with repeated injections in rats and whether a relationship between the hypophagic effects of both compounds exists. Only the first of three subsequent intraperitoneal injection of LPS (100 micrograms/kg body wt each), given every 2nd day, led to a significant reduction of food intake. In contrast, MDP (1.6 mg/kg body wt) did not lose its hypophagic effect with four subsequent intraperitoneal injections. Furthermore, the LPS tolerance did not alter the hypophagic response to subsequently injected MDP. Likewise, MDP pretreatment did not alter the hypophagic response to LPS. Doses of MDP and LPS that were individually below the threshold for a reliable reduction of food intake (0.4 mg MDP/kg body wt + 25 micrograms LPS/kg body wt) reduced food intake synergistically when injected together. The hypophagia produced by combined injections of MDP plus LPS slowly diminished with repeated injections. The results indicate that separate but interacting mechanisms are involved in the feeding responses to MDP and LPS. The observed synergism between MDP and LPS suggests a synergistic role of bacterial muramyl peptides and LPS in the anorexia during bacterial infections.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

[Regulation of food intake].

Regulation of food intake is commonly treated as a negative feedback-loop. Hunger and/or appetite lead man and animals to ingest food. The subsequent meal-contingent activation of pre- and postabsorptive mechanisms then leads to satiety. The activation of oral and gastrointestinal chemo- and mechanoreceptors is important on the preabsorptive site. The gastrointestinal hormone cholecystokinin may also have a physiological satiety effect. Preabsorptive satiety mechanisms are influenced by the rate of gastrointestinal transit. The pancreatic hormone glucagon, which is released during meal taking, and various metabolites contribute to the postabsorptive regulation of food intake through activation of hepatic chemoreceptors, which are connected to the brain via predominantly vagal afferents. In addition, glucoreceptors in the brain, in particular in the nucleus of the solitary tract, contribute to food intake regulation by monitoring blood glucose concentration or, more specifically, glucose utilization. The nucleus of the solitary tract, which relays vagal afferents from gut and liver and also gustatory afferents, projects to the hypothalamus and to other forebrain structures. In this neural network the informations from the periphery are integrated by various neurotransmitters and neuropeptides, but the exact role of the substances involved is not fully understood yet. Body weight and, hence, body fat presumably affects feeding through modulation of a postabsorptive mechanism.

Animals↗
PubMed1990

Comparison of the effects of bacterial lipopolysaccharide and muramyl dipeptide on food intake.

For further characterization of the mechanism involved in the anorexia during bacterial infection, we investigated whether muramyl dipeptide (MDP), the minimal immunologically active structure of gram-positive bacterial cell walls, affects rats' food intake in the same way as lipopolysaccharide (LPS) from E. coli. MDP (1.6 mg/kg body weight = b.wt.) injected intraperitoneally (IP) reduced food intake by decreasing meal frequency without affecting meal size. Indomethacin (2.5 mg/kg b.wt., IP) but not verapamil (5 mg/kg b.wt., IP) attenuated the hypophagic effect of MDP. In further experiments, MDP and LPS (100 micrograms/kg b.wt., IP) both inhibited gastric emptying and indomethacin failed to block this effect of LPS. Hepatic vagotomy did not attenuate the hypophagic effects of MDP or LPS. LPS reduced water intake only when food was available, but reduced food intake also during water deprivation. MDP did not affect water intake. MDP and LPS both had an aversive effect, but LiCl, which was also aversive, failed to reduce feeding under the conditions tested. This questions the role of a conditioned taste aversion in the hypophagia induced by MDP or LPS. The results suggest that a stimulation of eicosanoid synthesis contributes to MDP-induced hypophagia and may therefore also contribute to the anorexia during infection. In contrast, an inhibition of gastric emptying, an activation of hepatic satiety signals or a reduction of water intake, does not seem to be crucial for the hypophagic effects of MDP or LPS.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

Meal patterns of pygmy goats fed hay and concentrate ad lib.

The meal patterns of pygmy goats fed hay and pelleted concentrate ad lib were recorded and analyzed. The pygmy goats consumed 8 hay meals [6 during the light phase (= light)/2 during the dark phase (= dark)] and 10 concentrate meals (7 during light/3 during dark) during 24 hr (12 hr light/12 hr dark). Sixty-two percent of hay and 74% of concentrate intake occurred during light. Total 24-hr hay (280 g) and concentrate (264 g) intakes were similar, but concentrate was preferred during dark. Concentrate meals were smaller during light than during dark. The mean feeding rate (g/min) within meals for both hay and concentrate was higher during dark than during light. Meal size and duration of postmeal interval were positively correlated for concentrate but not for hay. No significant positive correlation was found between meal size and duration of premeal interval. Separate analysis of diurnal and nocturnal meals indicated that the postmeal correlation for concentrate was evident primarily during dark. The results demonstrate that food intake in pygmy goats shows distinct diurnal variations and suggest that food intake in ruminants is regulated from meal to meal, with different factors prevailing during light and dark.

Animal Feed↗
PubMed1989

Verapamil and indomethacin attenuate endotoxin-induced anorexia.

To characterize the mechanism of the anorexia during infection, we investigated the effect of E. coli lipopolysaccharide (LPS) on feeding in rats under various conditions: LPS (125, 100, 75, and 50 micrograms/kg body weight = b. wt.) injected intraperitoneally (IP) reduced food intake by decreasing meal frequency without affecting meal size. The Ca++-channel blocker verapamil (5 mg/kg b. wt., IP) or the antipyretic and antiphlogistic drug indomethacin (2.5 mg/kg b. wt., IP), but not combined alpha- and beta-adrenergic receptor blockade by IP phentolamine plus propranolol (500 micrograms/kg b. wt., each) attenuated the anorectic effect of LPS (125 or 100 micrograms/kg b. wt.). The results suggest that a phospholipase A2-sensitive mechanism contributes to the anorexia during injection.

Animals↗
PubMed1989

Hepatic vagotomy increases consumption of a novel-tasting diet presented immediately after surgery.

To further characterize the possible effect of hepatic vagotomy on food intake, rats adapted to a medium-fat diet (MF diet) were offered a novel-tasting diet immediately after hepatic branch vagotomy (HBX rats) or sham vagotomy (SHAM rats) and food intake as well as diet selection (novel-tasting vs. familiar diet) was measured. When a novel-tasting sweet medium-fat diet (SMF diet) was offered immediately after surgery, HBX rats ate transiently more (days 1-4 after surgery) and selected more (days 5 and 6 after surgery) of the SMF diet than SHAM rats. Similar results were obtained when a novel-tasting bitter diet (AMF diet) was offered instead of the SMF diet. In contrast, when rats adapted to the AMF diet prior to surgery were given normal MF diet as novel-tasting diet immediately after surgery, HBX and SHAM rats' postoperative food intake and diet selection did not differ. When rats were given only MF or SMF diet before and after surgery, HBX and SHAM rats' food intake during the initial postoperative period also did not differ. The results indicate that hepatic branch vagotomy and sham vagotomy have different aversive effects which lead to transient differences in postoperative food intake when diets with a novel and strong taste are presented during the initial postoperative period. Therefore, information conveyed by the hepatic branch of the vagus can apparently lead to a conditioned feeding response. This is evidence for a more subtle role of the liver in the control of food intake than previously thought.

Animals↗
PubMed1989

Vasopressin reduces food intake in goats.

The effect of arginine vasopressin (VP) on cumulative food intake and meal pattern was tested in pygmy goats. VP injected intraperitoneally (I.P.) (0.75, 1.5 and 3.0 micrograms kg-1 body weight) appeared to reduce food intake in a dose-dependent manner by reducing the size of the first meal and by increasing the first intermeal interval (IMI). The hypophagic effect of VP was reversed by both a V1-receptor antagonist and an alpha-adrenergic antagonist. Exogenous VP (0.75 and 1.5 microgram kg-1 body weight I.P.) produced increases in plasma VP concentration which also may occur in stressful situations. VP might therefore be related to stress-induced anorexia.

Animals↗
PubMed1989

[The regulation of feed intake in ruminants].

As in monogastric species, food intake in ruminants is regulated from meal to meal. The prandial stimulation of taste receptors and gastrointestinal chemo- and mechanoreceptors as well as hepatic chemoreceptors contributes to satiety. All these receptors are apparently connected with the brain by vagal afferents. A physiological satiety function of prandially released gastrointestinal and pancreatic hormones in ruminants is uncertain. Food stimuli affect feeding also through autonomic reflexes which regulate reticulo-rumen motility. All informations from the periphery are finally integrated in the hypothalamus. The exact role of the various neurotransmitters and neuropeptides involved in the control of feeding is as yet largely unknown.

Animal Feed↗
PubMed1989

[Taste].

Taste has a dual role. Like other senses it informs the individual about the external world, but unlike other senses it connects that perception with information about the internal environment. The principal function of taste is similar in all higher species. Molecules act on specialized sensory cells (= taste cells) in various regions of the oral cavity thus triggering signals, which are relayed to the cortex via afferent nerves, the caudal hindbrain and the thalamus. Taste afferents also reach the hypothalamus and the limbic system. The taste of food triggers physiological and behavioral reactions in man and animals. Stimulation of taste cells immediately elicits salivation, secretion of gastric acid and pancreatic juice as well as secretion of gastrointestinal and pancreatic hormones. Innate and learned taste preferences or aversions play an important role in food selection and taste aversions are considered to be reliable indicators of malaise. Neural signals from the periphery or humoral factors which are sensed by receptors in the central nervous system both can change the acceptance of a certain taste. Endogenous opiates in the brain seem to play a special role in the modulation of taste perception. The amygdala is apparently a brain area which is particularly important for taste perception.

Animals↗
PubMed1988

Metabolic and hormonal factors controlling food intake.

Food intake is controlled by stimuli acting at the pre- and postabsorptive levels. Preabsorptively, nutrients present in the stomach and intestine elicit signals contributing to meal-ending satiety. Neurally mediated signals and hormonal signals both seem instrumental in the production of this gastrointestinal satiety. Postabsorptively, metabolic receptors in the liver that sense the oxidation of metabolic fuels seem to play an important role in the control of post-meal satiety and meal initiation. These receptors are apparently connected with the brain by vagal afferents, because hepatic vagotomy eliminates the effects of various metabolites and metabolic inhibitors on food intake. Glucoreceptors in the hindbrain that sense the utilization of glucose are probably also involved in control of meal initiation. Finally, humoral factors reflecting the size of the fat depots may also function as feedback signals in the control of feeding.

Eating↗