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Biomedical subjects

W Langhans

Publications and source records attributed to W Langhans.

At least 55 records · Page 3Linked to original sources

The satiating potency of hepatic portal glucagon in rats is not affected by [corrected] insulin or insulin antibodies.

To characterize the interactive effects of acute prandial manipulations of insulin and glucagon on spontaneous feeding in adult male rats fed ad lib, glucagon (G) and insulin (1) or insulin antibodies (IAb) were confused into the hepatic portal vein during the first meal of the dark phase. Infusions (3-6 min, 33 microliters/min) were remotely controlled, and a computerized system recorded meal patterns. In Experiment 1, five separate factorial designs were used to test the effects of G (1.3 or 13 micrograms/meal) alone, I (1.3 or 2.7 mU/meal) alone, or both G + I. The peptides were infused either simultaneously or sequentially (G before I). The larger dose of G alone reduced meal size. I neither inhibited feeding nor increased the effects of either G dose. In one test, 13 micrograms/meal G did not block meal size when followed by 2.7 mU I, but this antagonism did not occur in a replication. In several tests, there was a trend for I to decrease the size of the spontaneous meal that followed the meal during which I was infused, but this was statistically significant only once. Intermeal intervals were not affected in any test. Experiment 2 tested coinfusions of 20 micrograms G and polyclonal IAb with an in vitro binding capacity of 40 mU rat insulin. G alone reduced meal size, IAb alone increased meal size, and G + IAb produced an additive effect. These data extend previous investigations of the satiating action of G and I in the rat and indicate 1. that exogenous I does not affect the satiating potency of G; 2. that exogenous G and endogenous I elicit an additive synergistic inhibition of spontaneous meal size; and 3. that G-induced I secretion does not mediate the satiating effect of G.

Animals↗

Labyrinth exploration, emotional reactivity, and conditioned fear in young Roman/Verh inbred rats.

An inbreeding program has been carried out with the Swiss sublines of Roman high- and low-avoidance rats since 1993. The present study reports the first experiments conducted with young animals of those inbred strains (RHA-I/Verh and RLA-I/Verh, respectively) from the sixth and seventh inbreeding generations. The results confirmed expected behavioral profiles. Compared to the RHA-I/Verh strain, RLA-I/Verh rats showed decreased entries into the illuminated central arena of an hexagonal tunnel maze, as well as decreased spontaneous locomotor activity and increased defecations, in two independent experiments. Young RLA-I/Verh females explored less than did their RHA-I/Verh counterparts during session 1 of a conditioned-fear experiment preceding shock administration, and in session 2 (conducted 24 h after the application of three footshocks), they showed greater conditioned behavioral inhibition (i.e., reduced amount of rearing), as well as higher defecation scores, than did RHA-I/Verh females.

Analysis of Variance↗

Differential circadian eating patterns in two psychogenetically selected strains of rats fed low-, medium-, and high-fat diets.

Spontaneous eating patterns in male, inbred Roman high- and low-avoidance rats (RHA/Verh, RLA/Verh) were continuously recorded while animals were successively offered three isocaloric (approximately 16.5-kJ/g) diets: a low-fat, high-carbohydrate diet (LF; 3.3% fat), a medium-fat diet (MF; 18% fat), and a high-fat diet (HF; 40% fat), the latter being followed once again by the LF diet. Under the conditions of this experiment, overall 24-h food intake did not differ significantly between RHA/Verh and RLA/Verh rats, but was significantly higher for both rat strains on the MF and HF diets than on the LF diet. Despite the similar 24 h-food intake, RHA/Verh rats ate transiently less than RLA/Verh rats during the third quarter of the dark phase under all dietary conditions. These differences were due to the RHA/Verh rats' longer intermeal intervals (with all diets) and smaller meals (with the MF and HF diets) and were compensated for during the last 3 h of the dark phase. On the LF diet, dark-phase meal frequency was higher and both nocturnal meal size and mean eating rate within meals were lower in RLA/Verh rats than in RHA/Verh rats. With the MF and HF diets, mean nocturnal meal size and meal duration were higher and mean eating rate was lower in RLA/Verh rats than in RHA/Verh rats. For both strains, nocturnal meal size was significantly higher with the MF and HF diets than with the LF diet, and nocturnal meal frequency was lower with the HF diet than with the other two diets. Although body weights were similar at the start of the study, RLA/Verh rats gained significantly more weight than did RHA/Verh rats by the end. As has often been the case with other aspects of behavior studied, differences in neuromodulatory systems (e.g., serotoninergic and dopaminergic) between RHA/Verh and RLA/Verh rats may directly or indirectly contribute to the subtle differences in eating patterns observed here.

Analysis of Variance↗

Subdiaphragmatic vagal deafferentation fails to block feeding-suppressive effects of LPS and IL-1 beta in rats.

To evaluate the role of subdiaphragmatic vagal afferent fibers in mediating the inhibition of food intake produced by peripheral administration of bacterial lipopolysaccharide (LPS) and the proinflammatory cytokine interleukin-1 beta (IL-1 beta), we assessed the ability of 100 micrograms/kg ip LPS and 2 micrograms/kg ip human recombinant IL-1 beta to suppress solid food intake during the first 3 and 6 h of the dark cycle in rats with selective vagal rootlet deafferentation (SDA, n = 15) and in sham surgical control rats (Con, n = 17). SDA was produced by a combination of dorsal subdiaphragmatic truncal vagotomy and left vagal afferent rootlet transection as the left vagus enters the caudal brain stem. Both LPS and IL-1 beta significantly suppressed food intake at 3 and 6 h in both Con and SDA rats, and SDA failed to attenuate the LPS- and IL-1 beta-induced reductions in food consumption relative to the suppression seen in controls. Peripheral administration of the gut-brain peptide cholecystokinin (CCK) suppressed 30-min 12.5% liquid glucose consumption in control, but not in SDA rats, consistent with previous demonstrations of the role of subdiaphragmatic vagal afferents in the mediation of CCK satiety. These data demonstrate that subdiaphragmatic vagal afferents are not necessary for the feeding-suppressive actions of peripherally administered LPS and IL-1 beta and suggest that peripheral LPS and IL-1 beta may inhibit food intake via humoral and/or splanchnic visceral afferent pathways.

Afferent Pathways↗

Effects of L-carnitine supplementation on physical performance and energy metabolism of endurance-trained athletes: a double-blind crossover field study.

A double-blind crossover field study was performed to investigate the effects of acute L-carnitine supplementation on metabolism and performance of endurance-trained athletes during and after a marathon run. Seven male subjects were given supplements of 2 g L-carnitine 2 h before the start of a marathon run and again after 20 km of the run. The plasma concentration of metabolites and hormones was analysed 1 h before, immediately after and 1 h after the run, as well as the next morning after the run. In addition, the respiratory exchange ratio (R) was determined before and at the end of the run, and a submaximal performance test was completed on a treadmill the morning after the run. The administration of L-carnitine was associated with a significant increase in the plasma concentration of all analysed carnitine fractions (i.e. free carnitine, short-chain acylcarnitine, long-chain acylcarnitine, total acid soluble carnitine, total carnitine) but caused no significant change in marathon running time, in R, in the plasma concentrations of carbohydrate metabolites (glucose, lactate, pyruvate), of fat metabolites (free fatty acids, glycerol, beta-hydroxybutyrate), of hormones (insulin, glucagon, cortisol), and of enzyme activities (creatine kinase, lactate dehydrogenase). Moreover, there was no difference in the result of the submaximal performance test the morning after the run. In conclusion, acute administration of L-carnitine did not affect the metabolism or improve the physical performance of the endurance-trained athletes during the run and did not alter their recovery.

Adult↗

Breakfasts with different fiber and macronutrient contents do not differentially affect timing, size or microstructure of the subsequent lunch.

The effects of four equienergetic breakfasts with varying fiber and macronutrient contents on hunger and satiety ratings, on subsequent lunch intake, and on postprandial carbohydrate and fat metabolism were investigated in normal weight male subjects in two experiments, in which lunch was offered at a predetermined time (Experiment 1) or in which the subjects were free to choose when to eat lunch (Experiment 2). Consumption of either a commercially available high fiber cereal (HFC, 10% fiber), a medium fiber cereal (MFC, 7% fiber), a low fiber cereal (LFC, 3% fiber), or a standard continental breakfast (0% fiber) on nonconsecutive days did not differentially affect hunger and satiety ratings, the size or microstructure of the subsequent lunch, and the breakfast to lunch intermeal interval (in Experiment 2). Plasma concentrations of glucose, lactate, and insulin increased more after the LFC breakfast than after the other breakfast varieties. A reactive postprandial hypoglycaemia occurred after the LFC breakfast, shortly before lunch. The plasma concentrations of fat metabolites (triglycerides, free fatty acids, beta-hydroxybutyrate) and of glucagon were not differentially affected by the breakfast varieties. The results are consistent with the assumption that energy content of a meal is the major determinant of subsequent energy intake in man and the fiber content and macronutrient composition have only a modulating effect.

3-Hydroxybutyric Acid↗

Role of the liver in the metabolic control of eating: what we know--and what we do not know.

Profound metal-related changes in the supply of metabolites to t he liver and in the hepatic metabolism occur, and there is ample evidence that neural signals from hepatic metabolic sensors can affect eating. Hepatic afferent nerves presumably represent glucosensors which contribute to the control of eating by monitoring their own glucose utilization. Yet, the nature of the putative sensors that respond to the oxidation of other metabolites than glucose had not been identified. ATP and sodium pump activity may link hepatic oxidative metabolism and membrane potential, because hepatic phosphate-trapping by 2,5-anhydro-mannitol, and inhibition of sodium pump activity by ouabain is associated with a stimulation of eating. Hepatocyte membrane potential is also subject to changes in transmembranal potassium flow through volumetrically controlled membranal potassium channels. Yet it is unknown if and how hepatocytes are linked to afferent nerves. It is also unclear how the effects of glucagon and insulin fit into the hepatic metabolic control of eating. Glucagon appears to induce satiety through its actions in the liver, but the involved mechanism is still unclear. Recent studies suggest that insulin, which has mainly been explored as a centrally acting long-term satiety signal, has an immediate effect on meal size, but is presently unknown whether an hepatic action of insulin is involved.

Animals↗

Effect of water deprivation on eating patterns of lactating cows fed grass and corn pellets ad lib.

The present study investigated the effect of 48 h of water deprivation on eating behavior of 12 lactating cows fed grass and corn pellets ad lib. Water deprivation reduced grass and corn pellet intake significantly, with corn pellet intake decreasing earlier than grass intake. The reduction of feed intake was entirely due to a reduction of meal size for both grass and corn-pellet meals. The size of the first meal of the water deprivation period was already reduced by about 30%. Grass-meal frequency increased, whereas corn-pellet meal frequency decreased during water deprivation. Water deprivation also decreased live weight and milk yield by about 12 and 30%, respectively. All parameters returned to baseline values with rehydration. With ad lib access to feed and water, 77% of drafts occurred in relation to meals, but the number of meals clearly exceeded the number of drafts. The results demonstrate that water deprivation rapidly leads to premature meal termination. This is in line with the assumption that an enhanced prandial increase in ruminal fluid osmotality contributes to dehydration-induced hypophagia. Yet, further studies are necessary to prove this assumption and to better understand the complex relationships between eating and drinking in ruminants.

Animals↗

Characterisation of the acute phase response of heifers to a prolonged low dose infusion of lipopolysaccharide.

The effect of a prolonged low dose infusion of bacterial lipopolysaccharide (LPS) on acute phase-like reactions was examined in heifers. LPS (2 micrograms kg-1 dissolved in 100 ml water), or saline was infused (at 1 ml min-1) intravenously for 100 minutes and blood samples were taken at various times before, during and after the infusion. The serum concentrations of tumour necrosis factor-alpha (TNF alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and serum amyloid A (SAA) and the rectal temperature increased in response to the LPS infusion. Serum TNF alpha increased before the increases in IL-1 beta and IL-6 and remained high from 20 minutes after the onset of the infusion until the end of the sampling period (six hours). The LPS-induced increases in serum IL-1 beta and IL-6 were biphasic. Plasma cortisol and lactate concentrations also increased, and plasma glucose and beta-hydroxybutyrate concentrations decreased in response to the LPS infusion. The similarity of these reactions to changes observed in response to bacterial infections shows that the prolonged infusion of low doses of LPS is a good model for studying the acute phase response to Gram-negative bacterial infection in heifers.

Acute-Phase Proteins↗

Bacterial products and the control of ingestive behavior: clinical implications.

Bacterial products such as lipopolysaccharides (LPS) and muramyl peptides are delivered in the course of infections. They trigger the host's acute phase responses to bacterial infections and are probably involved in the accompanying hypophagia because LPS and muramyl dipeptide (MDP, the minimal immunologically active muramyl peptide) reduce food intake after parenteral administration in animals. LPS and MDP inhibit feeding synergistically through separate but interacting mechanisms. The hypophagic effects of LPS and MDP are presumably mediated by the combined actions of interleukin-1, tumor necrosis factor, and other cytokines. More work is required to understand the interactions between these cytokines, and between bacterial products and cytokines, before cytokine antagonists can be used for treatment of the hypophagia during bacterial infections. As the hypophagia seems to be an early mechanism of host defense, a treatment should be carefully considered. If an intervention is indicated because of a patient's poor condition, inhibitors of eicosanoid synthesis and glucocorticoids may hold more promise for therapy because such substances block LPS and MDP hypophagia. Although LPS can reduce food intake by direct action on the brain, presently available evidence indicates that systemic LPS acts primarily in the periphery to generate a neural signal that is transmitted to the brain and inhibits feeding through the vagus. The exact site where LPS acts on peripheral nerves remains to be identified. LPS hypophagia is conditionable, but conditioning cannot solely account for LPS hypophagia under most test conditions. Whether MDP hypophagia is also conditionable and mediated by vagal afferents is not yet known. All in all, the putative mediators and mechanisms of LPS and MDP hypophagia suggest some options for a treatment of the hypophagia during bacterial infection, but present knowledge about the mechanisms and interactions of the involved substances is still fragmentary and requires further investigation.

Acetylmuramyl-Alanyl-Isoglutamine↗

ACTH, cortisol and glucose responses after administration of vasopressin in cattle and sheep.

The present study compared the effects of vasopressin on plasma concentrations of corticotropin, cortisol and glucose in cattle and sheep. After intravenous injection of 1, 0.1 and 0.01 microgram vasopressin per kg body weight, the plasma vasopressin concentration increased proportionally to the injected dose, and this increase was similar in cattle and sheep. Doses of 1 and 0.1 microgram per kg body weight of vasopressin triggered significant responses of corticotropin, cortisol and glucose in cattle and sheep. The corticotropin response to both doses was significantly greater in sheep, whereas the glucose response was greater in cattle. The cortisol response did not differ between species. The lowest dose of vasopressin (0.01 microgram per kg body weight) still induced a significant cortisol response without a substantial effect on plasma corticotropin, suggesting that a direct action of vasopressin on the adrenals may contribute to the observed cortisol response. The results demonstrate that vasopressin increases plasma levels of corticotropin, cortisol and glucose in cattle, as it does in sheep, but the intensities of the corticotropin and glucose responses to vasopressin differ between cattle and sheep. The reasons for these differences remain to be clarified.

Adrenocorticotropic Hormone↗

Limited importance of a learned aversion in the hypophagic effect of interleukin-1 beta.

This study addressed the possible role of a learned aversion in the hypophagic effect of interleukin-1 beta (IL-1 beta) in the rat. Two repetitive intraperitoneal injections of IL-1 beta (2 micrograms/kg body weight = b.wt.) progressively reduced intake of a novel-tasting saccharin diet (SD) presented immediately after injection. When SD and the familiar diet were offered some days after an injection, SD selection was in some but not all trials reduced by IL-1 beta pretreatment. When SD was offered alone several days after an injection, SD intake was not affected by the initial pairing of SD presentation with IL-1 beta injection. In further experiments, the novelty of a flavor added to the diet fed immediately after injection proved to be crucial for the aversive effect of IL-1 beta, and enhanced its hypophagic effect. Finally, lesion of the area postrema and the adjacent nucleus of the solitary tract failed to affect the hypophagia induced by IL-1 beta (1 microgram/kg b.wt.). The results indicate that, under certain conditions, IL-1 beta can induce an aversion to the taste and flavor of the food consumed after injection. This aversive effect of IL-1 beta appears to be rather weak and is presumably not involved in the hypophagic effect of IL-1 beta under normal feeding conditions. It may however enhance IL-1 beta's hypophagic effect under certain conditions, for instance after repeated injections.

Animals↗

Feeding patterns of lactating cows of three different breeds fed hay, corn silage, and grass silage.

Feeding behavior of 35 lactating cows of three different breeds (Holstein-Friesian = HF, Simmental = SI, and Jersey = JER) was compared in the present study. The cows were kept in a loose housing system and fed hay, corn silage (CS) and grass silage (GS) ad lib. Within 7 consecutive days, 2918 meals were recorded and analyzed: 2503 meals were eaten during the light phase (0430-2200), and 57% of these diurnal meals consisted of only one feedstuff (43% hay, 9% CS, 5% GS). During the dark phase, only 23% of the 415 meals consisted of hay alone, but 16% of CS and 21% of GS alone. This circadian distribution showed no breed differences, yet meal patterns did: HF and SI cows ate 11 meals per day, and JER cows ate more than 13 meals/day. Meal size was 9.8MJ, 7.9MJ, and 5.8MJ for HF, SI, and JER cows, respectively. HF cows had the highest 24 h energy intake and JER cows the lowest, but the latter spent the most time feeding. During the light phase all three breeds obtained the most energy from hay, followed by CS and GS. In contrast, during the dark phase most energy was derived from GS, and hay contributed the least. A significant premeal correlation was observed for cows of all breeds, in particular during the time with the highest feeding activity (0800-1300). During the dark phase no premeal correlation could be detected; instead a significant postmeal correlation appeared, in particular in HF and SI cows.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Feed↗

Effect of bovine leukemia virus infection on bovine peripheral blood monocyte responsiveness to lipopolysaccharide stimulation in vitro.

The effects of bovine leukemia virus (BLV) infection on cytokine activity of bovine monocytes stimulated with Escherichia coli lipopolysaccharide (LPS) were examined. Compared to supernatants of LPS-stimulated monocytes from BLV-negative cows, supernatants from BLV-positive cows contained about four times more interleukin-1 beta (IL-1 beta) (as measured by an enzyme-linked immunosorbent assay (ELISA) for bovine IL-1 beta). Despite their higher IL-1 beta concentration, supernatants from BLV-positive cows stimulated proliferation of murine thymocytes in the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-biphenyl tetrazolium bromide) assay similar to supernatants from BLV-negative cows, but showed about 30% less IL-1 activity than supernatants from BLV-negative cows on the IL-1-dependent cell line LBRM-33 1 A-5, and about five times more tumor necrosis factor (TNF) activity on the TNF-sensitive murine fibroblast cell line L-929. These results demonstrate that BLV infection changes the cytokine response of bovine monocytes to LPS stimulation in vitro. The results are consistent with the assumption that BLV infection leads to the production and secretion of a soluble IL-1 inhibitor by LPS-stimulated peripheral blood monocytes.

Animals↗

Hepatic portal insulin antibody infusion increases, but insulin does not alter, spontaneous meal size in rats.

To investigate the acute effects of pancreatic insulin on spontaneous feeding in rats fed ad libitum, insulin or insulin antibodies were infused into the hepatic portal vein during the first meal of either the light or dark phase. Infusions (3 min, 0.033 ml/min) were remotely controlled, and a computerized system recorded meal patterns. In separate crossover tests, 1, 2, 4, 8, and 16 mU insulin/meal did not affect meal size or subsequent intermeal interval (P > 0.10). In one test, nocturnal meal duration was decreased by 2 mU insulin/meal (19%, P < 0.05). Infusions of polyclonal antibodies to human insulin with in vitro rat insulin binding capacity of 20 or 50 mU increased the size of the first nocturnal meal by 24 and 29% (P < 0.05), respectively. Meal duration was reliably increased only by the smaller antibody dose. Subsequent intermeal interval was unaffected by either antibody dose. The stimulatory effect of insulin antibody infusion on meal size indicates that antagonism of circulating insulin during meals interferes with the control of meal termination. Thus insulin appears to play a role in the physiological control of nocturnal spontaneous feeding in rats. Exogenous insulin may have failed to decrease meal size because of a ceiling effect.

Animals↗

Caprine arthritis encephalitis virus infection changes caprine blood monocyte responsiveness to lipopolysaccharide stimulation in vitro.

The effects of caprine arthritis encephalitis virus (CAEV) infection on cytokine activity of caprine monocytes stimulated with Escherichia coli lipopolysaccharide (LPS) were examined. Compared with supernatants from LPS-stimulated monocytes of CAEV-negative goats, supernatants from CAEV-positive goats stimulated less proliferation of murine thymocytes in the MTT (3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide) assay, showed about 50% less IL-1 activity on the IL-1-dependent cell line LBRM-33 1 A-5, and showed about 200% more tumor necrosis factor (TNF) activity on the TNF-sensitive murine fibroblast cell line L-929. These results indicate that CAEV infection changes caprine monocyte cytokine responsivity.

Animals↗