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Biomedical subjects

W Langhans

Publications and source records attributed to W Langhans.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1987

Decreased feeding and supraphysiological plasma levels of glucagon after glucagon injection in rats.

The effects of intraperitoneally injected pancreatic glucagon on feeding and on plasma levels of pancreatic glucagon as well as on blood glucose levels and liver glycogen content were investigated in rats, in order to test the physiological relevance of exogenous glucagon's satiety effect. The rats were intraperitoneally injected with various doses of glucagon [60, 240 or 480 micrograms/kg body weight (b.wt.)] or vehicle when they started to eat after a 12 hr period of food deprivation. Only the highest dose of pancreatic glucagon (480 micrograms/kg b.wt.) decreased the size and duration of the first meal after injection. Hepatic vein, hepatic portal vein and aortal plasma pancreatic glucagon levels were increased about 10 fold by 60 and 240 micrograms/kg b.wt. of glucagon and about 30 to 70 fold by 480 micrograms/kg b.wt. of glucagon. All glucagon doses reduced liver glycogen content and increased hepatic vein blood glucose levels similarly. The results indicate that decreased feeding after intraperitoneal injection of glucagon is a pharmacological effect of the hormone, at least under the conditions tested.

Animals↗
PubMed1987

Evidence for a vagally mediated satiety signal derived from hepatic fatty acid oxidation.

To test the possibility that vagally mediated signals derived from hepatic fatty acid oxidation affect feeding, we investigated the influence of selective hepatic vagotomy on the acute hyperphagic effect of the fatty acid oxidation inhibitor 2-mercaptoacetate (MA) in rats kept on a medium fat diet (18% fat). An i.p. injection of MA (400 mumol/kg b.wt.) stimulated feeding in sham-vagotomized rats clearly more than in vagotomized rats. A high dose of MA (800 mumol/kg b.wt.) initially increased food intake in sham-vagotomized but not in vagotomized rats and later decreased food intake similarly in both surgical groups. MA retained its potency to stimulate feeding after an i.p. injection of atropine methylnitrate (5 mg/kg b.wt.). These results indicate that hepatic fatty acid oxidation provides a satiety signal that is mediated by vagal afferents.

Animals↗
PubMed1987

Evidence for a role of the sodium pump of hepatocytes in the control of food intake.

To test the hypothesis that the sodium pump of hepatocytes is involved in the control of food intake, we investigated the effect of ouabain, an inhibitor of the sodium pump, on feeding in intact and hepatic vagotomized rats. Ouabain (2 mg/kg b.wt.), injected intraperitoneally during the bright phase of the lighting cycle, stimulated feeding in intact and sham-vagotomized rats, but not in hepatic vagotomized rats. Atropinization did not block ouabain's hyperphagic effect. Ouabain did not affect portal blood glucose level. Rats started to eat sooner than normal when ouabain was injected, while their meal size and duration was unchanged. The results are consistent with a role of the sodium pump of hepatocytes in the control of food intake.

Animals↗
PubMed1987

Role of fatty acid oxidation in control of meal pattern.

To characterize the role of fatty acid oxidation in the control of food intake, we investigated the effect of 2-mercaptoacetate, which inhibits fatty acid oxidation, on meal patterns and cumulative food intake in rats. Rats were fed either a medium fat (MF, 18% fat) or a low fat (LF, 3.3% fat) diet. Mercaptoacetate (400 mumole/kg body wt), intraperitoneally injected in the middle of the bright or at the onset of the dark phase of the diurnal lighting cycle, increased cumulative food intake in MF rats by shortening the latency to eat after injection and the duration of the subsequent intermeal interval (IMI) without affecting the size of the first meal. Mercaptoacetate, injected in the middle of the bright phase, reduced the latency to eat but did not affect the duration of the subsequent IMI or cumulative food intake in LF rats. A higher dose of mercaptoacetate (600 mumole/kg body wt), initially increased and later decreased cumulative food intake in MF rats. The initial increase in food intake was due to shorter IMIs; the subsequent decrease in food intake was due to smaller meals after mercaptoacetate injection than after control injection. The results indicate that a drop in fatty acid oxidation caused by mercaptoacetate triggers a meal. This implicates fatty acid oxidation in the maintenance of postprandial satiety.

Animals↗
PubMed1986

Pancreatic glucagon's effects on satiety and hepatic glucose production are independently affected by diet composition.

We tested whether pancreatic glucagon's effects on satiety and hepatic glycogenolysis depend on variations in the macronutrient composition of the diet. Rats were kept on high carbohydrate, high fat, or high protein diets (HC-, HF- or HP-rats, respectively) and adapted to a 5 hour feeding (11:00-16:00)-19 hour deprivation (16:00-11:00) schedule. Glucagon (540 mcg/kg body weight) was intraperitoneally injected at 14:00. Glucagon stimulated similar amounts of hepatic glycogenolysis in HC- and in HF-rats and less glycogenolysis in HP-rats, but glucagon decreased food intake only in HC-rats. When HF- or HP-rats were prefed the HC-diet once for 1 hour (11:00-12:00) prior to injection, glucagon stimulated hepatic glycogenolysis similarly in both groups but decreased food intake only in HF-rats. Therefore, stimulation of hepatic glycogenolysis by glucagon is not sufficient to elicit satiety under all feeding conditions. The results also suggest that glucagon-induced satiety is not limited to carbohydrate intake.

Animals↗
PubMed1986

Selective hepatic vagotomy does not prevent compensatory feeding in response to body weight changes.

The effects of selective hepatic vagotomy on compensatory adjustments of feeding in response to experimentally induced changes in body weight were investigated in rats. Repeated injections of slow-acting insulin increased food intake and body weight in vagotomized as well as in sham-vagotomized rats. When the treatment was stopped, the rats of both surgical groups displayed a compensatory hypophagia of similar magnitude and body weight returned to preinjection levels. In turn, after 7 days of restricted feeding (5 g/day) with a concomitant loss of body weight, rats became hyperphagic and body weight approached the normal level. Again, the feeding responses or body weight changes did not differ between vagotomized and sham-vagotomized rats. The results demonstrate that selective hepatic vagotomy does not disrupt the putative feedback-loop between body weight and feeding, and raise questions concerning the role of the liver in the lipostatic control of food intake.

Animals↗
PubMed1986

Control of food intake by fatty acid oxidation.

The role of fatty acid oxidation in the control of food intake was studied using mercaptoacetate (MA), an inhibitor of fatty acid oxidation. Food intake, plasma free fatty acids (FFA) and ketone bodies, and blood glucose were measured. Rats were fed either a low-fat (LF, 3.33% fat) or a medium-fat (MF, 18% fat) diet. At the onset of the dark phase of the lighting cycle, MA did not affect food intake in LF rats but increased it 74% in MF rats in comparison to control. Four hours after the injection the effect of MA on food intake disappeared. In the middle of the bright phase of the lighting cycle, MA increased food intake in MF rats approximately 120% up to 6 h postinjection. After MA, plasma FFA concentration was elevated, and plasma 3-hydroxybutyrate concentration was lowered, indicating that fatty acid oxidation had been successfully reduced. MA did not affect blood glucose. These results indicate fatty acid oxidation is involved in the control of food intake, at least when the dietary fat level is relatively high.

3-Hydroxybutyric Acid↗
PubMed1985

Ketone kinetics and D-(-)-3-hydroxybutyrate-induced inhibition of feeding in rats.

For further investigation of the mechanism involved in D,L-3 hydroxybutyrate (DL3HB)-induced inhibition of feeding [5], we measured cumulative food intake following subcutaneous injections of DL3HB or D-(-)-3-hydroxybutyrate (D3HB), and plasma ketone levels following subcutaneous injections of D3HB or acetoacetate (ACAC) in rats. Subcutaneously injected DL3HB (10 mmoles/kg body weight) and D3HB (5 mmoles/kg body weight) reduced food intake a similar amount. After injection of D3HB or ACAC (5 mmoles/kg body weight) plasma concentrations of the injected ketone bodies reached a similar high level at 20 min and then decreased with time (40 and 60 min). Even though ACAC failed to reduce food intake, injected ACAC disappeared faster from the circulation than injected D3HB. The data are consistent with the idea that oxidation of injected D3HB to ACAC reduces food intake in rats.

3-Hydroxybutyric Acid↗
PubMed1985

Dissociation of epinephrine's hyperglycemic and anorectic effect.

The contributions of alpha- and beta-adrenergic receptor mechanisms to epinephrine-induced hyperglycemia, to prandial hepatic glycogenolysis, and to epinephrine-induced inhibition of feeding were investigated in rats, because epinephrine's hyperglycemic and anorectic effect might be related to each other. Intraperitoneal injection of the selective alpha-adrenergic receptor antagonist phentolamine (0.5 mg/kg body weight) but not of the selective beta-adrenergic receptor antagonist propranolol (0.5 mg/kg body weight) reduced the hyperglycemic effect of a subsequent epinephrine injection (0.05 mg/kg body weight). In addition, injection of phentolamine (0.5 mg/kg b.w.) or injection of phentolamine plus propranolol (0.5 mg/kg b.w. each) similarly inhibited epinephrine-induced hepatic glycogenolysis. In contrast, phentolamine injection did not affect prandial hepatic glycogenolysis. Neither phentolamine nor propranolol injection was sufficient to affect the inhibition of feeding induced by subsequent epinephrine injection, but the combination of both receptor blockers completely abolished epinephrine's effect on food intake. These findings are not consistent with the idea that epinephrine-induced hypophagia is related to epinephrine's effect on hepatic carbohydrate metabolism. In addition, the data suggest that catecholamines are not the main contributors to prandial hepatic glycogenolysis in rats.

Animals↗
PubMed1985

Selective hepatic vagotomy eliminates the hypophagic effect of different metabolites.

To test the hypothesis that vagally mediated metabolic signals from the liver affect feeding, we investigated the influence of selective hepatic vagotomy on the anorectic effect of different metabolites in rats. Subcutaneous injection of glycerol (GLY), D-3 hydroxybutyrate (DHB), L-malate (MAL), L-lactate (LAC), or pyruvate (PYR) (5.7 mmol/kg metabolic body weight = b.wt.0.75, each) reduced food intake in sham-vagotomized rats. Selective hepatic vagotomy eliminated the hypophagic effect of all metabolites. In an additional experiment, LAC retained its potency to inhibit feeding in sham-vagotomized rats after an intraperitoneal injection of atropine methylnitrate (5 mg/kg b.wt.0.75). The results demonstrate that the hypophagic effect of GLY, DHB, MAL, LAC and PYR originates in the liver and is mediated by hepatic vagal afferents. This implicates the existence of adequate hepatic receptors which might contribute to the control of food intake.

Animals↗
PubMed1985

Regulation of food intake by hepatic oxidative metabolism.

It has been proposed that the turnover of metabolic fuels affects feeding. In the present study the effects of different metabolites (glycerol, L-malate, D-3-hydroxybutyrate, L-lactate) or their oxidation products (dihydroxyacetone, oxaloacetate, acetoacetate, pyruvate) on food intake were investigated under various feeding conditions. The results of these experiments increase our knowledge about the nature and origin of metabolic signals in the energostatic control of food intake. In the experiments, glycerol, malate, 3-hydroxybutyrate, lactate or pyruvate (4.5-7.7 mmoles/kg metabolic body weight injected subcutaneously reduced food intake in rats, whereas dihydroxyacetone, acetoacetate or oxaloacetate did not. The effect of glycerol disappeared with high levels of dietary protein, whereas the effects of lactate and pyruvate disappeared with high levels of dietary fat. The hypophagic effects of glycerol, malate, 3-hydroxybutyrate, lactate and pyruvate were abolished by selective hepatic vagotomy. The results suggest that vagally mediated signals originating from hepatic oxidation of metabolic fuels contribute to the regulation of food intake.

3-Hydroxybutyric Acid↗
PubMed1985

Different metabolites might reduce food intake by the mitochondrial generation of reducing equivalents.

To test the possibility that hypophagic effects of injected metabolites are linked to a particular oxidative step in their metabolism, cumulative food intake in rats after subcutaneous injection of various metabolites or their immediate oxidation products was investigated. Glycerol was compared with dihydroxyacetone, L-malate with oxaloacetate, and L-lactate with pyruvate. Subcutaneous injection of 4.5 mmol/kg metabolic body weight (BW0.75) of glycerol or malate reduced food intake significantly, whereas the same doses of dihydroxyacetone or oxaloacetate did not. Lactate or pyruvate (4.5 mmol/kg BW0.75, each) both reduced food intake significantly. However, even higher doses (7.7 mmol/kg BW0.75) of lactate or pyruvate failed to affect food intake when rats were fed a high fat (HF) diet, which is known to decrease the activity of the enzyme pyruvate dehydrogenase. In an additional experiment, subcutaneous injection of lactate or pyruvate (7.7 mmol/kg BW0.75, each) increased plasma levels of lactate and pyruvate 2 h after the injection in HF-rats more than in rats fed the usual high-carbohydrate diet. The data are consistent with the hypothesis that the increased generation of reducing equivalents in the mitochondria, brought about by the oxidation of injected glycerol, malate, lactate, or pyruvate, reduces food intake in rats.

Animals↗