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Biomedical subjects

W Langhans

Publications and source records attributed to W Langhans.

108 records · Page 6Linked to original sources
PubMed1984

Subcutaneous glycerol injection fails to reduce food intake in rats fed a high protein diet.

To test whether glycerol utilization might contribute to glycerol-induced hypophagia, cumulative food intake was measured following subcutaneous glycerol injection in rats fed a high carbohydrate (HC), a high fat (HF) or a high protein (HP) diet, because food composition is known to influence the activity of several glycerol metabolizing enzymes. In additional experiments, the effect of glycerol injection on plasma glycerol, blood glucose, and liver glycogen levels was also investigated in HC-, HF-, and HP-rats. Subcutaneous glycerol injection (6.3 mmoles/kg b.w.) significantly reduced food intake in HC- and HF-rats, but failed to decrease feeding in HP-rats. Five hours after glycerol injection, plasma glycerol levels were significantly elevated in HP-rats, but did not differ from the glycerol levels of controls in HC- and HF-rats. Subcutaneous glycerol injection did not affect blood glucose concentration or liver glycogen content 5 hours after injection in any feeding group. The results suggest that oxidation of the injected glycerol might contribute to the glycerol-induced hypophagia in HC- and in HF-rats.

Animals↗
PubMed1984

Hepatic handling of pancreatic glucagon and glucose during meals in rats.

Prandial changes in plasma pancreatic glucagon, blood glucose, and liver glycogen levels were studied during the first meal after 12 h of food deprivation in rats. To determine whether pancreatic glucagon secretion is influenced by the composition of the diet, the experiments were performed in rats fed high-carbohydrate (HC), high-fat (HF), or high-protein (HP) diets. Plasma glucagon levels in the hepatic portal vein increased about 100% during meals in all feeding groups, whereas glucagon levels in the hepatic vein changed very little. Blood glucose concentration in the hepatic portal vein increased during meals in HC diet-fed rats but decreased in HF and in HP diet-fed rats. Blood glucose in the hepatic vein also increased in HC and HP diet-fed rats. In addition, liver glycogen content decreased during meals in HC and HP diet-fed rats and by 14 min after the meal in HF diet-fed rats. These results demonstrate that a considerable amount of the glucagon released during meals in HC, HF, and HP diet-fed rats remains in the liver. This is consistent with the hypothesis that the liver is important for the satiety effect of glucagon. The results also suggest that glucagon contributes to the meal-induced changes in hepatic carbohydrate metabolism observed in all groups.

Animals↗
PubMed1983

Plasma metabolites and food intake reduction following heparinoid injection in rats.

Behavioral and physiological consequences of heparinoid injections, which increase plasma levels of nonesterified fatty acids (NEFA) by releasing lipoproteinlipase into the circulation, were studied in rats, because, according to the lipostatic hypothesis of food intake control, changes in plasma metabolite levels should influence food intake. Subcutaneously injected 55 mg/kg body wt. of the heparinoid Na-pentosanpolysulfate (PPS) significantly reduced feeding in rats with ad lib access to either a high carbohydrate (HC) or a high fat (HF) diet. However, the reduction of food intake in HF-rats exceeded that in HC-rats. Moreover, the food intake reduction following PPS-injections was associated with greater increases in plasma levels of NEFA and free glycerol in HF-rats, whereas PPS increased plasma levels of D-(-)-3-hydroxybutyrate only in HF-rats, and did not alter blood glucose concentrations. Although PPS inhibited blood coagulation, it did not affect the hematocrit. Furthermore, PPS-injections that reduced feeding, failed to produce a conditioned taste aversion in a two bottle preference test. The data therefore strongly suggest that elevated levels of plasma NEFA and/or free plasma glycerol decrease food intake in rats. These metabolites might contribute to a lipostatic mechanism of feeding control.

3-Hydroxybutyric Acid↗
PubMed1983

Different effects of subcutaneous D,L-3-hydroxybutyrate and acetoacetate injections on food intake in rats.

Cumulative food intake following subcutaneous injection of D,L-3-hydroxybutyrate (DL3HB) or acetoacetate (AcAc) was investigated in rats, because ketone bodies might contribute to food intake regulation according to Kennedy's lipostatic hypothesis. In addition, the metabolic effects of DL3HB-injections were studied by measuring the levels of plasma D3HB, plasma non-esterified fatty acids (NEFA), plasma glycerol, blood glucose, and liver glycogen. Subcutaneously injected DL3HB (10 mmoles/kg body weight) significantly reduced feeding while equimolar AcAc did not. DL3HB-injection increased plasma D3HB and decreased plasma NEFA and plasma glycerol 1-2 hours after the injection but did not affect blood glucose or liver glycogen content. The data suggest that oxidation of D3HB to AcAc contributes to the inhibition of feeding following subcutaneous DL3HB-injection in rats.

3-Hydroxybutyric Acid↗
PubMed1983

Increases in plasma glycerol levels precede the hypophagia following subcutaneous glycerol injection in rats.

Cumulative food intake and plasma glycerol levels following subcutaneous glycerol injections were investigated in rats, because increases in plasma glycerol have been suspected to contribute to glycerol-induced hypophagia. Besides plasma glycerol, plasma non-esterified fatty acids (NEFA), plasma D-(-)-3-hydroxybutyrate (3-HB), blood glucose, and liver glycogen content were also measured. Two daily injections of 80 mg/kg body wt. glycerol did not affect food intake and failed to increase plasma glycerol 30 min after the injection. A single injection of 660 mg/kg body wt. glycerol reduced food intake and increased plasma glycerol 1-2 hours after the injection. This glycerol dose also increased liver glycogen content 1-2 hours after the injection but did not affect plasma NEFA and 3-HB. Rats injected with 660 mg/kg body wt. glycerol did not reduce feeding within the first 2 hours following the injection, when plasma glycerol levels were increased. Inhibition of feeding began at about 3 hours and continued up to 6 hours although plasma glycerol levels had declined to control values 5-6 hours after the injection. It is concluded that metabolic consequences of elevated plasma glycerol levels rather than increases in plasma glycerol levels per se elicit the food intake reduction following exogenous glycerol loads in rats.

3-Hydroxybutyric Acid↗
PubMed1983

Changes in food intake and meal patterns following injection of D-mannoheptulose in rats.

Behavioral and metabolic effects of intraperitoneal D-mannoheptulose (MH) injections were investigated in rats fed a high carbohydrate (HC) or a high fat (HF) diet. Injection of 125 or 250 mg/kg body weight (body wt) MH did not affect food intake in HC rats. Injection of 400 mg/kg body wt MH inhibited feeding in HC rats by primarily reducing meal size. In contrast, none of the MH doses tested (125, 250, 400, 800 mg/kg body wt) affected food intake or meal patterns in HF rats. The hyperglycemia following MH injection (400 mg/kg body wt) was more pronounced in HC compared to HF rats. MH injection (400 mg/kg body wt) induced a strong taste aversion in HC rats, but had only weak aversive consequences in HF rats. The data throw some doubt on the hypothetical role of insulin in the production of satiety. In addition, the results suggest that a hedonic shift takes place following MH injection in HC rats. The strong dislike for the HC diet after MH injection might be triggered by the severe disturbance of glucose homeostasis and might contribute to the transient hypophagia in HC rats by primarily reducing meal size.

Animals↗
PubMed1982

Stimulation of feeding in rats by intraperitoneal injection of antibodies to glucagon.

Intraperitoneal injections of antibodies to pancreatic glucagon at the onset of the first meal after 12 hours of food deprivation increased meal size 63 percent and meal duration 74 percent in rats. The antibodies also reduced the increase in hepatic vein blood glucose that occurred during meals in control rats, but did not affect the prandial increase in portal vein blood glucose. These results suggest that, under these conditions, pancreatic glucagon is necessary for the normal termination of meals.

Animals↗
PubMed1982

Liver glycogen content decreases during meals in rats.

The effects of feeding on liver glycogen content and blood glucose in the hepatic and hepatic portal veins were investigated in rats. Liver glycogen content decreased about 25% during meals both in rats refed after 12 h food deprivation (23 +/- 1 to 17 +/- 1 mg glycogen/g liver) and in ad libitum-fed rats taking fully spontaneous meals (44 +/- 2 to 32 +/- 2 mg/g). Liver glycogen began to increase within 30 min after meals in ad libitum-fed rats. Hepatic vein blood glucose levels at meal onset (118 +/- 4 mg/dl in the food-deprived rats, 127 +/- 4 in ad libitum-fed rats) and at meal end (155 +/- 3 and 166 +/- 5 mg/dl, respectively) were similar in the two groups. Portal vein blood glucose increased during meals in the previously food-deprived rats (83 +/- 4 to 116 +/- 6 mg/dl) but not in the ad libitum-fed rats (127 +/- 5 to 132 +/- 3 mg/dl). Mechanisms that may elicit prandial glycogenolysis and the possible role of this effect in the production of meal ending satiety are discussed.

Animals↗
PubMed1981

Metabolic concomitants of glucagon-induced suppression of feeding in the rat.

The suppression of food intake elicited in rats by injection of pancreatic glucagon and the accompanying changes in energy metabolite flux were investigated. Glucagon injections, 120-360 micrograms ip, were made as rats began the first meal of the dark phase after food deprivation during the light phase. Glucagon-injected rats terminated their meals sooner and ate smaller meals than vehicle-injected rats. For metabolic assays, rats were identically treated and killed just at meal onset or 15 min later. Portal vein blood glucose increased similarly in all rats allowed to feed, whereas plasma nonesterified fatty acid and D-(-)-3-hydroxybutyrate levels decreased during feeding. In contrast, hepatic vein and aorta blood glucose levels increased more after glucagon than after vehicle injections. Liver glycogen content decreased after glucagon injections. The highest glucagon dose only had slight lipolytic and ketogenic effects. It was concluded the glycogenolytic and hyperglycemic action of glucagon may generate a satiety signal sufficient to cause premature termination of meals. Changes in ketone and lipid fluxes do not appear necessary for this behavioral effect.

Animals↗
PubMedDate not supplied

Metabolic effects of a fat- and carbohydrate-rich meal in rats.

To investigate meal-induced changes in hepatic fat and carbohydrate metabolism in rats, hepatic venous, portal venous, and aortal plasma levels of several metabolites as well as changes in hepatic glycogen and lactate content were measured during and after the first nocturnal meal following a 12-h fast. The rats were fed a diet with about 46%, 41%, and 13% of the total energy (approximately 16.5 kJ/g) derived from carbohydrates, fats, and protein, respectively. During the later part of the meal and thereafter, plasma triglyceride level increased in all blood vessels. After a transient initial decrease, portal venous and aortal nonesterified fatty acid (NEFA) levels, net hepatic NEFA uptake, and hepatic beta-hydroxybutyrate (BHB) production increased and reached fasting (meal onset) values by 30 min after the meal. Although liver glycogen did not change significantly, the liver released glucose continuously. The liver initially accumulated lactate and maintained a high lactate concentration despite switching from lactate uptake to net release of lactate around 10 min into the meal. Taken together, these data indicate that hepatic glycolysis, gluconeogenesis, and considerable fatty acid oxidation occur concurrently in rat liver during and after a fat- and carbohydrate-rich meal. The findings are relevant to contemporary hypotheses of the metabolic control of eating and, in particular, to hypotheses linking hepatic fatty acid oxidation to postprandial satiety.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Meal patterns and meal-induced metabolic changes in calves fed milk ad lib.

The feeding behavior of 11 calves fed milk ad lib was characterized and analyzed at the age of 5 weeks, and the short-term changes in the plasma concentrations of various metabolites (glucose, lactate, free fatty acids, triglycerides, beta-hydroxybutyrate) and insulin in relation to a representative spontaneous milk meal were measured during the following week. In a 6-day period, the calves consumed 287 (=86%) of a total of 335 milk meals during the light phase from 0500-2200 [on average, 4.4 +/- 0.5 (mean +/- SEM) meals]. The meal size and duration during light were 2.0 +/- 0.3 kg and 5.3 +/- 0.3 min, respectively. However, only 0.7 +/- 0.1 milk meals of similar size and duration were consumed during the dark phase. The plasma concentrations of insulin and glucose increased in response to the spontaneous milk meal and remained elevated for at least 2 h after meal end. The plasma concentrations of triglycerides, free fatty acids, and beta-hydroxybutyrate also increased after meal termination, and remained elevated until 40 min (triglycerides, free fatty acids) and 60 min (beta-hydroxybutyrate) after meal end, respectively. The observed spontaneous milk intake patterns were similar to the natural suckling behavior described for calves, suggesting that the conditions of the present experiment did not disrupt the animals' natural feeding behavior. Some of the profound metabolic changes in relation to a spontaneous milk meal might contribute to the control of milk intake in calves, but further experiments are necessary to test this idea.

Animals↗
PubMedDate not supplied

Role of rumen fluid hypertonicity in the dehydration-induced hypophagia of cows.

Three experiments were performed in non-lactating, rumen-fistulated cows to assess the role of rumen fluid hypertonicity in dehydration-induced hypophagia. First, the course of rumen fluid and plasma osmolality before and after an individual test meal was recorded when water was offered ad libitum and on the fifth day of a 65% water restriction period. Then, the effects of intraruminal water infusions on food intake were examined in dehydrated cows. Finally, two doses of the local anesthetic mepivacaine HCl were given into the rumen in an attempt to inactivate the osmosensors potentially involved in dehydration-induced hypophagia. Water restriction reduced test meal size and increased rumen fluid and plasma osmolality. Despite the smaller meal, the prandial increase in rumen fluid osmolality was more pronounced during water restriction than with water ad libitum. Independent of treatment, the test meal had no effect on plasma osmolality. Intraruminal water infusions during water deprivation decreased rumen fluid osmolality below the control level and normalized food intake. Injection of 2 or 4 g mepivacaine/cow into the rumen did not attenuate dehydration-induced hypophagia. All in all, these results suggest that rumen fluid hypertonicity, perhaps in concert with plasma hypertonicity, contributes to the early satiation induced by dehydration.

Anesthetics, Local↗
PubMedDate not supplied

Effect of hydroxycitrate on food intake and body weight regain after a period of restrictive feeding in male rats.

We examined whether dietary supplementation of hydroxycitrate (HCA), a competitive inhibitor of the extramitochondrial enzyme ATP-citrate-lyase, which inhibits lipogenesis, reduces food intake and body weight regain in rats after 10-15% weight loss. In four experiments, 24 male rats were fed restrictively (10 g/day) for 10 days and then given ad lib access to one of four different diets (HI-Suc=high sucrose; HI-Glu=high glucose; Chow=grounded standard rat chow; HI-Glu+Fat=high glucose+fat) varying in the content of fat and low molecular carbohydrates for the following 10 days. For half of the rats (n=12), the ad lib diet was supplemented with 3% (w/w) HCA. HCA reduced body weight regain with all diets except Chow. HCA also reduced food intake temporarily with three of the four tested diets. The suppressive effect of HCA on food intake was particularly strong with the HI-Glu+Fat diet (fat=24% of energy). With Diet HI-Glu and HI-Glu+Fat HCA reduced the feed conversion efficiency (cumulative body weight regain (g)/cumulative food intake (MJ)) during the 10 ad lib days, suggesting that it also increased energy expenditure. This effect seemed to be positively related to the glucose content of the diet. All in all, HCA reduced body weight regain after substantial body weight loss, and the effects are presumably linked to its inhibiting effect on lipogenesis, but the exact mechanism still has to be determined.

Animals↗
PubMedDate not supplied

Suppression of hepatic fatty acid oxidation and food intake in men.

We investigated the effects of the fatty acid oxidation inhibitor etomoxir (ETO) on food intake and on fat and carbohydrate metabolism in two double-blind crossover studies in male, normal-weight subjects. In study 1, ETO (75 mg [+]-racemate) or placebo was given orally 30 min after completion of a standardized, fat-enriched (total energy: 2698 kJ, 40% from fat) lunch. The subjects (n = 15) were isolated from external time cues and free to choose when to eat dinner from an oversized serving (total energy: 6656 kJ, 60% from fat). In study 2, subjects (n = 13) were selected for habitually high fat intake (mean: 44% of energy intake). ETO (150 mg) or placebo was given after an overnight fast, 2.5 h before offering an oversized high fat breakfast (6960 kJ, 72% from fat). In both studies, blood samples were taken and the respiratory quotient (RQ) was measured several times during each test period. In study 1, ETO (75 mg) did not affect the timing and size of the dinner or subjective feelings of hunger and satiety. Although ETO (75 mg) did not affect the RQ, it decreased plasma beta-hydroxybutyrate (BHB) and increased plasma lactate compared with placebo. Plasma triacylglycerols (TG), free fatty acids (FFA), glucose, and insulin were not affected by ETO. In study 2, ETO (150 mg) enhanced hunger feelings and increased the size of the breakfast by 22.7%. ETO did not affect the RQ, but baseline RQ was lower in study 2 than in study 1 (0.83 versus 0.89, P < 0.01). Compared with placebo, ETO (150 mg) decreased plasma BHB and increased plasma FFA and plasma lactate. Baseline plasma concentrations of BHB, FFA, and lactate were higher in study 2 than in study 1 (BHB: 242 versus 81 mumol/L, P < 0.001; FFA: 0.674 versus 0.406 mmol/L, P < 0.01; lactate: 1.08 versus 0.74 mmol/L, P < 0.05). Plasma concentrations of TG, glucose, and insulin were not affected by ETO. The results suggest that inhibition of hepatic fatty acid oxidation stimulates eating in men when baseline fatty acid oxidation is sufficiently high and markedly suppressed by the treatment.

3-Hydroxybutyric Acid↗