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Biomedical subjects

D Rigaud

Publications and source records attributed to D Rigaud.

At least 37 records · Page 2Linked to original sources
PubMed1994

Palatability of a meal influences release of beta-endorphin, and of potential regulators of food intake in healthy human subjects.

The effect of the palatability of a meal was tested on the post-prandial release of several gut hormones or neuropeptides which are known to have an effect on intake and satiety. Hormonal response was determined in plasma during the 3 h after a highly palatable and energy-rich meal or after the same meal served cold in a poorly acceptable form, as well as while fasting. The early post-prandial pancreatic polypeptide and neurotensin response was significantly higher after the highly palatable meal than after the cold one. Later responses differed only for pancreatic polypeptide. No difference was observed in cholecystokinin and neuropeptide Y levels. Post-prandial levels of beta-endorphin were elevated only after the cold meal and were associated with an elevated response of ACTH. We suggest that beta-endorphin might be secreted in response to an aversion towards the non-palatable cold meal. This could, subsequently, inhibit the cephalic phase of pancreatic polypeptide response and the early post-prandial response of neurotensin by a central anticholinergic effect. This study evidences an effect of palatability on the modulation of the digestive hormonal response after a meal.

Adult↗
PubMed1994

Mechanisms of decreased food intake during weight loss in adult Crohn's disease patients without obvious malabsorption.

Because weight loss is common in colonic Crohn's disease and is poorly correlated with disease activity, we analyzed food intake in 63 patients without malabsorption, 30 patients with weight loss (9.2 +/- 4.2 kg), and 33 patients without weight loss. Energy and protein intakes were lower in patients with weight loss than in those with stable weight (P < 0.01). In the former group, food restrictions were more numerous (P < 0.01) and visual analog scales showed less hunger, decreased appetite, and fewer sensations of pleasure related to eating, as compared with the other group (P < 0.01). Food intake reduction was also related to depressive mood and medical advice. However, there was no difference between groups in fecal energy wasting and resting energy expenditure. Weight loss in Crohn's disease may be due to a decrease in food intake rather than to an increase in energy cost of the disease. Thus, focus of attention on the diet is crucial to prevent malnutrition.

Adult↗
PubMed1994

Influence of diet on experimental toxicity of amphotericin B deoxycholate.

The effects of pre- and postprandial levels of lipids in serum on the experimental in vivo and in vitro toxicities of amphotericin B deoxycholate (AmB-d) were studied. Normal OF1 mice were tested at baseline, after normal feeding, after 3 h of fasting, or after a sequence of feeding and fasting and vice versa. The 50% lethal dose (LD50) of AmB-d was significantly higher in fed mice than in mice which fasted or at baseline (2.38 +/- 0.12 versus 1.53 +/- 0.2 and 1.50 +/- 0.1 mg/kg of body weight, respectively; P < 0.05). When different nutritional regimens were alternated over a short period, the level of in vivo AmB-d toxicity was dictated by the last feeding regimen. Serum triglycerides, but not cholesterol in very-low-density and low-density lipoproteins, correlated significantly (P < 0.01) with the LD50 of AmB. In vitro experiments showed that the addition of human serum reduced AmB-d-induced toxicity against human erythrocytes, but serum drawn after fasting was less protective than postprandial serum. However, neither serum decreased the in vitro activity of AmB-d against Candida albicans. Circular dichroism, a method that enables the amount of free AmB to be measured, showed that both mouse and human total serum lipoproteins bound more AmB-d when serum was isolated postprandially than when it was obtained after fasting. Our results show that AmB-d toxicity is reduced by feeding-induced modifications in serum lipids. The influence of food intake on the clinical toxicity of the drug merits being investigated.

Amphotericin B↗
PubMed1994

Effect of postgastric energy loads on intake of sham meals of different palatability in rats.

Food intake depends on the palatability of the diet and on the energy delivered to the body. It is not known, however, whether the palatability of a diet is able to modulate the inhibitory effect of energy input on food intake. To address this question, we have measured intake during sham feeding for diets of different palatabilities in rats receiving varying levels of duodenal energy load. Rats were offered sucrose solutions (6, 10, or 30%) or mixed liquid diets without or with physiological duodenal energy loads using a mixed liquid diet. Compared with that seen during real feeding, meal size during sham feeding was increased for palatable diets but not for less palatable diets. Intraduodenal infusion of the mixed liquid diet inhibited the intake of all diets given by sham feeding. This inhibition was dependent on the level of duodenal energy load and was significantly greater for more palatable diets than for less palatable ones. We conclude that the inhibitory effects of intestinal nutrient load on intake are significant for all diets but have a more pronounced effect on the intake of highly palatable diets.

Animals↗
PubMed1994

Diaphragmatic function in severely malnourished patients with anorexia nervosa. Effects of renutrition.

The effects of malnutrition and refeeding on nutritional indices, pulmonary function, and diaphragmatic contractile properties were studied in severely malnourished patients with anorexia nervosa. Fifteen patients were evaluated upon hospital admission (Day 0) and on Days 7, 30, and 45 after starting feeding. Spirometry, lung volumes, and arterial blood gases were measured at each time interval, as were contractile properties of the diaphragm as assessed by transdiaphragmatic pressure generated during electrical phrenic nerve stimulation (Pdistim) and a maximal sniff maneuver (Pdisniff). Anthropomorphic and biochemical measurements were performed at each time interval. Patients were severely malnourished upon admission; mean body weight was 37.1 +/- 4.7 kg (63% ideal body weight). During nutritional support, body weight increased significantly to 42.9 +/- 4.6 kg on Day 45 (p < 0.01), as did muscle mass: 11.2 +/- 4.1 kg on Day 0, to 16.6 +/- 4.9 kg on Day 45 (p < 0.01). Vital capacity and FEV1 increased significantly by Day 30 (p < 0.05). Lung volumes were unchanged. Mean arterial blood gas values were also within the normal range at Day 0; PaO2, 92.6 +/- 2.4 mm Hg and PacO2, 41.0 +/- 1.5 mm Hg. Four patients, however, had an increased PacO2 (> 42 mm Hg) at Day 0, which returned to normal by Day 30. Diaphragmatic contractility was severely depressed initially; Pdistim, 15.9 +/- 1.4 cm H2O; Pdisniff, 65.4 +/- 5 cm H2O; but it significantly increased with nutritional support by Day 30 to 22.5 +/- 1.9 and 84.6 +/- 4.7 cm H2O, respectively. We conclude that diaphragmatic function is severely impaired in malnuorished patients free of other coexisting

Acute Disease↗
PubMed1994

[Cephalic phase of gastric secretion in dogs. Effect of palatability and caloric intake].

The purpose of this study was to analyze the relative part of the cephalic phase in the gastric secretory and circulating gastrin responses to meals of variable composition and palatability in dogs. Meal palatability was quantified by measuring the ingestion rate of a fixed amount of food. By progressively increasing the amount of carbohydrates or lipids added to a normal meat meal, it was possible to obtain eleven meals of progressively decreasing ingestion rate. When were offered as sham-feeding these eleven meals in dogs fitted with a cervical esophagostomy and a gastric fistula, gastric acid response decreased only after meals of very small ingestion rates. Moreover, neither gastrin, nor gastric pepsin responses changed significantly with ingestion rate of the sham-fed meals. By subtracting the response to sham-fed meals from the response to real meals of identical composition, it was possible to calculate the non-cephalic part of gastric responses. The non-cephalic part of gastric acid secretion and of circulating gastrin was significantly correlated to calorie intake; the slope of the best fitting regression line was greater after lipid meals than after carbohydrate meals. The non-cephalic part of pepsin secretion was very small, if any, and its level was not correlated to the amount of ingested calories. This work suggests that palatability has very little influence on gastric secretion control in dogs.

Animals↗
PubMed1993

Resting energy expenditure in human immunodeficiency virus-infected patients: comparison between patients with and without secondary infections.

Resting energy expenditure (REE) was measured in 165 malnourished patients with human immunodeficiency virus infection and compared with that of 31 control subjects. Of these patients, 129 had no symptoms of secondary infections (NI), whereas 36 had evolving secondary infection (I) despite a body temperature < 38 degrees C. Mean REE was 11% higher in the NI group than in the control group (P < 0.05); it was 34% higher in the I group than in the control group (P < 0.001) and 21% higher than in the NI group (P < 0.01). In all cases the best predictive variable for REE was the fat-free mass (FFM) (r = 0.77, P < 0.001 in NI; r = 0.70, P < 0.001 in I; r = 0.78 in the control group. The REE-FFM ratio was 152.5 +/- 1.2 and 207 +/- 5.4 kJ.kg-1.d-1 in the NI and I groups, respectively. A high energy expenditure may be a harbinger of secondary infection in acquired immunodeficiency syndrome and may participate in accelerated weight loss.

AIDS-Related Opportunistic Infections↗
PubMed1993

Gastric secretion of platelet activating factor and precursors in healthy humans: effect of pentagastrin.

The release of platelet activating factor (PAF-ACETHER or PAF) and its precursors in the gastric lumen was assessed in 13 normal subjects in basal condition and after stimulation by gastrin. Acid, pepsin, and sialic acid outputs were determined under the same conditions. Gastric juice was collected using a nasogastric tube after overnight fast in basal condition for 60 minutes, then under pentagastrin infusion (6 micrograms/kg/hr for 60 minutes). Platelet activating factor was detected at low concentration in 4/13 subjects under basal condition (mean (SEM) 1.2 (0.6) pg/hr) while high concentrations of lyso platelet activating factor (6.1 (1.8) microgram/hr) and of alkyl-acyl-glycerophosphocholine (AAGPC) (11.5 (3) micrograms/hr) were found in 13 and 11 subjects, respectively. Platelet activating factor was not detected during pentagastrin infusion, while lyso platelet activating factor and alkyl-acyl-glycerophosphocholine were detected in 13 and in 12 subjects, respectively. Compared with the basal condition these platelet activating factor precursors increased significantly (p < 0.001) going up to fivefold baseline (31.8 (6.8) micrograms/hr and 53 (9.3) micrograms/hr respectively) in response to pentagastrin. There was a positive correlation between platelet activating factor precursors and acid or pepsin output but not between platelet activating factor precursors and sialic acid. As sialic acid may be considered an index of mucus glycoprotein degradation, it seems that gastrin stimulation of gastric epithelial cells results in a concomittant secretion of platelet activating factor precursors, acid, and pepsin irrespective of mucus glycoprotein degradation.

Acetylation↗
PubMed1993

[Increase of resting energy expenditure during flare-ups in Crohn disease].

Crohn's disease is an inflammatory process commonly characterized by phases of flare-up. Weight loss and malnutrition are prominent features in the course of the disease, especially during acute episodes. It is therefore important to define energy needs. Curiously, resting energy expenditure (REE) has rarely been studied in Crohn's disease, and never in relation with the activity of the disease. We therefore determined REE together with body composition (fat free mass, FFM), Crohn's disease activity index (CDAI) and plasma acute phase proteins in 70 patients: during flare-up in 41 and during clinical remission (CDAI < 150) in 29. We found an increase in REE in patients with active disease (CDAI > 150), as compared with patients in remission, when REE was expressed as a function of FFM: 31.7 +/- 2.7 versus 29.4 +/- 3.3 kcal/kg FFM/day (P < 0.01). The mean REE/FFM was 8% higher during flare-up than during remission, and was correlated to both clinical (CDAI; P = 0.011) and biological inflammatory activity indices (C reactive protein, P = 0.018; orosomucoid, P = 0.024). In some patients, the REE was in the normal range, despite an increase in REE/FFM, because of a decrease in FFM due to hypermetabolism. In 8 patients treated successfully by total parenteral nutrition for a massive flare-up, REE/FFM was increased before TPN (36.6 +/- 3.0 kcal/kg/day), and decreased after 4 weeks of TPN (31.4 +/- 1.8 kcal/kg/day; P < 0.001), returning within normal values in 7 patients.

Adult↗
PubMed1992

Effect of a moderate alcohol intake on the lipoproteins of normotriglyceridemic obese subjects compared with normoponderal controls.

Moderate alcohol intake is frequently associated with an elevated concentration of high-density lipoprotein (HDL), which is one of the potential causes for the relative decrease in cardiovascular risk reported in moderate drinkers. Conversely, low HDL concentrations, particularly HDL2, in obese subjects may be a risk factor. The effect of 30 g alcohol daily (wine) during 14 days following a period of abstinence was studied in seven normolipidemic obese subjects (body mass index [BMI], 30 +/- 1.7 kg/m2) compared with seven normoponderal controls (BMI, 22 +/- 1.2 kg/m2). Alcohol caused apolipoprotein (apo) AI and apo AII concentrations to increase in all controls by 12% and 16% (P less than .05), but not in obese subjects. Lipoprotein (Lp) AI HDL particles (without AII) were initially in the same proportions in the two groups. Their increase in controls only (P less than .03) was not matched by an increase in HDL2 in all subjects. In obese subjects, neither Lp AI nor HDL2 were increased by alcohol, but their HDL-triglyceride (TG) contents, initially elevated, were normalized. Cholesterol ester (CE) transfer activity was not different in controls and obese subjects during abstinence (105.7 +/- 40.8 v 104.8 +/- 34.5 mmol/mg protein/h). It was notably depressed by alcohol in controls (74.2 +/- 27.4, P less than .002), but not in obese subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Lack of plasmic beta-endorphin response to a gastronomic meal in healthy humans.

In order to study the relationship between the endogenous opiate system and food intake in man, plasma concentrations of beta-endorphin were measured in ten healthy subjects. Time course of beta-endorphinemia was compared under the following conditions: basal (fasting), after an injection of pentagastrin (6 micrograms/kg), or after a gastronomic meal. No changes in plasma beta-endorphin or ACTH concentrations were observed with pentagastrin nor after the meal, despite the combination of very high sensory pleasure with intake of a very large amount of food. It is concluded that blood beta-endorphin concentration is not a sensitive index of the effects of food intake on the endogenous opioid system in man.

Adult↗
PubMed1991

Immunoreactive beta-endorphin increases after an aspartame chocolate drink in healthy human subjects.

It has been claimed that sucrose intake induces a rise in beta-endorphins. In an attempt to discriminate between the sensorial and metabolic effects of sucrose intake in this process, the effects of two chocolate drinks were compared: one sweetened with 50 g of sucrose, the other with 80 mg of aspartame. Plasma beta-endorphin concentrations were more elevated after the aspartame drink than after sucrose or fasting, while insulin increased after drinking as much with aspartame as with sucrose. We suggest that the increase in beta-endorphin after aspartame edulcorated chocolate is related with insulin secretion in the absence of marked changes in blood glucose or with a direct effect of aspartame itself on beta-endorphin liberation.

Adolescent↗
PubMed1991

Resting energy expenditure is increased in stable, malnourished HIV-infected patients.

Resting energy expenditure (REE) was measured by reference to body composition in 50 malnourished patients with human immunodeficiency virus (HIV) infection and compared with that of 14 healthy subjects. Among HIV patients, 40 had acquired immune deficiency syndrome (AIDS) and 10 had AIDS-related complex (ARC). All were in stable condition and had a previous history of progressive wasting, ie, a mean body weight loss of 14.2 +/- 8.1 kg over 16.6 mo (range 2-49 ms). The mean REE was 14% higher than estimated basal energy expenditure (EBEE), according to the Harris and Benedict formula. Thirty-four patients (68%) were classified as hypermetabolic (REE greater than 110% EBEE). The best predictable variable for REE was fat-free mass (FFM), as determined by an anthropometric method (r = 0.72; P less than 0.001). The mean REE was 12% higher in HIV patients than in the control group FFM (156 +/- 19 vs 124 +/- 17 kJ.kg FFM-1.d-1). We concluded that in stable and malnourished HIV patients, the progressive wasting may be partly related to an increase in REE. The mechanism of this hypermetabolic state remains to be established.

Body Composition↗
PubMed1991

Controlled trial comparing two types of enteral nutrition in treatment of active Crohn's disease: elemental versus polymeric diet.

To determine whether an elemental diet or a polymeric defined formula diet would be more effective for treating active Crohn's disease, we conducted a prospective randomised clinical trial in 30 patients with active Crohn's disease unresponsive to steroids and/or complicated by malnutrition. They received a four to six week enteral nutrition course with either an elemental diet or a polymeric diet. Clinical remission occurred in 10 of the 15 patients on elemental diet compared with 11 of the 15 patients assigned to polymeric diet. Both groups showed similar improvements in nutritional status, biological inflammation, alpha 1 antitrypsin clearance, and colonoscopic lesions (diminished in 17 out of 24 patients). Most patients relapsed during the year after discharge. We conclude that enteral nutrition, whatever the diet, is an efficient primary therapy for active Crohn's disease but does not influence the long term outcome.

Adult↗
PubMed1991

Sequential somatostatin and gastrin releases in response to secretin in rat in vivo.

Secretin in known to inhibit gastric acid secretion. Exogenous secretin has also been shown to have a biphasic effect on acid secretion, being stimulatory then inhibitory. To explain this effect, we studied the timing of gastrin, somatostatin, and HCl releases in the gastric lumen in response to an i.v. bolus of secretin (360 pmol) or saline in conscious rats provided with a chronic double gastric fistula and having had or not antrectomy. After secretin but not saline, an immediate and transient increase in acid and gastrin secretions was first observed. After a 4 min lag, a dramatic increase in somatostatin secretion was then observed, together with a 90 percent inhibition of acid secretion and a return of gastrin release to basal level. Twenty min after secretin administration, a rebound increase in acid and gastrin outputs occurred, whereas somatostatin output returned to basal level. The secretin-induced somatostatin release was higher in rats with antrectomy than in those without antrectomy suggesting that the observed somatostatin output mostly originated from the fundus. This present study suggests that a bolus of secretin induced a gastrin release and thus could stimulate acid secretion. These pharmacological findings could provide an explanation for the so-called paradoxical secretin-induced stimulation of gastrin secretion in particular conditions.

Animals↗