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PubMed1991

Optimization of gut structure and diet for higher vertebrate herbivores.

A generalized herbivore gut is modelled as (i) a well-stirred anterior chamber in which microbial fermentation occurs; (ii) a tubular reactor in which digestion but no fermentation occurs; and (iii) a posterior fermentation chamber. The rate at which the herbivore gains metabolizable energy is calculated for diets that can be eaten at different rates and contain different energy densities of easily digested cell contents, and of cell wall materials that can be fermented but not digested. The optimum gut structure for each diet is determined. Chewing probably speeds digestion and fermentation but reduces eating time. Optimal chewing times are determined for particular diets and guts. Herbivores often have a choice between poorer food that can be eaten fast and richer food that can only be eaten more slowly. Energy costs may be incurred in travelling between patches of the richer food. Optimal diet choices are predicted for herbivores with particular gut structures.

Animals↗
PubMed1992

Differential inhibition of fat intake in two strains of rat by the peptide enterostatin.

The effect of enterostatin, the amino-terminal pentapeptide of pancreatic procolipase, on food intake was investigated in two strains of rat, the dietary fat-sensitive Osborne-Mendel (OM) rat and the dietary fat-resistant S5B/Pl rat. After an overnight fast, enterostatin inhibited intake of high-fat (HF) but not low-fat (LF) diets in OM rats, but had no effect in S5B/Pl rats. When fed a macronutrient three-choice diet, OM rats selected fat preferentially, whereas S5B/Pl rats selected carbohydrate. Enterostatin specifically inhibited the intake of fat in OM rats but not S5B/Pl rats fed a three-choice macronutrient diet. The activity of pancreatic colipase was increased in S5B/Pl rats on both HF and LF diets compared with OM rats. Pancreatic colipase activities were negatively related to the voluntary intake of fat on three-choice macronutrient diets. The data support the hypothesis that enterostatin may control the intake of dietary fat.

Animals↗
PubMed1982

The effect of chronic alpha-glycosidase inhibition on diabetic nephropathy in the db/db mouse.

Acarbose, a complex oligosaccharide, is a potent competitive inhibitor of sucrase and decreases postprandial hyperglycemia when administered with food. To evaluate its potential for metabolic control and prevention of diabetic nephropathy, groups of gentically diabetic mice (C57 BLKsJ db/db) were treated with Acarbose for 10 wk. Control mice received normal chow and experimental groups were given Acarbose prepared as a drug-food mixture in doses of 10, 20, and 40 mg/100 g of food. Acarbose did not influence fasting blood glucose, food intake, or the normal development of obesity in the mice. Urinary glucose excretion and glycosylated hemoglobin was significantly reduced in animals receiving high-dose Acarbose (40 mg/100 g food). Immunopathologic examination of the kidneys showed a dose-dependent decrease in glomerular mesangial immunoglobulin deposition. By light microscopy, glomerular mesangial thickening was significantly reduced in the group receiving high-dose Acarbose (40 mg/100 g food). To the extent that Acarbose improves metabolic control in the db/db mouse, chronic treatment with this agent produces a dose-dependent amelioration of diabetic nephropathy. Alphaglycosidase inhibition may be a useful adjunctive therapy for blood glucose control in diabetes mellitus.

Acarbose↗
PubMed1979

[Circadian rhythm of poly A polymerase in rat liver nuclei].

Isolated nuclei from the liver of rats maintained under daily scheduled conditions of light (12 hrs) and food (8 hrs) showed a peak of Mn2+-dependent poly (A) polymerase activity 6 hrs after the beginning of the feeding period, as shown by DNA dependent RNA polymerase B. In fasting animals the peak of poly (A) polymerase occurs at 18.00.

Animals↗
PubMed1999

Corticotropin-releasing hormone-binding protein in brain and pituitary of food-deprived obese (fa/fa) Zucker rats.

The present study was conducted to verify whether experimental conditions such as obesity and food deprivation, which promote food intake and reduce thermogenesis, could modify the expression of the corticotropin-releasing hormone (CRH)-binding protein (BP) in the rat brain. In situ hybridization, histochemistry, and immunohistochemistry were used to assess the expression of CRH-BP in lean (Fa/?) and obese (fa/fa) Zucker rats that were fed ad libitum, food deprived for 24 h, or food deprived for 24 h and refed for 6 h. In both lean and obese rats, food deprivation led to a reduction in body weight that was accompanied by a reversible increase in plasma corticosterone levels. Food deprivation and, to a lesser degree, obesity induced the expression of CRH-BP mRNA in the dorsal part of the medial preoptic area (MPOA). This induction of the CRH-BP gene led to by food deprivation was confirmed by the appearance in the dorsal part of the MPOA of neurons immunoreactive to CRH-BP. Food deprivation (in particular) and obesity also increased the levels of CRH-BP mRNA in the basolateral amygdala (BLA). The enhanced CRH-BP expression in the MPOA and BLA in response to food deprivation was reversed by refeeding. In lean Fa/? rats, the CRH-BP mRNA level in the pituitary cells was significantly decreased after food deprivation and restored after refeeding. When food was provided ad libitum, the number of cells expressing CRH-BP in the anterior pituitary was significantly higher in lean rats than in obese animals. Food deprivation for 24 h decreased dramatically the number of pituitary cells expressing CRH-BP in lean rats. Altogether, the present results demonstrate that food deprivation and, to a lesser extent, obesity can selectively affect the expression of CRH-BP. Given both the inactivating effect of CRH-BP on the CRH system and the potential roles played by the MPOA and BLA in the thermogenic and anorectic effects of CRH, it can be argued that the induction of the CRH-BP gene in obesity and after food deprivation occurs as a mechanism to reduce energy expenditure and to stimulate food intake.

Amygdala↗
PubMed1983

Gastrin production following antrectomy. A study on the occurrence of gastrin-producing cells and the serum gastrin response to feeding.

Fifteen patients were studied 3 to 35 years after antrectomy, with a gastroduodenal (Billroth I (BI)) anastomosis in 8, and a gastrojejunal (Billroth II (BII)) anastomosis in 7. The investigations included gastric acid secretion, serum gastrin response to feeding and immunohistochemical search for gastrin-producing cells in gastric remnant mucosal biopsies. All of the patients had hypochlorhydria. The gastrin response to feeding was minimal. Apart from a significantly higher value of serum gastrin 3 hours post-prandial in BI operated as compared to BII operated patients, no greater differences were found in the gastrin production between the two groups of patients. No gastrin-producing cells could be identified in the gastric remnant, not even in areas of pseudopyloric metaplasia. It is concluded that the gastrin production following antrectomy is caused by extragastric G-cells; these cells are poorly stimulated by food, and do not respond to hypochlorhydria with hypergastrinaemia.

Aged↗
PubMed2000

Differential effects of melanocortin peptides on ingestive behaviour in rats: evidence against the involvement of MC(3) receptor in the regulation of food intake.

The pro-opiomelanocortin-derived peptides decrease food intake possibly via MC4 receptor. In this study we compared the effects of alpha-melanocyte-stimulating hormone (MSH), beta-MSH and gamma(1)-MSH (0.2, 1.0 and 5.0 microg, i.c.v.) on food intake. alpha-MSH and beta-MSH inhibited spontaneous food intake in a dose dependent manner, whereas the gamma(1)-MSH did not. alpha-MSH and beta-MSH but not gamma(1)-MSH (all 5.0 microg, i.c.v.) inhibited fasting-induced food intake about 50%. None of the three peptides inhibited fluid consumption in water-deprived (24 h) rats. It is suggested that MC(3) receptor, activated selectively by gamma(1)-MSH, is not involved in the regulation of food intake.

Animals↗
PubMed1981

Influence of study design in assessing food effects on absorption of erythromycin base and erythromycin stearate.

We performed a series of six single-dose and multiple-dose studies to evaluate the effect of food on the absorption of erythromycin base and erythromycin stearate. When we used a single-dose design, we found that an unprotected erythromycin base preparation was absorbed extensively if a prolonged fast preceded administration of the drug. A shorter faster period (as occurs in clinical settings) dramatically reduced the absorption of unprotected base; however, film-coated tablets seemed to be as well protected as and were absorbed more rapidly than enteric-coated tablets when they were evaluated by single-dose testing procedures. In contrast, when a commercially available film-coated preparation of erythromycin base was evaluated in multidose fashion between meals (fasting), the drug was about 25% less well absorbed than commercially available enteric-coated base tablets. Finally, when commercially available film-coated erythromycin base and stearate formulations were administered with meals, both film-coated preparations were 43 to 59% less well absorbed than the enteric-coated base formulation. Furthermore, the enteric-coated base formulation performed equally well when administered either every 6 h between meals (fasting) or four times a day (immediately after meals and at bedtime). These studies document the need for multidose bioavailability techniques when the bioavailabilities of acid-labile drugs are evaluated.

Adult↗
PubMed2004

Relationship between ghrelin and energy expenditure in healthy young women.

Ghrelin is a novel peptide that has been isolated from human and rat stomach tissues. Despite its known stimulatory effects on appetite and eating behavior, little information is available regarding its relationship with energy expenditure in normal-weight humans. To address this issue, we examined the relationship between serum ghrelin and resting metabolic rate (RMR), the thermic effect of food (TEF), fasting and postprandial respiratory quotient, physical activity level, peak aerobic capacity (VO(2 peak)), energy intake, and psychological measures of feeding behavior. We recruited 65 young healthy women and determined RMR and TEF by indirect calorimetry after a 12-h fast. Physical activity was determined by a leisure time physical activity questionnaire; VO(2 peak) was determined by bicycle ergometer test to exhaustion; energy intake was determined by a 24-h dietary recall; and food behavior was determined by a three-factor eating questionnaire. Our cohort showed a broad range of body mass index (range, 16.8-28.3 kg/m2), RMR (range, 820-1550 kcal/d), TEF (range, 74.4-136.5 kcal/d), and percent body fat (range, 14.0-37.7%). We noted significant inverse correlations between ghrelin and RMR (r = -0.350, P = 0.004) and TEF (r = -0.396, P = 0.001). These inverse correlations persisted after statistical control for both fat-free mass and fat mass (ghrelin vs. RMR partial, r = -0.284, P = 0.024; and ghrelin vs. TEF partial, r = -0.329, P = 0.01) and insulin levels (ghrelin vs. RMR partial, r = -0.255, P = 0.046; and ghrelin vs. TEF partial, r = -0.287, P = 0.024) using partial correlation analysis. We also observed a significant inverse correlation between ghrelin and daily caloric intake (r = -0.266, P = 0.032), but ghrelin levels were not significantly correlated with fasting (r = -0.002), postprandial respiratory quotient (r = -0.016), leisure time physical activity (r = 0.104), VO(2 peak) (r = 0.138), dietary disinhibition (r = -0.071), dietary restraint (r = 0.051), or feeling of general hunger (r = -0.028). These results suggest that higher levels of ghrelin are associated with low levels of resting and postprandial thermogenesis, which is independent of individual differences in fat-free mass and fat mass. Although speculative, serum ghrelin may play a role in the regulation of energy homeostasis by acting as a hormonal marker of increased energy efficiency.

Adult↗
PubMed1978

Effect of fasting, glucose, amino acids and food intake on in vivo insulin release in the chicken.

Insulin release was studied in vivo in the chicken using the radioimmunoassay previously described (Simon, Freychet and Rosselin 1974). An orally administered glucose load (2 g/kg b.w.) stimulated insulin release and was rapidly metabolized. A prolonged fasting period (65 hr) increased both initial plasma glucose and initial plasma insulin levels and highly impaired the glucose tolerance. A fasting-impaired insulin release and/or a fasting tissue "insulin resistance" accounted for this fasting-impaired glucose tolerance. An orally administered amino acid mixture (1 g/kg b.w.) stimulated insulin release to a very low extent. The effect was however sufficient to decrease the plasma glucose level. In combination with glucose, the oral amino acid load potentiated the effect of a dose of glucose on insulin release and highly improved the glucose tolerance. This synergism was still observed with the intake of a mixed and balanced diet. Therefore, except for some characteristics observed in the chicken which are discussed, the insulin regulation and the pancreatic beta-cell function are qualitatively similar in the chicken and in mammals.

Amino Acids↗
PubMed1981

Effect of food and GH on the binding of 125I-somatomedin A to the membranes of rat lung and kidney.

Studies were undertaken to examine the relationship between serum levels of somatomedin A and its binding sites in the lung and kidney of rats. After three days of fasting, serum levels of somatomedin A decreased, accompanied by increases of 17.5% and 21.4% in binding to the plasma membranes from lung and kidney, respectively. After two days of refeeding, this binding decreased with the increase in the serum level of somatomedin A. There was observed a negative correlation between the serum level of somatomedin A and the percentage of labelled somatomedin A bound to the membranes. These observations suggest that somatomedin down-regulates its own receptor under these conditions. A similar regulatory mechanism was not observed with either hypophysectomized- or GH-treated rats.

Animals↗
PubMed2002

Clinical pharmacokinetics of tegaserod, a serotonin 5-HT(4) receptor partial agonist with promotile activity.

Tegaserod, a selective serotonin (5-hydroxytryptamine; 5-HT) 5-HT(4) receptor partial agonist, is indicated in patients with irritable bowel syndrome (IBS) who identify abdominal pain or discomfort and constipation as their predominant symptoms. Tegaserod at dosages of 1 to 12 mg/day exerts pharmacodynamic actions in the upper and the lower gastrointestinal tract, accelerating small bowel and colonic transit in patients with IBS. Tegaserod is rapidly absorbed following oral administration; peak plasma concentrations (C(max)) are reached after approximately 1 hour. Absolute bioavailability is about 10% under fasted conditions. Food reduces the bioavailability of tegaserod by 40 to 65% and the C(max) by 20 to 40%. Systemic exposure to tegaserod is not significantly altered at neutral gastric pH compared with the fasted state (pH 2). Tegaserod is approximately 98% bound to plasma proteins, primarily to alpha(1)-acid glycoprotein, and has a volume of distribution at steady-state of 368 +/- 223L. Tegaserod is metabolised mainly via two pathways. The first is a presystemic acid-catalysed hydrolysis in the stomach followed by oxidation and conjugation which produces the main metabolite of tegaserod, 5-methoxyindole-3-carboxylic acid glucuronide (M 29.0). This metabolite has negligible affinity for 5-HT(4) receptors and is devoid of promotile activity. The second is direct glucuronidation which leads to generation of three isomeric N-glucuronides. The plasma clearance of tegaserod is 77 +/- 15 L/h, with an estimated terminal half-life of 11 +/- 5 hours following intravenous administration. Approximately two-thirds of the orally administered dose of tegaserod is excreted unchanged in faeces, with the remainder excreted in urine, primarily as M 29.0. The pharmacokinetics of tegaserod are dose-proportional over the range 2 to 12mg given twice daily for 5 days, with no relevant accumulation. The pharmacokinetics of tegaserod in patients with IBS are comparable to those in healthy individuals, and similar between men and women. No dosage adjustment is required in elderly patients or those with mild to moderate hepatic or renal impairment. Tegaserod should not be used in patients with severe hepatic or renal impairment. No clinically relevant drug-drug interactions with tegaserod have been identified. In vivo drug-drug interaction studies with theophylline [a cytochrome P450 (CYP) 1A2 prototype substrate], dextromethorphan (a CYP2D6 prototype substrate), digoxin, warfarin and oral contraceptives have indicated no clinically relevant interactions and no requirement for dosage adjustment.

Animals↗
PubMed2004

Mice with deletion of the mitochondrial glycerol-3-phosphate dehydrogenase gene exhibit a thrifty phenotype: effect of gender.

To define the role of mitochondrial glycerol-3-phosphate dehydrogenase (mGPD; EC 1.1.99.5) in energy balance and intermediary metabolism, we studied transgenic mice not expressing mGPD (mGPD-/-). These mice had approximately 14% lower blood glucose; approximately 50% higher serum glycerol; approximately 80% higher serum triglycerides; and at thermoneutrality, their energy expenditure (Qo(2)) was 15% lower than in wild-type (WT) mice. Glycerol-3-phosphate levels and lactate-to-pyruvate ratios were threefold elevated in muscle, but not in liver, of mGPD-/- mice. WT and mGPD-/- mice were then challenged with a high-fat diet, fasting, or food restriction. The high-fat diet caused more weight gain and adiposity in mGPD-/- than in WT female mice, without the genotype differentially affecting Qo(2) or energy intake. After a 30-h fast, WT female lost 60% more weight than mGPD-/- mice but these latter became more hypothermic. When energy intake was restricted to 50-70% of the ad libitum intake for 10 days, mGPD-/- female mice lost less weight than WT controls, but they had lower Qo(2) and body temperature. WT and mGPD-/- male mice did not differ significantly in their responses to these challenges. These results show that the lack of mGPD causes significant alterations of intermediary metabolism, which are more pronounced in muscle than liver and lead to a thrifty phenotype that is more marked in females than males. Lower T(4)-to-T(3) conversion in mGPD-/- females and a greater reliance of normal females on mGPD to respond to high-fat diets make the lack of the enzyme more consequential in the female gender.

Animals↗
PubMed1990

Regulation of cholecystokinin secretion by food, hormones, and neural pathways in the rat.

Regulation of cholecystokinin (CCK) secretion was studied in conscious unrestrained rats by simultaneous duodenal perfusion with foodstuffs, intravenous infusion of hormones or neural agents, and arterial blood sampling for CCK bioassay. Duodenal infusion of casein resulted in elevation of plasma CCK from fasting level of 0.5 +/- 0.1 to 3.8 +/- 0.4 pM. Casein hydrolysate, calcium, and glucose did not elevate plasma CCK. Infusion of intact fat had a small, but nonsignificant, effect (1.4 +/- 0.4 pM), whereas infusion of oleate increased plasma CCK to 3.7 +/- 0.6 pM. Thus intact protein and fatty acids are the major dietary intestinal stimuli for CCK release in the rat. The CCK response to protein could be inhibited by somatostatin but not by peptide YY (0.2, 2, or 20 micrograms.kg-1.h-1); intravenous infusion of 1 or 10 micrograms.kg-1.h-1 somatostatin decreased casein-stimulated CCK levels to 1.5 +/- 0.2 and 0.9 +/- 0.3 pM, respectively. Stimulation of vagal discharge with 2-deoxy-D-glucose had no effect on basal or protein-stimulated plasma CCK levels; thus CCK release in the rat does not appear to be modulated by central vagal pathways. Gastrin-releasing peptide increased fasting plasma CCK levels to 1.6 +/- 0.1 pM. Administration of the cholinergic agonist bethanechol, while having no effect on fasting CCK level, inhibited protein-stimulated plasma CCK from 3.9 +/- 0.6 to 1.3 +/- 0.3 pM. Cholinergic blockade with atropine, in contrast, had no effect on basal or protein-stimulated plasma CCK. Thus CCK release is stimulated by dietary protein or fatty acid and by gastrin-releasing peptide and inhibited by somatostatin and bethanechol.

Animals↗
PubMed1998

Neuropeptide Y Y1 receptor antisense oligodeoxynucleotides enhance food intake in energy-deprived rats.

In the literature, conflicting data on the effect of NPY Y1 antisense oligodeoxynucleotides (ODNs) on food intake have been reported, describing either an increase or a decrease in feeding in antisense-treated animals. In the present studies antisense oligodeoxynucleotides targeted to the Y1 receptor (Y1 antisense ODNs) were used to re-investigate the functional importance of this receptor subtype in vivo in the regulation of feeding in rats. We used phosphothioate-terminal protected derivatives of two ODN sequences used in previous reports. In addition, as one of these sequences was not tested in vitro, we demonstrated its efficacy in LMTK-cells transfected with the Y1 receptor subtype. In vivo, repeated intracerebroventricular (i.c.v.) injections of Y1 antisense ODNs did not affect basal food intake or the increase in food intake after i.c.v. injection of neuropeptide Y (NPY, 300 pmol). Y1 antisense ODNs given intracerebroventricularly enhanced food intake in energy-deprived rats (+175% and +60% vs. control scrambled and sense sequences, respectively after 2 h of refeeding). Analysis of the structure of feeding behaviour revealed that Y1 antisense ODNs enhanced fasting-induced food intake during the first hour of refeeding by inducing increases in meal size (+143% and +155% vs. sense and scrambled ODNs) but not meal duration. These data suggest that the NPY Y1 receptor is not directly implicated in feeding in the rat when calorie intake is normal but might be specifically activated during energy deprivation.

Animals↗
PubMed1990

Patterns of weight loss and regain in wrestlers: has the tradition changed?

To assess current weight loss practices in wrestlers, 63 college wrestlers and 368 high school wrestlers completed a questionnaire that examined the frequency and magnitude of weight loss, weight control methods, emotions associated with weight loss, dieting patterns, and preoccupation with food. Clear patterns emerged showing frequent, rapid, and large weight loss and regain cycles. Of the college wrestlers, 41% reported weight fluctuations of 5.0-9.1 kg each week of the season. For the high school wrestlers, 23% lost 2.7-4.5 kg weekly. In the college cohort, 35% lost 0.5-4.5 kg over 100 times in their life, and 22% had lost 5.0-9.1 kg between 21 and 50 times in their life. Of the high school wrestlers, 42% had already lost 5.0-9.1 kg 1-5 times in their life. A variety of aggressive methods wer used to lose weight including dehydration, food restriction, fasting, and, for a few, vomiting, laxatives, and diuretics. "Making weight" was associated with fatigue, anger, and anxiety. Thirty to forty percent of the wrestlers, at both the high school and college level, reported being preoccupied with food and eating out of control after a match. The tradition of "making weight" still appears to be integral to wrestling. The potential physiological, psychological, and health consequences of these practices merit further attention.

Adolescent↗
PubMed1989

Pharmacokinetics of halofantrine in man: effects of food and dose size.

1. Plasma concentrations of halofantrine (Hf) and its putative principal plasma metabolite desbutyl halofantrine (Hfm) have been measured in two separate studies after oral administration of the hydrochloride salt. 2. Six healthy male volunteers each received single oral doses of 250, 500 and 1000 mg administered after an overnight fast. A washout period of at least 6 weeks was allowed between each dose. A further 250 mg single oral dose was administered to the same six subjects in a fasting state and after a standardised fatty meal in a randomised study, again with a washout period of at least 6 weeks. 3. AUC and maximum plasma concentration (Cmax) for Hf increased in proportion to the dose from 250-500 mg. This increase was non-proportional when the dose was increased from 500 to 1000 mg. For Hfm, in the dose range 250-500 mg, AUC but not Cmax increased in proportion in the increase in dose size. The increase in these parameters was non-proportional when the dose was increased from 500 to 1000 mg. Time to reach peak concentrations for Hf and Hfm and the elimination half-life of Hf remained unchanged across the dosage range. 4. Following a fatty meal, Cmax for Hf was increased from 184 +/- 115 micrograms l-1 (fasting) to 1218 +/- 464 micrograms l-1 (fed). AUC for Hf was increased from 3.9 +/- 2.6 mg l-1 h (fasting) to 11.3 +/- 3.5 mg l-1 h following a fatty meal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗