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At least 739 records · Page 41Linked to original sources
PubMed1996

Comparison between activation of ornithine decarboxylase and histidine decarboxylase in rat stomach.

We compared the responses of rat stomach ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) to food intake, oral treatment with antisecretagogues, NaHCO3, and hypertonic NaCl, antrectomy, intravenous infusion of gastrin-17, the selective cholecystokinin (CCK)-B/gastrin receptor antagonist L-365,260, and the somatostatin analogue RC-160. The serum gastrin concentration and oxyntic mucosal ODC and HDC activities were higher in freely fed rats than in fasted rats. Food intake in fasted rats raised the serum gastrin concentration and the ODC and HDC activities. Ranitidine, omeprazole, and NaHCO3 raised the serum gastrin concentration and activated ODC and HDC. Hypertonic NaCl raised the ODC activity 200-fold, whereas circulating gastrin and HDC activity were increased only moderately. Infusion of gastrin-17 activated HDC but not ODC. L-365,260 prevented the activation of HDC but not of ODC in response to food intake and treatment with omeprazole, NaHCO3, or hypertonic NaCl. Antrectomy prevented the food- and omeprazole-evoked rise in oxyntic mucosal HDC activity but not the rise in ODC activity. RC-160 suppressed HDC activity after food intake and treatment with omeprazole, NaHCO3, or NaCl. In contrast, RC-160 suppressed omeprazole- and NaHCO3-evoked ODC activation but not that evoked by food intake or NaCl. The results support the view that HDC in the oxyntic mucosa is activated by gastrin and suppressed by somatostatin. The induction of ODC is not mediated by gastrin; ODC activation appears to be related to acid inhibition per se or to mucosal maintenance and repair; somatostatin, or rather the lack of it, might contribute to the induction of ODC after acid blockade. The mechanism behind the activation of rat stomach ODC seems to differ depending on the type of stimulus.

Analgesics↗
PubMed2005

Arousal and differential Fos expression in histaminergic neurons of the ascending arousal system during a feeding-related motivated behaviour.

Arousal depends on the concerted activity of the ascending arousal system (AAS) but specific stimuli may primarily activate some nuclei of this system. Motivated behaviours are characterized by behavioural arousal, although it is not known which AAS nuclei are active during a motivated behaviour. To address this issue, rats were rendered motivated for food by fasting them for 1 day and then were enticed with food that they could not obtain for varying periods of time. We studied the level of arousal by polysomnography or radiotelemetry, and Fos-ir in the AAS, during food enticing. We found a strong arousal and an early increase in Fos-ir in the histaminergic neurons from the tuberomammillary nucleus, after 30 min of enticing, followed by increased Fos-ir in the whole AAS if food enticing was prolonged to 1 or 2 hours. In contrast, food presentation to non-motivated rats did not increase arousal or Fos-ir in the tuberomammillary nucleus. As opposed to the active arousal of the motivated rats, passive arousal induced by sensory stimulation was associated with increased Fos-ir in the locus coeruleus and the orexin neurons, but not with increased Fos-ir in the tuberomammillary nucleus or in the other nuclei of the AAS. We conclude that the arousal during feeding-related motivated behaviour is associated primarily with the activation of the tuberomammillary nucleus, while the other arousal-related nuclei become active later on.

Afferent Pathways↗
PubMed2006

Peroxisome proliferator-activated receptor (PPAR)-alpha agonism prevents the onset of type 2 diabetes in Zucker diabetic fatty rats: A comparison with PPAR gamma agonism.

Peroxisome proliferator-activated receptor (PPAR)-gamma agonists are insulin sensitizers, whereas PPAR alpha agonists are lipid-lowering agents in humans. Chronic treatment with PPAR gamma agonists has been shown to prevent the onset of diabetes in young Zucker diabetic fatty (ZDF) rats; however, the effects of PPAR alpha agonists have not been well characterized in this model. Here we investigated chronic efficacy of PPAR alpha and nonthiazolidinedione (nTZD) PPAR gamma agonists on the onset of diabetes in 6-wk-old male ZDF rats. Whereas treatment with the nTZD PPAR gamma agonist completely prevented development of hyperglycemia, PPAR alpha activation was associated with lowering of food intake and body weight and reductions in fed and fasting hyperglycemia, with prevention of the hyperinsulinemic peak preceding the development of hyperglycemia in ZDF rats. Both compounds improved glucose tolerance during an oral glucose tolerance test with concomitant increases in insulin response. Such improvements of insulin secretion were associated with increased islet to total pancreatic area ratio and pancreatic insulin contents. Hyperinsulinemic-euglycemic clamp studies demonstrated that nTZD PPAR gamma reduced basal endogenous glucose production and increased insulin-stimulated glucose disposal, consistent with an improved insulin action as a cause of the improved glucose homeostasis. In contrast, activation of PPAR alpha did not significantly improve glucose metabolism during the hyperinsulinemic-euglycemic clamp. In conclusion, chronic treatment of ZDF rats with a PPAR gamma agonist completely prevented the onset of diabetes by improving both insulin action and secretion, whereas PPAR alpha agonism was partially effective, primarily by improving the pancreatic islet insulin response. Unlike the PPAR gamma agonist, the PPAR alpha agonist demonstrated efficacy without inducing body weight gain and cardiomegaly. This study suggests a possible role for PPAR alpha agonists in the prevention of type 2 diabetes mellitus.

Animals↗
PubMed2003

Regulation of ghrelin secretion and action.

The pulsatile release of growth hormone (GH) from anterior pituitary gland is regulated by the interplay of at least two hypothalamic hormones, GH-releasing hormone (GHRH) and somatostatin, via their engagement with specific cell surface receptors on the anterior pituitary somatotroph. Furthermore, release of GH in vivo may also be controlled by a third type of receptor, the growth hormone secretagogue receptor, a G-protein-coupled receptor, called GHS receptor type 1a (GHSR1a), which was identified in the pituitary and the hypothalamus in humans using a nonpeptidyl growth hormone secretagogue (MK-0677). Ghrelin, the endogenous ligand for the GHS-R1a, is a 28-amino-acid peptide isolated from human stomach that is modified by a straight chain octanoyl group covalently linked to Ser3, which is essential for its endocrine activity. This hormone, predominantly expressed and secreted by the stomach, has a dual action on GH secretion and food intake, showing interdependency between these actions. The finding that fasting and food intake, respectively, increase and decrease the secretion of ghrelin suggests that this hormone may be the bridge connecting somatic growth and body composition with energy metabolism, and appears to play a role in the alteration of energy homeostasis and body weight in pathophysiological states such as hypothyroidism and hyperthyroidism. Despite this, little is known about the intracellular signaling through which ghrelin exerts its regulatory actions. Activation of intracellular calcium mobilization is one of the earliest known cellular signals elicited by ghrelin. In HEK- 293 cells expressing the GHS-R1a, ghrelin induces a biphasic cytosolic calcium elevation characterized by a spike phase of the response, which reflects Ins(1,4,5)P3- dependent calcium mobilization of intracellular stores, and a sustained phase of the response, which is due to calcium influx across the plasma membrane triggered by aperture of capacitative calcium channels (store-operated calcium channels). Upon repeated administration, ghrelin showed a marked suppression of ghrelin-mediated elevations of intracellular calcium. This homologous desensitization represents an important physiological mechanism that modulates receptor responsiveness and acts as an information filter for intracellular signaling system. The discovery of ghrelin adds a new component to the complex machinery responsible for regulation of GH secretion in connection with the regulation of appetite and energy homeostasis.

Animals↗
PubMed1986

Vagal control of canine postprandial upper gastrointestinal motility.

The role of the vagus nerves in the control of postprandial motility in the upper gastrointestinal tract was investigated in four dogs by use of a bilateral cervical cooling blockade technique. On administration of food, the fasting migrating motor complex (MMC) was replaced by the postprandial (feeding) pattern. Feeding pattern duration varied in a dose-dependent manner with either total volume or calories of food. During the feeding pattern, oscillations in lower esophageal sphincter (LES) pressure occurred at time intervals equivalent to the MMC cycle period. Twenty-one control feeding experiments and 17 postprandial vagal blockade experiments were performed, with a minimum of three of each type in each dog. Vagal blockade, initiated at times ranging from 15 min to 4 h after feeding and maintained for up to 5 h, abolished the postprandial activity in the upper gastrointestinal tract. During postprandial vagal blockade, LES pressure was abolished and bursts of contractions were observed only in the upper small bowel, a pattern resembling that observed during vagal blockade in the fasted state. These bursts occurred at the expected times relative to, and their cycle period was not significantly different from, that of the MMCs recorded prior to feeding. Vagal blockade started prior to feeding prevented initiation of the fed pattern, which appeared immediately on termination of the blockade. We conclude that initiation and maintenance of the postprandial pattern in the upper gastrointestinal tract with concurrent inhibition of the fasting MMC normally require vagal integrity. The "clock" controlling the MMC cycle period is not reset by feeding, but its effect on motility is suppressed.

Animals↗
PubMed1996

Gender-specific changes in thyroid hormone-glucuronidating enzymes in rat liver during short-term fasting and long-term food restriction.

Glucuronidation is a major pathway of thyroid hormone metabolism in rats, involving at least three different hepatic UDP-glucuronyltransferases (UGTs): bilirubin UGT, phenol UGT and androsterone UGT. We have studied the effects of short-term (3 days) fasting and long-term (3 weeks) food restriction to one-third of normal intake (FR33) on hepatic UGT activities for thyroxine (T4), triiodothyronine (T3), bilirubin and androsterone in male and female Wistar rats with either a functional (high activity, HA) or a defective (low activity, LA) androsterone UGT gene. Because food deprivation is known to induce centrally mediated hypothyroidism in rats, results were compared with those obtained in methimazole (MMI)-induced hypothyroid rats. Both fasting and FR33 produced largely parallel increases in T4 and bilirubin UGT activities. These effects were greater in males than in females, and were reproduced in MMI-treated rats. In male and female HA rats, fasting induced insignificant increases in T3 UGT activity and had no effect on androsterone UGT activity. In male HA rats, FR33 was associated with an increase in T3 UGT activity, while androsterone UGT activity showed little change. However, in female HA rats both T3 and androsterone UGT activities were markedly decreased by FR33. Triiodothyronine UGT activity in LA rats was strongly decreased compared with HA rats, but was not further decreased by FR33 in female LA rats, supporting the importance of androsterone UGT for T3 glucuronidation. These results demonstrate different sex-dependent effects of food deprivation on hepatic T4 and T3 glucuronidation that are associated with changes in the expression of bilirubin UGT and androsterone UGT, respectively. For the increased T4 and bilirubin UGT activities at least, these effects appear to be mediated by the hypothyroid state of the (semi)starved animals.

Androsterone↗
PubMed1975

Serum gastrin level in early childhood.

Serum gastrin concentration was measured in newborns and infants with no gastrointestinal disorders, in the fasting state and after food stimulation. Mean fasting concentration in 14 newborns aged 1 to 12 days (130 . 4 pg/ml +/- 11 . 4 SE) was significantly higher than the mean value in 23 infants aged 1.5 to 22 months (101.4 +/- 6.6 pg/ml). Ingestion of the usual milk meal resulted in a definite rise of the serum gastrin level in the 5 subjects tested (3 newborns and 2 infants). The mean fasting serum gastrin level in 6 babies with hiatus hernia and gastro-oesophageal reflux was found to be no different from the corresponding value in 8 age-matched controls. However, a conspicuously raised fasting gastrin concentration was observed in one infant with lower oesophageal dyskinesia. The results indicate that the release of gastrin and the reactivity of the hormone-producing sites to food stimulation in early life are similar to those in adult humans. No defect of gastrin release was shown in patients with gastro-oesophageal reflux.

Animals↗
PubMed1982

Reciprocal changes in serum 3, 3', 5'-tri-iodothyronine concentration and the peripheral thyroxine inner ring monodeiodination during food restriction in the young pig.

Utilizing the difference in pH optima between two distinct enzyme systems responsible for the thyroxine (T4) inner and outer ring monodeiodination, and a specific radioimmunoassay for iodothyronines, the net T4 conversion to 3, 3', 5'-tri-iodothyronine (rT3) and 3, 5', 3'-tri-iodothyronine (T3) in growing pigs kept under various food restrictions was determined in vitro. It has been found that fasting lowers deiodination of T4 to T3 by liver and kidney homogenates. The conversion of T4 to rT3 was reduced in the liver but not in the kidney, unless the animals were completely fasted. During food restriction serum T4 and T3 decreased whereas rT3 increased, which indicated that the serum rT3 level is not a good reflection of T4 to rT3 converting activity in the liver or kidney. The data suggest that a rise in rT3 reflects a lowered degradation rate of the hormone or an increased secretion by the thyroid gland rather than changes in rT3 neogenesis in the periphery.

Adaptation, Physiological↗
PubMed1996

Stimulation of luteinizing hormone secretion by food intake: evidence against a role for insulin.

In adult male rhesus monkeys, 1 day of fasting leads to a profound suppression of LH secretion that is rapidly reversed with refeeding. To test the hypothesis that changes in insulin secretion during fasting and refeeding mediate the changes in LH secretion, blood samples for LH measurement were obtained between 0900-2400 h from adult male rhesus monkeys (n = 9) on 1) a day when monkeys were refed their normal meal after a day of fasting, and 2) a day when monkeys were refed their normal meal, but endogenous insulin secretion was suppressed. Diazoxide (7.5-9.5 mg/kg.h) caused a 40-99% suppression of postmeal insulin secretion. However, no significant differences in LH pulse frequency, pulse amplitude, or mean serum LH levels were detected between control and diazoxide trials, even in animals in which insulin was markedly suppressed. Further, no correlation existed between the degree of insulin suppression and the magnitude of the meal-induced stimulation of LH. We conclude that meal-induced insulin secretion does not provide the stimulus mediating the meal-induced increase in LH secretion.

Animals↗
PubMed2003

[Food residues identified in the pharynx of a patient with a cleft palate].

Solid food residues were identified in the pharynx of a 17-month-old infant with a cleft palate at the time of anesthesia induction, although nothing-by-mouth directions for more than four hours had been strictly followed. Preoperative airway management, e.g. gargling and nose blowing, is necessary in patients with a cleft palate even after an appropriate period of fasting because food residues may remain in the nose due to the anatomical abnormality.

Anesthesia, General↗
PubMed1984

The effect of food restriction during rearing on fasting heat production of layer strain pullets and hens.

Fasting heat production was measured in darkened respiration chambers at three chronological and three physiological ages during rearing and laying in a layer strain to determine the effects of food restriction during rearing. There were three rearing treatments (42 to 162 days of age) in which birds were allowed ad libitum food intake (F) or were restricted by time (TR), in which birds were allowed continuous ad libitum food intake for about 24 hr in every 72 hr, or by proportion (PR), in which birds were offered each day 60 to 70% of the quantity consumed by F birds the previous day. Liveweight at 163 days of age was reduced by 19 and 15% for TR and PR birds, respectively, compared to F birds. Ad libitum food consumption was allowed during the laying period. Chronological age measurements were carried out at 140 days of age (prelay), 332 days of age, and 370 days of age. Physiological age measurements were carried out at sexual maturity (first egg), peak production (28 days after first egg) and postpeak production (98 days after first egg). Fasting heat production, measured under conditions that minimized physical activity, was not altered after correction for liveweight changes by the food restriction treatments. Based on this and other published studies, it was postulated that physical activity may play an important role in determining the effects of food restriction in poultry.

Animals↗
PubMed2000

Ghrelin induces adiposity in rodents.

The discovery of the peptide hormone ghrelin, an endogenous ligand for the growth hormone secretagogue (GHS) receptor, yielded the surprising result that the principal site of ghrelin synthesis is the stomach and not the hypothalamus. Although ghrelin is likely to regulate pituitary growth hormone (GH) secretion along with GH-releasing hormone and somatostatin, GHS receptors have also been identified on hypothalamic neurons and in the brainstem. Apart from potential paracrine effects, ghrelin may thus offer an endocrine link between stomach, hypothalamus and pituitary, suggesting an involvement in regulation of energy balance. Here we show that peripheral daily administration of ghrelin caused weight gain by reducing fat utilization in mice and rats. Intracerebroventricular administration of ghrelin generated a dose-dependent increase in food intake and body weight. Rat serum ghrelin concentrations were increased by fasting and were reduced by re-feeding or oral glucose administration, but not by water ingestion. We propose that ghrelin, in addition to its role in regulating GH secretion, signals the hypothalamus when an increase in metabolic efficiency is necessary.

Adipose Tissue↗
PubMed1977

Gastroduodenostomy in dogs with and without parietal cell vagotomy. Effect upon gastric emptying and motility, Heidenhain pouch acid secretion and serum gastrin concentration.

Heidenhain pouch (HP) dogs were studied. After gastroduodenostomy (GD) gastric emptying time was unaffected, but cineradiography showed that the strength of the antral contractions diminished considerably, while the number of peristaltic waves increased. "Circus movements" of the barium meal through the GD to the duodenum and back to the stomach through the pylorus occurred. No significant changes in food-stimulated HP acid secretion or serum gastrin response were observed. After parietal cell vagotomy (PCV) gastric emptying and motility was unaffected, but food-stimulated HP acid secretion and serum gastrin response increased significantly. After addition of a GD to PCV gastric emptying time decreased significantly but similar changes in antral motility occurred as after GD alone. The food-stimulated HP acid secretion and serum gastrin response became significantly reduced. Fasting HP acid secretion and serum gastrin concentration were not significantly altered by any of the surgical procedures.

Animals↗
PubMed1991

Serum pattern of thyroxine (T4), 3,3',5-triiodothyronine (T3) and 3,3',5'-triiodothyronine (rT3) in fed and fasted cocks following TRH stimulation.

Food deprivation for 27 and 75h in cocks decreased serum levels of T3 maximally by 61.1% and increased the level of rT3 by 51.4% and that of T4 by 22.4%. Injection of a single dose of TRH (10 micrograms/kg b.w.) increased serum levels of all 3 iodothyronines in both fed and food-deprived animals. In fasted, TRH-treated birds the peak of serum rT3 was 80.5 and 73.3% above control levels in 27- and 75-hr food-deprived cocks, respectively (fed birds: 14.6 and 9.7%); the relevant data for T3 were: 78.3 and 40.4% (fed birds: 95.7 and 127.5%); for T4: 30.0 and 27.0% (fed birds: 9.2 and 6.1%). The greater relative increment of serum rT3 than T3 in food-deprived and TRH-treated cocks was supported by a fall of the serum T3/rT3 ratio to 78.7 and 27.9% in fed cocks and 27- and 75-hr fasted animals, respectively. We conclude, that food deprivation modifies the response of the hypophysis-thyroid axis to exogenous TRH in the sense that during fasting the production of rT3 is enhanced relative to T3.

Animals↗