Appetite In Rats Research Articles

Soybean β-Conglycinin Bromelain Hydrolysate Stimulates Cholecystokinin Secretion by Enteroendocrine STC-1 Cells to Suppress the Appetite of Rats under Meal-Feeding Conditions

A peptic digest of soybean β-conglycinin (BconP) suppresses the appetite in rats through cholecystokinin (CCK) secretion by enteroendocrine cells. We investigate in this study more appetite-suppressing hydrolysates. β-Conglycinin hydrolyzed with food-processing proteases thermolysin (BconT), bromelain (BconB), chymotrypsin, protease S, and protease M was examined for CCK-secreting activity in a CCK-producing cell line for comparison with BconP. The potent CCK-releasing hydrolysates were then tested for their suppression of the food intake by rats. BconB, BconT, and BconP stimulated high CCK secretion, with the highest by BconB. Orogastric preloading by BconB, but not by BconT, suppressed the 60-min food intake. A meal-feeding trial twice a day in the morning (a.m.) and evening (p.m.) for 10 d showed that BconB preloading before every meal attenuated the p.m. meal size, but not that a.m., resulting in an overall reduction of the daily meal size. These results demonstrate that the bromelain hydrolysate of β-conglycinin having potent CCK-releasing activity suppressed the appetite of rats under meal-feeding conditions.

Central mineralocorticoid receptor blockade reduces sodium appetite in rats: new evidence for an old effect

In a previous study we showed that chronic infusion of the mineralocorticoid hormone aldosterone into the fourth ventricle (4V) induces robust dose‐dependent daily sodium intake. In the present study we investigated the effects of the mineralocorticoid receptor (MR) antagonist, RU 28318, injected into the 4V or lateral ventricle (LV) on sodium intake induced by 24 h of sodium depletion (treatment with furosemide, 20 mg/kg b.w., s.c., followed by 24 h of sodium deficient diet), 9 days of sodium deficient diet (0.005% Na+) or chronic treatment with deoxycorticosterone acetate (DOCA, 2 mg/day, s.c. for 7 days). Male Wistar Hannover rats (280–350 g, n=4–7/group) with stainless steel guide cannulas implanted into the 4V or into the LV were used. RU 28318 (100 ng) into the 4V reduced 0.3 M NaCl intake induced by 24 h of sodium depletion (6±1 vs. vehicle: 12±2 mL/2 h) or by sodium deficient diet (1±1 vs. vehicle: 9.5±3 mL/2 h). However, injection of RU 28318 (100 ng) into the LV did not affect sodium intake induced by 24 h of sodium depletion (15±3 vs. vehicle: 15±3 mL/2h). RU 28318 (500 ng) into the 4V also produced no effect on sodium intake induced by DOCA (14±3 vs. vehicle: 11±2 mL/2 h). These data reinforce findings suggesting that hindbrain MRs are involved on aldosterone‐induced sodium appetite. However, it seems they are not involved on DOCA‐induced sodium intake.Supported by: FAPESP, CNPq, CAPES.

A Mechanism of Diminished Appetite in Rats Ingested Cadmium

A Mechanism of Diminished Appetite in Rats Ingested Cadmium

Dietary sodium deprivation evokes activation of brain regional neurons and down-regulation of angiotensin II type 1 receptor and angiotensin-convertion enzyme mRNA expression

Previous studies have indicated that the renin-angiotensin-aldosterone system (RAAS) is implicated in the induction of sodium appetite in rats and that different dietary sodium intakes influence the mRNA expression of central and peripheral RAAS components. To determine whether dietary sodium deprivation activates regional brain neurons related to sodium appetite, and changes their gene expression of RAAS components of rats, the present study examined the c-Fos expression after chronic exposure to low sodium diet, and determined the relationship between plasma and brain angiotensin I (ANG I), angiotensin II (ANG II) and aldosterone (ALD) levels and the sodium ingestive behavior variations, as well as the effects of prolonged dietary sodium deprivation on ANG II type 1 (AT1) and ANG II type 2 (AT2) receptors and angiotensin-convertion enzyme (ACE) mRNA levels in the involved brain regions using the method of real-time polymerase chain reaction (PCR). Results showed that the Fos immunoreactivity (Fos-ir) expression in forebrain areas such as subfornical organ (SFO), paraventricular hypothalamic nuclei (PVN), supraoptic nucleus (SON) and organum vasculosum laminae terminalis (OVLT) all increased significantly and that the levels of ANG I, ANG II and ALD also increased in plasma and forebrain in rats fed with low sodium diet. In contrast, AT1, ACE mRNA in PVN, SON and OVLT decreased significantly in dietary sodium depleted rats, while AT2 mRNA expression did not change in the examined areas. These results suggest that many brain areas are activated by increased levels of plasma and/or brain ANG II and ALD, which underlies the elevated preference for hypertonic salt solution after prolonged exposure to low sodium diet, and that the regional AT1 and ACE mRNA are down-regulated after dietary sodium deprivation, which may be mediated by increased ANG II in plasma and/or brain tissue.

Effects of age on DOCA salt appetite in rats

Effects of age on DOCA salt appetite in rats

ラットを用いたD-Histidineの摂食抑制効果の検討

ラットを用いたD-Histidineの摂食抑制効果の検討

Salt Appetite in Sodium-Depleted or Sodium-Replete Conditions: Possible Role of Opioid Receptors

Background/Aims: Acute sodium depletion by the combination of pharmacological natriuresis via furosemide administration and a sodium-deficient diet results in a strong induction of salt appetite in rats. Recent evidence suggests that acute furosemide decreases both dopamine uptake and striatal dopamine transporter density and increases enkephalin mRNA levels in the nucleus accumbens (Acb). Therefore, it has been hypothesized that the motivational/attentional circuit in the brain is activated in salt-appetitive rats. Methods: To determine which loci along the dopaminergic circuit are responsible for this behavior, 10–15 min before furosemide-treated adult male Sprague-Dawley rats were allowed 2-hour access to 2% salt solution (2-bottle choice), we pharmacologically blocked dopamine receptor subtype 1 (D1r) and subtype 2 (D2r) with SCH23390 or raclopride, respectively, and stimulated D1r with SKF81297 or D2r with quinpirole in the shell of the Acb (AcbSh). Furthermore, delta opioid receptors were blocked with naltrindole in the AcbSh or ventral tegmental area (VTA). Results: We found that microinjections (1 µg) of SCH23390, raclopride, SKF81297, quinpirole, or naltrindole into the AcbSh had no effect. However, infusion of naltrindole into the VTA attenuated salt intake, whereas [D-Ser²,Leu⁵,Thr⁶]-enkephalin had no effect. Additionally, in rats previously primed with furosemide to crave salt in a ‘need-free’ manner, salt intake was augmented in the VTA and reduced in the AcbSh after infusion of [D-Ser²,Leu⁵,Thr⁶]-enkephalin. Conclusion: These data provide evidence that mesolimbic opioid systems are involved in the facilitation of salt-appetitive behavior.

Gastric/Intestinal Electrical Stimulation Modulates Appetite Regulatory Peptide Hormones in the Stomach and Duodenum in Rats

Gastric/intestinal electrical stimulation (GIES) has been used to suppress appetite in the treatment of obesity with promising results. However, the mechanisms by which GIES benefits obese patients are not completely understood. This study investigated the acute effects of GIES on gastric and intestinal tissue levels of peptide hormones related to satiety and appetite in rats. 32 rats were divided into 4 groups: 1) sham stimulation, 2) gastric electrical stimulation (GES) with pulse trains, 3) GES with long pulse, and 4) duodenal electrical stimulation (DES) with pulse trains. After 2 hours of GIES, the rats were sacrificed immediately, and gastric fundus, duodenum and distal colon were harvested and extracted. Hormone levels of ghrelin, obestatin, cholecystokinin-8 (CCK-8) and peptide YY (PYY) were measured by radioimmunoassay (RIA). 1) The mean gastric fundus ghrelin level was 1789.04+/-362.81 pg/mg in the sham stimulation and significantly decreased with GES of pulse trains (597.85+/-195.33 pg/mg, P=0.012), GES of long pulse (754.6+/-282.6 pg/mg, P=0.039) and DES (731.69+/-110.84 pg/mg, P=0.037). 2) The mean duodenal CCK-8 concentration was 413.27+/-42.14 pg/mg in the sham stimulation and significantly increased by DES (762.6+/-98.75 pg/mg, P=0.013) but not in others. 3) Neither gastric obestatin nor distal colonic PYY was altered by any of GES or DES. GIES significantly impacts appetite-related peptide hormones in gastric and duodenal tissues. Acute GIES-induced manipulation of gut peptide hormones related to appetite and satiety is a nonpharmacologic, well-tolerated clinical procedure that could substantially contribute to the successful treatment and long-term management of obesity.

Pork Peptone Stimulates Cholecystokinin Secretion from Enteroendocrine Cells and Suppresses Appetite in Rats

We found that soybean beta-conglycinin peptone (BconP) suppresses food intake through cholecystokinin (CCK) release from enteroendocrine cells in association with binding of the peptone to rat small intestinal brush border membrane (BBM). The aim of the present study was to find new appetite suppressing peptides. Peptones from chicken, pork, beef, beef liver, and egg white were examined for activities to bind with rat BBM, CCK-release from enteroendocrine cell line STC-1, and induce satiety in rats. Chicken and pork peptone (ChickP and PorkP) bound to BBM with highest ability as evaluated with a surface plasmon biosensor. PorkP and ChickP released CCK in higher amounts than BconP from STC-1 cells dose-dependently, with highest stimulation by PorkP. An orogastric preload of PorkP, but not ChickP, suppressed food intake similarly to BconP, dose-dependently. These results suggest that PorkP interacts directly with the small intestinal CCK cells to release CCK, and that it suppresses appetite in rats.

WITHDRAWN: Control of thirst and salt appetite in rats by pre-systemic stimuli

The publisher regrets that this article is an accidental duplication of an article that has already been published, doi:10.1016/j.appet.2006.03.001. The duplicate article has therefore been withdrawn.

Control of thirst and salt appetite in rats: Early inhibition of water and NaCl ingestion

Most previous studies on the controls of thirst and salt appetite in rats have focused on systemic factors. Our recent experiments suggest that presystemic factors also are likely to play an important role. For example, dehydrated rats were found to consume similar volumes in an initial drinking bout when given access either to water or 0.05, 0.10, 0.15, or 0.20 M NaCl solution. Thus, cessation of the bouts evidently was not related to the concentration of fluid consumed but to its volume. It occurred despite the continued presence of known systemic stimuli for thirst (i.e. either increased plasma osmolality or decreased plasma volume), and therefore it resulted from inhibition rather than satiation. This inhibition appeared to derive from signals related to the cumulative volume of ingested fluid in the stomach and small intestine. Similar findings were obtained in studies of NaCl solution intake by NaCl-deprived adrenalectomized rats. These and other observations suggest that gastrointestinal fill generates stimuli that inhibit drinking in rats regardless of whether thirst or salt appetite motivates fluid consumption and regardless of whether rats consume water or NaCl solution.

Olfactory stimulation with scent of lavender oil affects autonomic neurotransmission and blood pressure in rats

Previously, we observed that olfactory stimulation with scent of lavender oil (SLVO) suppressed sympathetic nerve activities and elevated gastric vagal (parasympathetic) nerve activity (GVNA), decreased plasma glycerol concentration and body temperature, and enhanced appetite in rats. Here, we further showed that olfactory stimulation with SLVO lowered renal sympathetic nerve activity (RSNA) and blood pressure (BP) and elevated GVNA in urethane-anesthetized rats. Olfactory stimulation with linalool, a component of lavender oil, also elicited decreases in RSNA and BP and an increase in GVNA in urethane-anesthetized rats. Anosmia induced by pretreatment of the nasal cavity by application of ZnSO 4 eliminated the effects of both SLVO and scent of linalool on RSNA, GVNA and BP. Furthermore, intracerebroventricular administration of thioperamide, a histaminergic H3-antagonist, abolished the suppression of RSNA and BP as well as the elevation of GVNA mediated by both SLVO and scent of linalool. Finally, bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) eliminated RSNA and BP suppression and the elevation of GVNA due to SLVO or linalool. Thus, it was concluded that scent of lavender oil and its active component, linalool, affects autonomic neurotransmission and reduces blood pressure through the central histaminergic nervous system and the SCN.

Corticotropin-releasing hormone in the lateral parabrachial nucleus inhibits sodium appetite in rats

The present study investigated the role of corticotropin-releasing hormone (CRH) in the lateral parabrachial nucleus (LPBN) in the behavioral control of body fluid homeostasis by determining the effect of bilateral injections of the CRH receptor antagonist, alpha-helical corticotropin-releasing factor (CRF)(9-41), and the CRH receptor agonist, CRH, on sodium chloride (salt appetite) and water (thirst) intake. Groups of adult, male Sprague-Dawley rats had stainless-steel cannulas implanted bilaterally into the LPBN and were sodium depleted or water deprived. Bilateral injections of alpha-helical CRF(9-41) into the LPBN significantly potentiated water and salt intake in the sodium-depleted rats when access to fluids was restored. Bilateral injections of alpha-helical CRF(9-41) into the LPBN (1.0 microg) also increased sodium appetite in water-deprived rats. Conversely, in sodium-depleted animals, bilateral injections of CRH inhibited sodium chloride intake. These results suggest that there is an endogenous CRH inhibitory mechanism operating in the LPBN to modulate the intake of sodium (salt appetite). This mechanism may contribute to the behavioral control of restoration of body fluid homeostasis in sodium-deficient states.

Olfactory stimulation with scent of essential oil of grapefruit affects autonomic neurotransmission and blood pressure

Previously, we observed that olfactory stimulation with scent of grapefruit oil (SGFO) enhances sympathetic nerve activities and suppresses gastric vagal (parasympathetic) nerve activity (GVNA), increases plasma glycerol concentration and body temperature, and decreases appetite in rats. Here, we show that olfactory stimulation with SGFO for 10 min elevates renal sympathetic nerve activity (RSNA) and blood pressure (BP) and lowers GVNA in urethane-anesthetized rats. Olfactory stimulation with limonene, a major component of grapefruit oil, also elicited increases in RSNA and BP in urethane-anesthetized rats. Anosmic treatment with ZnSO 4 eliminated both the effects of SGFO and scent of limonene on RSNA and BP. Intracerebral administration of diphenhydramine, a histaminergic H1-antagonist, abolished SGFO- or scent of limonene-mediated increases in RSNA and BP as well as the decrease in GVNA. Moreover, bilateral lesions of the hypothalamic suprachiasmatic nucleus (SCN) eliminated the SGFO- and limonene-mediated increases in RSNA and BP and decrease in GVNA, but bilateral lesions of the cerebral cortex did not have any affect on these parameters. These findings suggest that scent of grapefruit oil and its active component, limonene, affect autonomic neurotransmission and blood pressure through central histaminergic nerves and the suprachiasmatic nucleus.

Olfactory stimulation with scent of lavender oil affects autonomic nerves, lipolysis and appetite in rats

In a previous study, we presented evidence that scent of grapefruit oil excites sympathetic nerves innervating white and brown adipose tissues and the adrenal gland, inhibits the vagal nerve innervating the stomach, increases lipolysis and heat production (energy consumption), and reduces appetite and body weight. Here, we examined the effects of olfactory stimulation with scent of lavender oil (SLVO) in rats and observed that in contrast to grapefruit oil, it inhibits the sympathetic nerves innervating the white and brown adipose tissues and adrenal gland and excites the parasympathetic gastric nerve. Local anesthesia of the nasal mucosa with xylocaine or anosmic treatment using ZnSO 4 eliminated the autonomic changes caused by SLVO. Moreover, stimulation with SLVO lowered the plasma glycerol level, and treatment with either ZnSO 4 or an intracranial injection of thioperamide, a histamine H3 receptor-antagonist, abolished SLVO-mediated glycerol decline. Furthermore, a 15-min daily exposure to SLVO increased food intake and body weight. Finally, linalool, a component of lavender oil, induced responses similar to those caused by SLVO, and the glycerol response to linalool was eliminated by thioperamide. Thus, scent of lavender oil and its active component, linalool, affect autonomic nerves, suppress lipolysis through a histaminergic response, and enhance appetite and body weight.

Olfactory stimulation with scent of grapefruit oil affects autonomic nerves, lipolysis and appetite in rats

In a previous study, we found that olfactory stimulation with scent of grapefruit oil (SGFO) excites the sympathetic nerve innervating the white adipose tissue in rats. Here we further examined the effects of SGFO in rats and observed that olfactory stimulation with SGFO excited the sympathetic nerves innervating the brown adipose tissue and adrenal gland and inhibited the parasympathetic gastric nerve. Local anesthesia of the nasal mucosa with xylocaine or anosmic treatment using ZnSO 4 eliminated the autonomic changes caused by SGFO. Moreover, stimulation with SGFO elevated the plasma glycerol level, and treatment with either ZnSO 4 or an intraperitoneal injection of diphenhydramine, a histamine H1 receptor-antagonist, abolished the glycerol elevation by SGFO. Furthermore, a 15-min exposure to SGFO three times a week reduced food intake and body weight. Finally, limonene, a component of grapefruit oil, induced reponses similar to those caused by SGFO, and diphenhydramine eliminated the glycerol response to limonene. Thus, the scent of grapefruit oil, and particularly its primary component limonene, affects autonomic nerves, enhances lipolysis through a histaminergic response, and reduces appetite and body weight.

Sodium preference and appetite in rats in an operant protocol

An operant task that may simulate natural foraging was used to study in Sprague–Dawley rats the need-free choice between water and various concentrations of NaCl solution, and the induction of sodium appetite during chronic deoxycorticosterone acetate (DOCA) treatment. The task imposed a fixed ratio foraging or procurement cost for access to each fluid. The relative preference for NaCl over water when both had the same procurement cost was similar to the preference/aversion function that has been reported for this strain of rat under free drinking conditions. As the procurement cost increased, the number of bouts taken per day of both water and NaCl decreased and the mean bout size increased. Administration of DOCA produced an increase in NaCl intake under all conditions, and this appetite was manifest as discrete episodes whose frequency and size were inversely related. Natural observations of sodium appetite in mammals, such as excursions to, often remote, mineral deposits, imply an episodic organization of this behavior. This report is the first laboratory simulation of environmental factors that affect the episodic or temporal organization of sodium appetite.

A novel method for induction of salt appetite in rats

A number of procedures exist for the experimental induction of sodium appetite. With the exception of a low sodium diet, nearly all of these methods are invasive, requiring injections, surgery, or both. In addition to stimulating intake of concentrated salt, some of them produce substantial side-effects like reduced food intake and weight gain. The present experiment was designed to evaluate the efficacy of a novel non-invasive method to induce a salt appetite. We investigated the effects of ingesting 100 μM amiloride, a diuretic and natriuretic compound, on urine quantity, electrolyte balance, 0.51 M sodium chloride (NaCl) intake, water intake, and Na +-free chow intake, and weight gain in rats. A water ingestion only group served as control. Consumption of amiloride in mixture with water produced greater loss of urinary Na + and intake of 0.51 M NaCl compared with controls. This treatment was without effect on food intake and only modestly influenced weight gain. These results demonstrate a rapid and non-invasive method for the induction of salt appetite free of unwanted side-effects.

P0026 PP EFFECT OF GHRELIN ON THE GASTROINTESTINAL MOTILITY IN CONSCIOUS RATS

Introduction: Ghrelin, a novel growth-hormone-releasing peptide isolated from rat and human stomachs, has been reported to increase appetite in rats and humans. The clinical usefulness of this novel substance is currently under investigation. However, little is known about its direct effects on the alimentary. In the present study, we examined its effects on intestinal motility in conscious rats. Methods: Male Wistar rats weighing 300–400 g were fasted for more than 24 hours before experiments. After being anesthetized with pentobarbital, the abdominal wall was opened by mid-line laparotomy, and a miniature strain-gauge force transducer was sutured on the serosal site of intestinal wall 5 cm from the anal side of Treizüfs ligament. Five to 10 days after operation, and confirming the stability of the basal intestinal motility, various concentrations (1, 5, 10, 25, 50, and 100 ƒÊ g/kg, intravenous (IV) injection) of rat ghrelin or saline were given through the caudal vein after 4 minutes of phase 3 contractions. Intestinal motility was quantified by frequency and the mean amplitude of clusters, drug-cluster intervals, duration of clusters, and counting the number of phase 3 contractions. Results: When IV injections of ghrelin (over than 5ƒÊ g/kg) were given to animals, clusters appeared immediately and these patterns consisted of phase 3-like contractions. IV administration of ghrelin increased the frequency of clusters in a dose-dependent manner (Table 1). The mean amplitude of clusters was approximately 50% compared with that of previous natural phase 3 contractions. Drug-cluster intervals were shortened in a dose-dependent manner (Regression analysis: p=0.045). Each duration of clusters was about 2 min, and was shorter than that of natural phase 3 contractions 291 plus-minus 34 min. The number of phase 3contractions for one hour did not change before or after IV injections of ghrelin.Table 1: Induction of intestinal clusters by ghrelinConclusion: Exogenous ghrelin modulated small intestinal motility in conscious rats.

Leptin gene expression and serum leptin levels in zinc deficiency: implications for appetite regulation in rats.

Zinc deficiency in animals causes impaired growth and anorexia, and the mechanisms for these symptoms of zinc deficiency are not yet clear. We investigated whether circulating leptin levels and gene expression would be dysregulated under zinc deficiency and what would be the implications for appetite in rats. In study 1, 24 Sprague-Dawley rats were provided consecutively with three different dietary zinc intake levels: Zn-adequate (30 mg/kg of diet), Zn-depleted (1 mg/kg of diet), and Zn-replete (50 mg/kg of diet), for 1, 2, and 2 weeks, respectively. At the end of each dietary period, one-third of the rats were killed. In study 2, rats were assigned to one of the four Zn diet groups: Zn-adequate (30 mg/kg of diet), pair-fed (30 mg/kg of diet), Zn-deficient (1 mg/kg of diet), or Zn-sufficient (50 mg/kg of diet), and were fed for 4 weeks. Tissue Zn and serum leptin were measured, and leptin gene expression in adipose tissues (inguinal and abdominal) was determined by reverse transcription-polymerase chain reaction and northern blotting. Blood subfractions as plasma, red blood cells, and mononuclear cells and liver Zn level were decreased during the Zn-depletion period (P <.05). Serum leptin showed a tendency to increase during the Zn-depletion period and decreased back to the level of the Zn-repletion period. Leptin mRNA levels in inguinal adipocytes also increased during the Zn-depletion (P <.05) and Zn-deficient periods, which is consistent with the change in serum leptin. However, the decrease in leptin mRNA in abdominal adipocytes was not consistent with the increase in inguinal leptin levels and the change in serum leptin. Increased leptin levels in linguinal adipocytes is consistent with the expected physiological change of a decrease in appetite under Zn deficiency. However, before coming to any firm conclusion, further studies on adipose tissue-specific leptin expression, including the appetite-related neuropeptides, are necessary for clarifying the cause of lower appetite in zinc deficiency.