Appetite In Rats Research Articles

Brain Perception of Different Oils on Appetite Regulation: An Anorectic Gene Expression Pattern in the Hypothalamus Dependent on the Vagus Nerve.

(1) Background: We examined the effect of the acute administration of olive oil (EVOO), linseed oil (GLO), soybean oil (SO), and palm oil (PO) on gastric motility and appetite in rats. (2) Methods: We assessed food intake, gastric retention (GR), and gene expression in all groups. (3) Results: Both EVOO and GLO were found to enhance the rate of stomach retention, leading to a decrease in hunger. On the other hand, the reduction in food intake caused by SO was accompanied by delayed effects on stomach retention. PO caused an alteration in the mRNA expression of NPY, POMC, and CART. Although PO increased stomach retention after 180 min, it did not affect food intake. It was subsequently verified that the absence of an autonomic reaction did not nullify the influence of EVOO in reducing food consumption. Moreover, in the absence of parasympathetic responses, animals that received PO exhibited a significant decrease in food consumption, probably mediated by lower NPY expression. (4) Conclusions: This study discovered that different oils induce various effects on parameters related to food consumption. Specifically, EVOO reduces food consumption primarily through its impact on the gastrointestinal tract, making it a recommended adjunct for weight loss. Conversely, the intake of PO limits food consumption in the absence of an autonomic reaction, but it is not advised due to its contribution to the development of cardiometabolic disorders.

Diet Protein Content and Individual Phenotype Affect Food Intake and Protein Appetence in Rats

BackgroundA low-protein diet can induce compensatory intake of excess energy. This must be better evaluated to anticipate the obesogenic risk that may result from the dietary recommendations for reducing animal protein consumption. ObjectivesWe aimed to further characterize the behavioral and physiological responses to a reduction in dietary protein and to identify the determinants of protein appetite. MethodsThirty-two male Wistar rats [4 wk old, (mean ± SEM) 135 ± 32 g body weight] were fed a low-protein (LP; 6% energy value) or normal-protein (NP; 20%) diet for 8 wk. Food intake and body mass were measured during the entire intervention. During self-selection sessions after 4 wk of experimental diets, we evaluated rat food preference between LP, NP, or high-protein (HP; 55%) pellets. At the end of the experiment, we assessed their hedonic response [ultrasonic vocalizations (USVs)] and c-Fos neuronal activation in the olfactory tubercle and nucleus accumbens (NAcc) associated with an LP or HP meal. ResultsRats fed an LP diet had greater food intake (24%), body weight (5%), and visceral adiposity (30%) than NP rats. All LP rats and half of the NP rats showed a nearly exclusive preference for HP pellets during self-selection sessions, whereas the other half of the NP rats showed no preference. This suggests that the appetite for proteins is driven not only by a low protein status but also by individual traits in NP rats. LP or HP meal induced similar USV emission and similar neuronal activation in the NAcc in feed-deprived LP and NP rats, showing no specific response linked to protein appetite. ConclusionsProtein appetite in rats is driven by low protein status or individual preferences in rats receiving adequate protein amounts. This must be considered and further analyzed, in the context of current recommendations for protein intake reduction.

Despite increasing aldosterone, elevated potassium is not necessary for activating aldosterone-sensitive HSD2 neurons or sodium appetite.

Restricting dietary sodium promotes sodium appetite in rats. Prolonged sodium restriction increases plasma potassium (pK), and elevated pK is largely responsible for a concurrent increase in aldosterone, which helps promote sodium appetite. In addition to increasing aldosterone, we hypothesized that elevated potassium directly influences the brain to promote sodium appetite. To test this, we restricted dietary potassium in sodium‐deprived rats. Potassium restriction reduced pK and blunted the increase in aldosterone caused by sodium deprivation, but did not prevent sodium appetite or the activation of aldosterone‐sensitive HSD2 neurons. Conversely, supplementing potassium in sodium‐deprived rats increased pK and aldosterone, but did not increase sodium appetite or the activation of HSD2 neurons relative to potassium restriction. Supplementing potassium without sodium deprivation did not significantly increase aldosterone and HSD2 neuronal activation and only modestly increased saline intake. Overall, restricting dietary sodium activated the HSD2 neurons and promoted sodium appetite across a wide range of pK and aldosterone, and saline consumption inactivated the HSD2 neurons despite persistent hyperaldosteronism. In conclusion, elevated potassium is important for increasing aldosterone, but it is neither necessary nor sufficient for activating HSD2 neurons and increasing sodium appetite.

Limbic control over the homeostatic need for sodium

The homeostatic need for sodium is one of the strongest motivational drives known in animals. Although the brain regions involved in the sensory detection of sodium levels have been mapped relatively well, data about the neural basis of the motivational properties of salt appetite, including a role for midbrain dopamine cells, have been inconclusive. Here, we employed a combination of fiber photometry, behavioral pharmacology and c-Fos immunohistochemistry to study the involvement of the mesocorticolimbic dopamine system in salt appetite in rats. We observed that sodium deficiency affected the responses of dopaminergic midbrain neurons to salt tasting, suggesting that these neurons encode appetitive properties of sodium. We further observed a significant reduction in the consumption of salt after pharmacological inactivation of the nucleus accumbens (but not the medial prefrontal cortex), and microstructure analysis of licking behavior suggested that this was due to decreased motivation for, but not appreciation of salt. However, this was not dependent on dopaminergic neurotransmission in that area, as infusion of a dopamine receptor antagonist into the nucleus accumbens did not alter salt appetite. We conclude that the nucleus accumbens, but not medial prefrontal cortex, is important for the behavioral expression of salt appetite by mediating its motivational component, but that the switch in salt appreciation after sodium depletion, although detected by midbrain dopamine neurons, must arise from other areas.

Effects of CeA lesions on the initiation and expression of sodium appetite in sodium-deficient rats

To investigate the effects of central nucleus of amygdala (CeA) lesion on the initiation and expression of sodium appetite in sodium-deficient rats. Three groups of SD rats (n=6 in each group) were treated with bilateral CeA lesion, sham lesion or no lesion. After the recovery, the rats were fed with low-sodium diets for 14 days to establish a sodium-deficient rat model. The double-bottle selection in single cage test was used to observe the intake of 0.3 mol/L NaCl and DW in 5 timepoint with 24 hours in sodium-deficient rats. Immunofluorescence staining of aldosterone-sensitive neurons in the nucleus tractus solitarii (NTS)was used to investigate the effect of CeA lesion or not on the activity of aldosterone-sensitive neurons in rats with or without sodium deficiency. After fed with low-sodium diet for14 days, the volume and preference rate of 0.3 mol/L NaCl intake of the rats within 24 h were significantly increased compared with those before low-sodium diet (P＜0.01). The intake volume and the preference rate of 0.3 mol/L NaCl in CeA lesion rats were significantly decreased than those in CeA sham lesion rats and normal rats in the sodium-deficient condition (P＜0.01). The CeA lesion had no effects on the activity of aldosterone-sensitive neurons in NTS in rats with low-sodium diet. Low-sodium diet induces an increase in the expression of sodium appetite in rats. CeA lesions inhibit the behavioral expression of sodium appetite in sodium-deficient rats but have no effects on the initiation of sodium appetite in rats with sodium-deficient rats.

Synthesis of New 7-bromo-5-(2’-chlorophenyl)-3-arylamino-1,2-dihydro-3H-1,4-benzodiazepine Derivatives and Their Influence on Appetite in Rats

A series of new 7-bromo-5-(2′-chlorophenyl)-3-arylamino-1,2-dihydro-3H-1,4-benzodiazepine derivatives (II-VIII) were synthesized. The series of synthesized compounds included those that had a substantial effect on appetite in rats, exhibiting both orexigenic and anorexigenic effects at low doses (2.07 – 2.21 μM). Compound VI had anorexigenic activity comparable with that of the hormone leptin, which reduces the appetite and food intake. Co-administration of leptin and III, which exhibited a pronounced orexigenic effect, reduced appetite by 73%.

Синтез новых производных 7-бром-5-(2’-хлор)фенил-3-ариламино-1,2-дигидро-3<i>H</i>-1,4-бенздиазепин-2-онов и их влияние на аппетит крыс

Синтезированы новые производные 7-бром-5-(2’-хлор)фенил-3-ариламино-1,2-дигидро-3H-1,4-бенздиазепина (II – VIII). В ряду синтезированных соединений обнаружены вещества, которые в низких дозах (2,07 – 2,21 мкМ) оказывали существенное влияние на аппетит крыс, проявляя как орексигенное, так и анорексигенное действие. Обнаружено соединение VI, которое по анорексигенному действию не уступает гормону лептину, снижающему аппетит и потребление пищи. При сочетанном введении лептина с соединением III, проявляющим выраженный орексигенный эффект, отмечается снижение аппетита на 73 %.

The effect of hydro-alcoholic extract of Achillea millefolium on appetite hormone in rats.

Achillea millefolium (A. millefolium) is known as an orexigenic herb in Iranian traditional medicine. In this study, the possible orexigenic effect of hydro-alcoholic extract of A. millefolium was investigated by measuring plasmaghrelin level. Thirty male Wistar rats were divided into five groups. Control group received water. Treatment groups received 50, 100 or 150 mg/kg of A. millefolium extract for 7 days via gavage. Before the intervention, daily amount of the food eaten by each rat was measured for 10 days. During the investigation, the amount of energy intake of each rat was also estimated 1, 2, 4, 6 and 24 hr after each intake, for 7 days. Later, the orexigenic dose of extract and distilled water was fed to two separate groups of 6 male Wistar rats. Plasma ghrelin level was measured 0.5, 1, 2 and 4 hrafter extract intake. The change in energy intake after treatment by 50and 100mg/kg of the extract was significantly higher than other groups (p<0.001).Administration of Achillea 100mg/kg significantly (p<0.05) decreased ghrelin level one hrafter intervention but there was no significant (p>0.05) difference among control and treated group. This study indicated that A. millefolium had positive dose-related effects on appetite in rats. It seems that the orexigenicactivity of extract was not related to changes in plasma ghrelin levels.

Oxytocin Acting in the Nucleus Accumbens Core Decreases Food Intake.

Central oxytocin (OT) promotes feeding termination in response to homeostatic challenges, such as excessive stomach distension, salt loading and toxicity. OT has also been proposed to affect feeding reward by decreasing the consumption of palatable carbohydrates and sweet tastants. Because the OT receptor (OTR) is expressed in the nucleus accumbens core (AcbC) and shell (AcbSh), a site regulating diverse aspects of eating behaviour, we investigated whether OT acts there to affect appetite in rats. First, we examined whether direct AcbC and AcbSh OT injections affect hunger- and palatability-driven consumption. We found that only AcbC OT infusions decrease deprivation-induced chow intake and reduce the consumption of palatable sucrose and saccharin solutions in nondeprived animals. These effects were abolished by pretreatment with an OTR antagonist, L-368,899, injected in the same site. AcbC OT at an anorexigenic dose did not induce a conditioned taste aversion, which indicates that AcbC OT-driven anorexia is not caused by sickness/malaise. The appetite-specific effect of AcbC OT is supported by the real-time polymerase chain reaction analysis of OTR mRNA in the AcbC, which revealed that food deprivation elevates OTR mRNA expression, whereas saccharin solution intake decreases OTR transcript levels. We also used c-Fos immunohistochemistry as a marker of neuronal activation and found that AcbC OT injection increases activation of the AcbC itself, as well as of two feeding-related sites: the hypothalamic paraventricular and supraoptic nuclei. Finally, considering the fact that OT plays a significant role in social behaviour, we examined whether offering animals a meal in a social setting would modify their hypophagic response to AcbC OT injections. We found that a social context abolishes the anorexigenic effects of AcbC OT. We conclude that OT acting via the AcbC decreases food intake driven by hunger and reward in rats offered a meal in a nonsocial setting.

Abstract 4514: PQR309: A potent, brain-penetrant, dual pan-PI3K/mTOR inhibitor with excellent oral bioavailability and tolerability

Abstract The phosphatidylinositol 3-kinase (PI3K) signaling pathway is frequently activated in tumors and promotes oncogenic cell transformation, proliferation and tumor growth. PQR309, a novel dual inhibitor of PI3K and mTOR, is currently in Phase I clinical development in cancer patients. PQR309 binds potently and specifically to the ATP binding pocket of all PI3K class I isoforms and mTORC1/2, attenuates PI3K signaling and inhibits tumor cell growth. The preclinical pharmacological and toxicological characterization of PQR309 is presented here. Methods: PQR309 pharmacokinetics/-dynamics (PK/PD) were investigated in rats and mice. Tissue samples from plasma, brain and liver were analyzed by LC/MS detecting PQR309 distribution as well as blood insulin and glucose. Toxicological studies were performed in rats and dogs. Effects on neurological, hematopoietic, respiratory, lymphoid, reproductive and cardiovascular system as well as general health were monitored. The metabolic fate of PQR309 was analyzed in rat, dog and human hepatocytes. Results: PQR309 PK studies in rats, mice and dogs revealed dose-proportional PK, both PO and IV, with a half-life of 5-8 hours in plasma, brain and liver, allowing for once a day oral application. As on-target effect, increase of blood insulin and glucose could be observed within hours after oral dosage in rats, which makes both molecules suitable as PD markers. In in vivo PC-3 rat tumor xenograft models, PQR309 effectively inhibited PI3K signaling in tumors and reduced tumor growth at 10 mg/kg oral dosing. Preclinical toxicity testing showed no signs of cardiotoxicity (including lack of hERG binding), phototoxicity (3T3 NRU test) or mutagenicity (AMES test) for PQR309. No marked effect on CYP450 activity was observed making PQR309 a good combination partner in cancer therapy. As for other PI3K inhibitors, PQR309 leads at elevated doses to a fully reversible loss of body weight and appetite in rats and dogs. No further significant adverse events were observed when testing PQR309 for 28 days in these species. Conclusions: PQR309 potently inhibits class I PI3K isoforms and mTORC1/2 and shows anti-tumor effects in vitro and in vivo. The physico-chemical properties of PQR309 result in good oral bioavailability and equal distribution between plasma and brain. Pre-clinical data led to initiation of a Phase I clinical study of PQR309 in solid tumors. Citation Format: Vladimir Cmiljanovic, Robert A. Ettlin, Florent Beaufils, Walter Dieterle, Petra Hillmann, Juergen Mestan, Anna Melone, Thomas Bohnacker, Marc Lang, Natasa Cmiljanovic, Bernd Giese, Paul Hebeisen, Matthias P. Wymann, Doriano Fabbro. PQR309: A potent, brain-penetrant, dual pan-PI3K/mTOR inhibitor with excellent oral bioavailability and tolerability. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4514. doi:10.1158/1538-7445.AM2015-4514

Thirst and sodium appetite in rats with experimental nephrotic syndrome

Nephrotic syndrome is a renal disease accompanied by abnormal body fluid balance. The present experiments investigated the role of behavioral mechanisms in contributing to disordered fluid homeostasis in rats with experimentally-induced nephrotic syndrome. The studies examined water and sodium ingestion under ad libitum conditions and in response to dehydration-related challenges in rats made nephrotic by treatment with the antibiotic, adriamycin. Rats with nephrotic syndrome had greater ad libitum water intakes beginning 3weeks after treatment, but daily sodium (0.3M NaCl) intakes were not affected. Nephrotic rats showed attenuated water and sodium intakes after combined treatment with furosemide (10mg/kg) and captopril (2mg/kg), reduced water intakes after 20h of water deprivation, and diminished water intakes, plasma renin activity and aldosterone secretion after subcutaneous isoproterenol (30μg/kg). However, the adriamycin-treated animals had normal water intakes in response to subcutaneous hypertonic saline (4% at 0.75ml/100g) and central injections of angiotensin II (10, 20, and 50ng). The results suggest that water and sodium ingestion in response to hypovolemic/hypotensive stimuli are disturbed in nephrotic rats, and provide evidence that the disordered behaviors reflect disturbances of the peripheral renin–angiotensin–aldosterone system.

The effect of hydro-alcoholic extract of Artemisia absinthium on appetite in male rats.

weight loss as a consecution of losing appetite in post-operative patients and those suffering from HIV, cancer, cachexia and inflammatory diseases are the main inducements of morbidity and mortality. There is an increasing demand for more efficacious and endurable appetite stimulating treatment for patients with cachexia. Health economics is influenced by the malnutrition which was accounted for 5% of Iranian populations in 2011. Artemisia absinthium is known as an orexigenic herb in Iranian traditional medicine. Little evidence is available about its orexigenic effect and mechanism. So, the present study evaluated the possible effect on appetite of hydroalcoholic extract of Artemisia absinthium . Thirty male Wistar rats were randomly divided into five groups. Vehicle group received 0.5 ml water per day, control group did not receive anything and other 3 groups received 50, 100 and 150 mg/kg of Artemisia absinthium for 7 days respectively. The daily amount of the food eaten by each rat was measured for 10 consecutive days. The amount of energy intake for each rat was also calculated for 7 days during the intervention. The difference in energy intake was calculated and compared between groups. The results suggest that there was no significant (p>0.05) differences in energy received before and during intervention between three case groups compared with the control group. The energy intake in 1-2 hours after extract injection in all groups, and energy intake after 24 hours interval in third case group (receiving 150 mg/kg extract) is higher compared to other intervals, but it is not significant (p>0.05). So, it can be stated that there was no significant differences between energy intake of 3 case groups and control group. Artemisia absinthium had no positive and dose-related effects on appetite of rats. Future studies are needed to evaluate the orexigenic effect of this plant.

The effect of hydroalcoholic extract of Cannabis Sativa on appetite hormone in rat.

Ghrelin is an orexigenic peptide which is secreted from stomach. Cannabis sativa is known as an orexigenic herb in Iranian traditional medicine. Little evidence is published about its effect on energy intake and its mechanism. In the current study, the possible effect of hydroalcoholic extract of C. sativa on appetite and ghrelin is evaluated. Thirty male Wistar rats were randomly divided into five groups. Two control groups were selected, the first group received 0.5 mL water per day (vehicle group) and another group did not receive anything (control group). The other three groups were treated daily with 50, 100 or 150 mg/kg of C. sativa for 7 days, respectively. Daily energy intake of the rats was calculated for 10 days prior to the> intervention and for the 7 day intervention. To investigate changes in plasma ghrelin as a potential mechanism, an orexigenic dose (150 mg/kg) of C. sativa or distilled water (vehicle) was fed to two separate groups of six rats by gavage. Total ghrelin levels in plasma were measured for 3 h post-gavage. There was no significant difference in energy intake between control and vehicle groups. Treatment with 100 and 150 mg/kg of the extract significantly increased energy intake vs the other groups (p<0.05). Total ghrelin levels were significantly elevated in the C. sativa group vs vehicle 30 and 60 min post-gavage. This study showed that C. sativa had both positive and dose-related effects on appetite of rats. Future studies are warranted to evaluate the orexigenic effect of this plant in human.

Salt appetite is reduced by a single experience of drinking hypertonic saline in the adult rat.

Salt appetite, the primordial instinct to favorably ingest salty substances, represents a vital evolutionary important drive to successfully maintain body fluid and electrolyte homeostasis. This innate instinct was shown here in Sprague-Dawley rats by increased ingestion of isotonic saline (IS) over water in fluid intake tests. However, this appetitive stimulus was fundamentally transformed into a powerfully aversive one by increasing the salt content of drinking fluid from IS to hypertonic saline (2% w/v NaCl, HS) in intake tests. Rats ingested HS similar to IS when given no choice in one-bottle tests and previous studies have indicated that this may modify salt appetite. We thus investigated if a single 24 h experience of ingesting IS or HS, dehydration (DH) or 4% high salt food (HSD) altered salt preference. Here we show that 24 h of ingesting IS and HS solutions, but not DH or HSD, robustly transformed salt appetite in rats when tested 7 days and 35 days later. Using two-bottle tests rats previously exposed to IS preferred neither IS or water, whereas rats exposed to HS showed aversion to IS. Responses to sweet solutions (1% sucrose) were not different in two-bottle tests with water, suggesting that salt was the primary aversive taste pathway recruited in this model. Inducing thirst by subcutaneous administration of angiotensin II did not overcome this salt aversion. We hypothesised that this behavior results from altered gene expression in brain structures important in thirst and salt appetite. Thus we also report here lasting changes in mRNAs for markers of neuronal activity, peptide hormones and neuronal plasticity in supraoptic and paraventricular nuclei of the hypothalamus following rehydration after both DH and HS. These results indicate that a single experience of drinking HS is a memorable one, with long-term changes in gene expression accompanying this aversion to salty solutions.

Effects of aging on mineralocorticoid-induced salt appetite in rats

This work examined the effects of age on salt appetite measured in the form of daily saline (i.e., 0.3 M NaCl) drinking in response to administration of deoxycorticosterone acetate (DOCA; 5 mg/kg body wt) using young (4 mo), "middle-aged" adult (12 mo), and old (30 mo) male Brown Norway rats. Water and sodium intakes, excretions, and balances were determined daily. The salt appetite response was age dependent with "middle-aged" rats ingesting the most saline solution followed in order by young and then old rats. While old rats drank the least saline solution, the amounts of saline ingested still were copious and comprise an unambiguous demonstration of salt appetite in old rats. Middle-aged rats had the highest saline preference ratios of the groups under baseline conditions and throughout testing consistent with an increased avidity for sodium taste. There were age differences in renal handling of water and sodium that were consistent with a renal contribution to the greater saline intakes by middle-aged rats. There was evidence of impaired renal function in old rats, but this did not account for the reduced saline intakes of the oldest rats.

The Role of Angiotensin II on Sodium Appetite After a Low‐Sodium Diet

The present study aimed to investigate the role of angiotensin II (AngII) on sodium appetite in rats subjected to a normal or a low-sodium diet (1% or >0.1% NaCl) for 4days. During sodium restriction, a reduction in water intake, urinary volume and sodium excretion was observed. After a low-sodium diet, we observed decreased plasma protein concentrations and haematocrit associated with a slight reduction in arterial pressure, without any significant changes in heart rate, natraemia, corticotrophin-releasing hormone mRNA expression in the paraventricular nucleus and corticosterone levels. After providing hypertonic saline, there was an increase in saline intake followed by a small increase in water intake, resulting in an enhanced saline intake ratio and the recovery of arterial pressure. Sodium deprivation increased plasma but not brain Ang I and II concentrations. A low-sodium diet increased kidney renin and liver angiotensinogen mRNA levels but not lung angiotensin-converting enzyme mRNA expression. Moreover, Ang II type 1a receptor mRNA expression was increased in the subfornical organ and the dorsal raphe nucleus and decreased in the medial preoptic nuclei, without changes in the paraventricular nucleus and the nucleus of solitary tract after a low-sodium diet. Blockade of AT(1) receptors or brain Ang II synthesis led to a reduction in sodium intake after a low-sodium diet. Intracerebroventricular injection of Ang II led to a similar increase in sodium and water intake in the control and low-sodium diet groups. In conclusion, the results of the present study suggest that Ang II is involved in the increased sodium appetite after a low-sodium diet.

The effect of hydroalcoholic extract of Coriandrum sativum on rat appetite.

Losing weight in consequence of appetite loss can be a sign of a serious underlying condition. Currently, the most widely prescribed medication for anorexia is cyproheptadine hydrochloride. However, the clinical use of cyproheptadine hydrochloride is limited by its side effects. In Iranian traditional medicine, Coriandrum sativum stimulates the appetite. Therefore, the effect of Coriandrum sativum (coriander) hydroalcoholic extract was investigated on food intake in rats. Thirty male Wistar rats were randomly divided into five groups. Two control groups were used, one group received 0.5 ml water per day (vehicle group), and another group did not receive anything (control group). The other 3 groups were daily treated by 50, 100 or 150 mg/kg of coriander for 7 days, respectively. The daily amount of the food eaten by each rat was measured for 10 days. The amount of energy intake of each rat was also calculated for 7 days during the intervention. The difference in energy intake was calculated and compared between groups. There was no significant change in energy intake between control and vehicle groups. The change in energy intake after treatment by 100 and 150 mg/kg of the extract was significantly higher than other groups (p=0.030 and p=0.007) CONCLUSION: This study indicated that coriander had positive effects on appetite of rats. Future studies are needed to evaluate the mechanisms of the effects of this plant on appetite.

Variable effects of parabrachial nucleus lesions on salt appetite in rats depending upon experimental paradigm and saline concentration.

Previous studies have demonstrated that bilateral lesions of the gustatory (medial) zone of the parabrachial nucleus (PBN) in the pons eliminate the salt (sodium chloride; NaCl) appetite induced in rats by treatment with the diuretic drug, furosemide. The present studies reexamined NaCl intake of rats with PBN lesions induced by ibotenic acid, using multiple models of salt appetite. The impairment of a conditioned taste aversion, an established consequence of PBN damage, was used as an initial screen with which to assess the effectiveness of the lesions. Rats with PBN lesions did not drink either 0.3 of a molar (M) solution of NaCl or 0.5 M NaCl in response to daily treatment with desoxycorticosterone acetate. These findings suggest that the excitatory stimulus of salt appetite mediated by mineralocorticoids is abolished by PBN lesions. In contrast, rats with PBN lesions drank some 0.5 M NaCl and more 0.3 M NaCl, in addition to water, in response to hypovolemia induced by subcutaneous injection of 30% polyethylene glycol solution. Those findings suggest that an excitatory stimulus of salt appetite, presumably mediated by Angiotensin II, is not abolished by PBN lesions. These and other observations indicate that lesions of the gustatory PBN in rats may or may not eliminate salt appetite, depending on which model is used and which concentration of NaCl solution is available.

Is Cannabis sativa an effective drug to increase appetite in rats?

Is Cannabis sativa an effective drug to increase appetite in rats?

Central alpha 2-adrenoceptors mediate the inhibitory effect of lipopolysaccharide on sodium appetite independently from systemic inhibitory factors in rats

Lipopolysaccharide (LPS) injected ip reduces sodium appetite in rats. In the present work we investigated a role for systemic inhibitory factors and alpha2-adrenoceptors on the effect of LPS on a sodium appetite test. Adult male rats (n=5–7/group) were depleted of sodium by a combination of the natriuretic furosemide sc plus 24h removal of ambient sodium to produce sodium appetite. LPS (2mg/kg) vs. saline ip increased the stomach liquid content (an index of gastric emptying and early pre-systemic gastrointestinal inhibitory signals) 5min after an intragastric load of 3ml of 0.3M NaCl given by gavage (4.4±0.4 vs.