scholarly journals Possible Mechanisms of Circulating PYY-Induced Satiation in Male Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (1) ◽  
pp. 193-204 ◽  
Author(s):  
Ulrike Stadlbauer ◽  
Myrtha Arnold ◽  
Elisabeth Weber ◽  
Wolfgang Langhans
Keyword(s):  
Plasma Levels ◽  
Jugular Vein ◽  
Area Postrema ◽  
Central Area ◽  
Male Rats ◽  
Acute Effects ◽  
Paraventricular Nuclei ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
The Brain

Peptide tyrosine-tyrosine (PYY) is implicated in eating control, but the site(s) and mechanism(s) of its action remain uncertain. We tested acute effects of intrameal hepatic portal vein (HPV) PYY3-36 infusions on eating in adult, male rats and measured HPV and jugular vein (JV) plasma levels of PYY in response to a solid, mixed-nutrient meal. We also examined the effects of HPV PYY3-36 infusions on JV plasma levels, flavor acceptance, and neuronal activation. Intrameal HPV PYY3-36 infusions [1 and 3 nmol/kg body weight (BW)] selectively reduced (P < 0.05) ongoing meal size. HPV PYY levels increased (P < 0.05) during a chow (12.5 kcal) or an isocaloric high-fat meal. JV PYY levels were generally lower than HPV levels but also increased in response to the chow meal. HPV PYY3-36 infusion (1 nmol/kg BW) caused a greater increase in JV PYY than a meal, but neither 1 nor 3 nmol/kg BW PYY3-36 caused conditioned flavor avoidance. HPV PYY3-36 (1 nmol/kg BW) increased the number of c-Fos-expressing cells in the nucleus tractus solitarii, the hypothalamic arcuate and paraventricular nuclei, the central area of the amygdala, and the nucleus accumbens but not in the area postrema and parabrachial nucleus. These data show that HPV infusions of PYY3-36 inhibit eating in rats without causing avoidance, and they identify some brain areas that might be involved. Endogenous PYY may induce satiation by acting directly in the brain, but further studies should examine whether PYY3–36 administrations that mimic the meal-induced increase in plasma PYY are sufficient to inhibit eating.

scholarly journals Circulating Glucagon-like Peptide-1 (GLP-1) Inhibits Eating in Male Rats by Acting in the Hindbrain and Without Inducing Avoidance

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1690-1699 ◽  
Author(s):  
Mukesh Punjabi ◽  
Myrtha Arnold ◽  
Elisabeth Rüttimann ◽  
Mariana Graber ◽  
Nori Geary ◽  
...  
Keyword(s):  
Area Postrema ◽  
Vena Cava ◽  
Inhibitory Effect ◽  
Male Rats ◽  
Physiological Relevance ◽  
Hepatic Portal Vein ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Hepatic Portal ◽  
Conditioned Flavor

To address the neural mediation of the eating-inhibitory effect of circulating glucagon-like peptide-1 (GLP-1), we investigated the effects of 1) intra-fourth ventricular infusion of the GLP-1 receptor antagonist exendin-9 or 2) area postrema lesion on the eating-inhibitory effect of intrameal hepatic portal vein (HPV) GLP-1 infusion in adult male rats. To evaluate the physiological relevance of the observed effect we examined 3) the influence of GLP-1 on flavor acceptance in a 2-bottle conditioned flavor avoidance test, and 4) measured active GLP-1 in the HPV and vena cava (VC) in relation to a meal and in the VC after HPV GLP-1 infusion. Intrameal HPV GLP-1 infusion (1 nmol/kg body weight-5 min) specifically reduced ongoing meal size by almost 40% (P < .05). Intra-fourth ventricular exendin-9 (10 μg/rat) itself did not affect eating, but attenuated (P < .05) the satiating effect of HPV GLP-1. Area postrema lesion also blocked (P < .05) the eating-inhibitory effect of HPV GLP-1. Pairing consumption of flavored saccharin solutions with HPV GLP-1 infusion did not alter flavor acceptance, indicating that HPV GLP-1 can inhibit eating without inducing malaise. A regular chow meal transiently increased (P < .05) HPV, but not VC, plasma active GLP-1 levels, whereas HPV GLP-1 infusion caused a transient supraphysiological increase (P < .01) in VC GLP-1 concentration 3 minutes after infusion onset. The results implicate hindbrain GLP-1 receptors and the area postrema in the eating-inhibitory effect of circulating GLP-1, but question the physiological relevance of the eating-inhibitory effect of iv infused GLP-1 under our conditions.

Chronic immobilization stress induces anxiety-related behaviors and affects brain essential minerals in male rats

2020 ◽  
pp. 1-8
Author(s):  
Zafer Sahin ◽  
Alpaslan Ozkurkculer ◽  
Omer Faruk Kalkan ◽  
Ahmet Ozkaya ◽  
Aynur Koc ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Central Area ◽  
Essential Elements ◽  
Male Rats ◽  
Control Group ◽  
Male Wistar Rats ◽  
Swimming Test ◽  
The Brain ◽  
Center Area ◽  
Chronic Immobilization Stress

Abstract. Alterations of essential elements in the brain are associated with the pathophysiology of many neuropsychiatric disorders. It is known that chronic/overwhelming stress may cause some anxiety and/or depression. We aimed to investigate the effects of two different chronic immobilization stress protocols on anxiety-related behaviors and brain minerals. Adult male Wistar rats were divided into 3 groups as follows ( n = 10/group): control, immobilization stress-1 (45 minutes daily for 7-day) and immobilization stress-2 (45 minutes twice a day for 7-day). Stress-related behaviors were evaluated by open field test and forced swimming test. In the immobilization stress-1 and immobilization stress-2 groups, percentage of time spent in the central area (6.38 ± 0.41% and 6.28 ± 1.03% respectively, p < 0.05) and rearing frequency (2.75 ± 0.41 and 3.85 ± 0.46, p < 0.01 and p < 0.05, respectively) were lower, latency to center area (49.11 ± 5.87 s and 44.92 ± 8.04 s, p < 0.01 and p < 0.01, respectively), were higher than the control group (8.65 ± 0.49%, 5.37 ± 0.44 and 15.3 ± 3.32 s, respectively). In the immobilization stress-1 group, zinc (12.65 ± 0.1 ppm, p < 0.001), magnesium (170.4 ± 1.7 ppm, p < 0.005) and phosphate (2.76 ± 0.1 ppm, p < 0.05) levels were lower than the control group (13.87 ± 0.16 ppm, 179.31 ± 1.87 ppm and 3.11 ± 0.06 ppm, respectively). In the immobilization stress-2 group, magnesium (171.56 ± 1.87 ppm, p < 0.05), phosphate (2.44 ± 0.07 ppm, p < 0.001) levels were lower, and manganese (373.68 ± 5.76 ppb, p < 0.001) and copper (2.79 ± 0.15 ppm, p < 0.05) levels were higher than the control group (179.31 ± 1.87 ppm, 3.11 ± 0.06 ppm, 327.25 ± 8.35 ppb and 2.45 ± 0.05 ppm, respectively). Our results indicated that 7-day chronic immobilization stress increased anxiety-related behaviors in both stress groups. Zinc, magnesium, phosphate, copper and manganese levels were affected in the brain.

Hepatic modulation of insulin-induced gastric acid secretion and EMG activity in rats

1980 ◽  
Vol 238 (5) ◽  
pp. R346-R352 ◽  
Author(s):  
J. Granneman ◽  
M. I. Friedman
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Emg Activity ◽  
Glucose Levels ◽  
Hepatic Portal Vein ◽  
Inhibited Acid ◽  
Hepatic Portal ◽  
The Brain

Intravenous infusions of fructose, a hexose that does not cross the blood-brain barrier, suppressed insulin-induced gastric acid secretion and electromyographic (EMG) activity despite continuing hypoglycemia. Hepatic portal vein infusions of 0.15 M fructose inhibited acid output while the same concentration delivered via the jugular vein did not, suggesting a hepatic site of action of the hexose. Only infusions of fructose that began before onset of the insulin-induced gastric responses were effective, whereas glucose infusions, which elevated plasma glucose levels, readily reversed ongoing gastric activity. The suppressive effects of fructose on gastric activity were prevented by prior section of the hepatic branch of the vagus nerve. In contrast, hepatic vagotomy did not prevent suppression of gastric responses by infusions of glucose, a hexose utilized by both brain and liver. These results suggest that receptors in the brain may initiate and terminate insulin-induced gastric acid secretion and motor activity, whereas sensors in the liver may inhibit these responses.

Hepatic contribution to satiation of salt appetite in rats

1986 ◽  
Vol 251 (6) ◽  
pp. R1095-R1102 ◽  
Author(s):  
M. G. Tordoff ◽  
J. Schulkin ◽  
M. I. Friedman
Keyword(s):  
Portal Vein ◽  
Sodium Concentration ◽  
Reciprocal Relationship ◽  
Dietary Sodium ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Portal Vein Infusion ◽  
The Brain

We examined the influence of hepatic-portal vein infusion of NaCl and of hepatic vagotomy on 3% NaCl solution drinking by sodium-deficient rats. Combined dietary sodium restriction and administration of the natriuretic agent, furosemide (5 mg), produced a vigorous appetite for 3% NaCl solution that was attenuated by portal infusion of NaCl. Whereas infusions (1 ml/30 min) of NaCl into the hepatic-portal vein in concentrations as low as 0.15 M (isotonic) significantly reduced 3% NaCl consumption, a higher concentration (0.6 M) infused into the jugular vein, or portal infusions of KCl (0.6 M) or sucrose (1.2 M), were ineffective. Rats with selective hepatic vagotomy displayed an attenuated appetite for salt whether or not they received hepatic-portal NaCl. This was not due to altered excretion of sodium. Taken together, these results suggest that the liver or portal vein can provide a sodium-specific neural signal capable of attenuating the appetite for salt and this information is transferred to the brain by fibers in the hepatic vagus that fire in reciprocal relationship with portal sodium concentration.

scholarly journals Effects of infusions of lysine, leucine and ammonium chloride into the hepatic portal vein of chickens on voluntary food intake

1987 ◽  
Vol 58 (2) ◽  
pp. 325-331 ◽  
Author(s):  
Audrey A. Rusby ◽  
J. M. Forbes
Keyword(s):  
Food Intake ◽  
Portal Vein ◽  
Ammonium Chloride ◽  
Jugular Vein ◽  
Free Access ◽  
Delayed Effect ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Access To Food ◽  
Portal Infusion

1. Adolescent cockerels of a laying strain were prepared with catheters whose tip lay in the hepatic portal vein, to study the effect of 3-h infusions of nutrients on food intake.2. Lysine, infused into the hepatic portal vein at rates of 150–450 mg/3 h reduced 3-h food intake by up to 58%, for a period of 6 h in previously starved birds, but had no effect on birds allowed free access to food. Infusions made into the jugular vein had no effect, suggesting a role for the liver in monitoring lysine levels.3. Portal infusion of leucine had a delayed effect while ammonium chloride, infused at isomolar rates to those of the lysine infusions, had very little effect on intake.4. The results support the concept of liver sensitivity to amino acids, but the mode of action is not clear; it appears not to be via the effects of ammonia.

scholarly journals Metabolic Sensing and the Brain: Who, What, Where, and How?

Endocrinology ◽  
2011 ◽  
Vol 152 (7) ◽  
pp. 2552-2557 ◽  
Author(s):  
Barry E. Levin ◽  
Christophe Magnan ◽  
Ambrose Dunn-Meynell ◽  
Christelle Le Foll
Keyword(s):  
Energy Homeostasis ◽  
Distributed Network ◽  
Metabolic Substrates ◽  
Hepatic Portal Vein ◽  
Metabolic Sensing ◽  
Hepatic Portal ◽  
And Function ◽  
The Brain ◽  
Local Brain ◽  
Brain Barriers

Unique subpopulations of specialized metabolic sensing neurons reside in a distributed network throughout the brain and respond to alterations in ambient levels of various metabolic substrates by altering their activity. Variations in local brain substrate levels reflect their transport across the blood- and cerebrospinal-brain barriers as well as local production by astrocytes. There are a number of mechanisms by which such metabolic sensing neurons alter their activity in response to changes in substrate levels, but it is clear that these neurons cannot be considered in isolation. They are heavily dependent on astrocyte and probably tanycyte metabolism and function but also respond to hormones (e.g. leptin and insulin) and cytokines that cross the blood-brain barrier from the periphery as well as hard-wired neural inputs from metabolic sensors in peripheral sites such as the hepatic portal vein, gastrointestinal tract, and carotid body. Thus, these specialized neurons are capable of monitoring and integrating multiple signals from the periphery as a means of regulating peripheral energy homeostasis.

Evidence for gut factor in K+ homeostasis

2007 ◽  
Vol 293 (2) ◽  
pp. F541-F547 ◽  
Author(s):  
Felix N. Lee ◽  
Gisuk Oh ◽  
Alicia A. McDonough ◽  
Jang H. Youn
Keyword(s):  
Portal Vein ◽  
Jugular Vein ◽  
Deficient Diet ◽  
Apparent Increase ◽  
Marked Enhancement ◽  
Hepatic Portal Vein ◽  
Hepatic Portal ◽  
Fasted Rats ◽  
Intraportal Infusion

We tested the hypothesis that K+ intake is sensed by putative K+ sensors in the splanchnic areas, and renal K+ handling is regulated by this signal. K+ was infused for 2 h into overnight-fasted rats via the jugular vein (systemic infusion), hepatic portal vein (intraportal infusion), or stomach (intragastric infusion) ( n = 5 each), and plasma K+ concentration ([K+]) and renal K+ excretion were measured during the 2-h preinfusion, 2-h K+ infusion, and 3-h washout periods. During systemic K+ infusion, plasma [K+] increased by ∼1.3 mM ( P < 0.05), and, on cessation of the K+ infusion, plasma [K+] fell to the preinfusion level within 1–2 h. Renal K+ excretion changed in proportion to the changes in plasma [K+]. During intraportal or intragastric K+ infusion, plasma [K+] and renal K+ excretion profiles were similar to those with systemic infusion. The effects of K+ infusions via the different routes ( n = 5 or 6 each) were also studied during simultaneous feeding of overnight-fasted rats with a K+-deficient diet. During the meal, intraportal infusion resulted in increases in plasma [K+] similar to those with the systemic K+ infusion, while intragastric K+ infusion did not significantly increase plasma [K+]. Thus, when the intragastric K+ infusion was combined with a meal, there was marked enhancement of clearance of the K+ infused, which was associated with an apparent increase in renal efficiency of K+ excretion. These data suggest that there may be a gut factor that enhances renal efficiency of K+ excretion during meal (or dietary K+) intake.

Food reward and gut-brain signalling

Neuroforum ◽  
2020 ◽  
Vol 26 (1) ◽  
pp. 1-9
Author(s):  
Sharmili Edwin Thanarajah ◽  
Marc Tittgemeyer
Keyword(s):  
Food Reward ◽  
Food Selection ◽  
Eating Behaviour ◽  
Processed Food ◽  
Hepatic Portal Vein ◽  
Reward Pathways ◽  
Hepatic Portal ◽  
The Brain ◽  
Possible Cause ◽  
Specific Food

AbstractThe increasing availability of ultra-processed, energy dense food is contributing to the spread of the obesity pandemic, which is a serious health threat in today’s world. One possible cause for this association arises from the fact that the brain is wired to derive pleasure from eating. Specifically, food intake activates reward pathways involving dopamine receptor signalling. The reinforcing value of specific food items results from the interplay between taste and nutritional properties. Increasing evidence suggests that nutritional value is sensed in the gut by chemoreceptors in the intestinal tract and the hepatic portal vein, and conveyed to the brain through neuronal and endocrine pathways to guide food selection behaviour. Ultra-processed food is designed to potentiate the reward response through a combination of high fat and high sugar, therebye seeming highly appetizing. There is increasing evidence that overconsumption of processed food distorts normal reward signalling, leading to compulsive eating behaviour and obesity. Hence, it is essential to understand food reward and gut-brain signalling to find an effective strategy to combat the obesity pandemic.

cAMP in temperature- and ADH-regulating centers after thermal stress

1977 ◽  
Vol 42 (2) ◽  
pp. 257-261 ◽  
Author(s):  
I. Kornbluth ◽  
R. A. Siegel ◽  
N. Conforti ◽  
I. Chowers
Keyword(s):  
Thermal Stress ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
The Body ◽  
Neural Mechanisms ◽  
Male Rats ◽  
Paraventricular Nuclei ◽  
Regulate Body Temperature ◽  
Camp Levels ◽  
The Brain

cAMP concentrations in temperature-regulating sites of the brain and plasma osmolality were measured after exposure of male rats to 36 degrees C and 37–42% rh. for 10, 20, or 30 min. Plasma osmolality was affected by none of the heat exposures. In both the preoptic area and the posterior medial hypothalamus, cAMP concentrations were increased compared to controls, after 10, 20 and 30 min of heat exposure. In the supraoptic-paraventricular nuclei, neither 10 nor 20 min of exposure resulted in augmented cAMP concentrations; but after 30 min of heat exposure, cAMP levels in these nuclei were significantly greater than in controls. Neurohypophysial cAMP concentrations were increased after both 10 and 30 min of exposure. Cerebral cortical cAMP concentrations were not affected by thermal stress. It is concluded that cAMP is involved in the neural mechanisms which are brought into play to regulate body temperature during acute heat exposure. The significance of this involvement and its relation to the overall temperature-regulating mechanisms of the body are discussed.

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