scholarly journals Diurnal rhythm of cerebrospinal fluid and plasma leptin levels related to feeding in non-lactating and lactating rats

2004 ◽  
Vol 180 (2) ◽  
pp. 283-286 ◽  
Author(s):  
S Asakuma ◽  
O Hiraku ◽  
Y Kurose ◽  
S Kobayashi ◽  
Y Terashima
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Feeding Behavior ◽  
Physiological Condition ◽  
Plasma Concentrations ◽  
Dark Phase ◽  
Light Phase ◽  
Daily Food ◽  
Plasma Leptin ◽  
The Brain

Leptin suppresses food intake and increases energy expenditure in the hypothalamus. Rats consume most of their daily food intake during the dark phase of the diurnal cycle. Lactating rats have increased food intake, but the involvement of leptin in the regulation of food intake in this physiological condition is not well understood. The present experiment was carried out to determine the circadian pattern of leptin concentrations in plasma and cerebrospinal fluid (CSF) in relation to the feeding behavior of non-lactating and lactating rats.Female rats were maintained on a controlled lighting schedule (lights on between 0600 and 1800 h) and the food intake of lactating rats was two- or threefold higher than that of non-lactating rats. In both groups, food intake was three times greater in the dark phase (P<0.01) compared with the light phase. The plasma concentrations of leptin were lower (P<0.01) in lactating rats than non-lactating rats in both light and dark phases, but there were no differences in plasma leptin levels between light and dark phases. In contrast, and in both groups, the leptin concentrations in CSF were lower (P<0.01) in the dark phase than in the light phase. Leptin levels in CSF were lower (P<0.01) in lactating rats than in non-lactating rats. We conclude that a diurnal pattern of leptin levels within the brain (but not in plasma) reflects characteristics of feeding behavior in lactating and non-lactating rats.

scholarly journals Diurnal Rhythm of Apolipoprotein A-IV in Rat Hypothalamus and Its Relation to Food Intake and Corticosterone

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3232-3238 ◽  
Author(s):  
Min Liu ◽  
Ling Shen ◽  
Yin Liu ◽  
Daisuke Tajima ◽  
Randall Sakai ◽  
...  
Keyword(s):  
Food Intake ◽  
Dark Phase ◽  
Light Phase ◽  
Daily Food Intake ◽  
Protein Levels ◽  
Diurnal Patterns ◽  
Apolipoprotein A ◽  
Daily Food ◽  
Gene And Protein Expression ◽  
Low Levels

Abstract Apolipoprotein A-IV (apo A-IV) is a satiety protein synthesized in the small intestine and hypothalamus. To further understand the roles of central apo A-IV in the management of daily food intake, we have examined the diurnal patterns of hypothalamic apo A-IV gene and protein expression in freely feeding and food-restricted (food provided 4 h daily between 1000 h and 1400 h) rats. In freely feeding rats, the hypothalamic apo A-IV mRNA and protein levels fluctuated, with high levels during the light phase, peaking at 0900 h (3 h after lights on), and low levels during the dark phase, with a nadir at 2100 h (3 h after lights off). The daily patterns of the fluctuation, however, were altered in food-restricted rats, which had a marked decrease in hypothalamic apo A-IV mRNA and protein levels during the 4 h-feeding period of the light phase. Although corticosterone (CORT) secretion temporally coincided with the decreasing phase of apo A-IV in the hypothalamus, depletion of CORT by adrenalectomy significantly decreased, rather than increased, hypothalamic apo A-IV mRNA and protein levels. These results indicate that the diurnal expression of hypothalamic apo A-IV is regulated by factors other than the circulating CORT, for example, the reduced food intake and body weight in adrenalectomized animals. The fact that hypothalamic apo A-IV level and food intake were inversely related during the normal diurnal cycle as well as in the period of restricted feeding suggests that hypothalamic apo A-IV is involved in the regulation of daily food intake.

scholarly journals PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin

2015 ◽  
Vol 309 (10) ◽  
pp. G816-G825 ◽  
Author(s):  
John P. Vu ◽  
Deepinder Goyal ◽  
Leon Luong ◽  
Suwan Oh ◽  
Ravneet Sandhu ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Peptide Yy ◽  
Dark Phase ◽  
Dependent Manner ◽  
Pac1 Receptor ◽  
Intraperitoneal Treatment ◽  
Regulate Food Intake ◽  
Feeding Parameters ◽  
Glucagon Like Peptide 1

Pituitary adenylate cyclase-activating peptide (PACAP) is expressed within the gastroenteric system, where it has profound physiological effects. PACAP was shown to regulate food intake and thermogenesis centrally; however, PACAP peripheral regulation of appetite and feeding behavior is unknown. Therefore, we studied PACAP's effect on appetite and food intake control by analyzing feeding behavior and metabolic hormones in PAC1-deficient (PAC1−/−) and age-matched wild-type (WT) mice intraperitoneally injected with PACAP1–38 or PACAP1–27 before the dark phase of feeding. Food intake and feeding behavior were analyzed using the BioDAQ system. Active ghrelin, glucagon-like peptide-1 (GLP-1), leptin, peptide YY, pancreatic polypeptide, and insulin were measured following PACAP1–38 administration in fasted WT mice. PACAP1–38/PACAP1–27 injected into WT mice significantly decreased in a dose-dependent manner cumulative food intake and reduced bout and meal feeding parameters. Conversely, PACAP1–38 injected into PAC1−/− mice failed to significantly change food intake. Importantly, PACAP1–38 reduced plasma levels of active ghrelin compared with vehicle in WT mice. In PAC1−/− mice, fasting levels of active ghrelin, GLP-1, insulin, and leptin and postprandial levels of active ghrelin and insulin were significantly altered compared with levels in WT mice. Therefore, PAC1 is a novel regulator of appetite/satiety. PACAP1–38/PACAP1–27 significantly reduced appetite and food intake through PAC1. In PAC1−/− mice, the regulation of anorexigenic/orexigenic hormones was abolished, whereas active ghrelin remained elevated even postprandially. PACAP significantly reduced active ghrelin in fasting conditions. These results establish a role for PACAP via PAC1 in the peripheral regulation of appetite/satiety and suggest future studies to explore a therapeutic use of PACAP or PAC1 agonists for obesity treatment.

scholarly journals Fluoxetine Mimics the Anorectic Action of Estrogen and Its Regulation of Circadian Feeding in Ovariectomized Female Rats

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 849 ◽  
Author(s):  
Yuri Nishimura ◽  
Kaori Mabuchi ◽  
Natsumi Omura ◽  
Ayako Igarashi ◽  
Megumi Miura ◽  
...  
Keyword(s):  
Food Intake ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Body Weight Gain ◽  
Treated Group ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Dark Phase ◽  
Light Phase ◽  
Serotonergic Neurons ◽  
Fos Expression

Our previous study demonstrated that chronic estrogen replacement in ovariectomized rats reduces food intake and augments c-Fos expression in the suprachiasmatic nucleus (SCN), specifically during the light phase. Here, we hypothesized that serotonergic neurons in the central nervous system (CNS), which have anorectic action and play a role in regulating circadian rhythm, mediate the light phase-specific anorectic action of estrogen, and that selective serotonin reuptake inhibitors (SSRIs) mimic the hypophagic action of estrogen. Female Wistar rats were ovariectomized and treated with estradiol (E2) or cholesterol by subcutaneously implanting a silicon capsule containing E2 or cholesterol. Then, half of the cholesterol-treated rats were injected with the SSRI fluoxetine (5 mg/kg) (FLX group), while the remaining rats in the cholesterol-treated group (CON group) and all those in the E2 group were injected with saline subcutaneously twice daily at the onsets of the light and dark phases. Both E2 and FLX reduced food intake during the light phase but not the dark phase, and reduced body weight gain. In addition, both E2 and FLX augmented the c-Fos expression in the SCN, specifically during the light phase. These data indicate that FLX exerts estrogen-like antiobesity and hypophagic actions by modifying circadian feeding patterns, and suggest that estrogen regulates circadian feeding rhythm via serotonergic neurons in the CNS.

Intravenous nutrient-induced satiety depends on feeding-related gut signals

1991 ◽  
Vol 261 (2) ◽  
pp. R313-R322 ◽  
Author(s):  
E. K. Walls ◽  
A. E. Willing ◽  
H. S. Koopmans
Keyword(s):  
Amino Acids ◽  
Food Intake ◽  
Light Phase ◽  
Dark Cycle ◽  
Intravenous Glucose ◽  
Daily Food Intake ◽  
Daily Food

To determine whether feeding-generated gut signals act in conjunction with intravenous nutrients to suppress food intake, nutrients were infused intravenously to dark-fed rats during different portions of the 12:12 h light-dark cycle. During 4-day test periods rats received 35.5-37 kcal/day of a solution containing 25% glucose-4.25% amino acids. Food intakes were reduced by 40.5 +/- 1.1 and 30.7 +/- 1.8 kcal or 110 and 87% of the calories infused in the dark (fed) phase over 8 and 12 h, respectively. When administered in the light phase while rats were fasted, 8- and 12-h infusions reduced food intake significantly less than in the dark: 21.3 +/- 1.1 and 19.6 +/- 0.7 kcal/day or only 57 and 55% of the infused calories, respectively. With 24-h infusions, as in previous studies, food intake was reduced by 24.5 +/- 2.1 kcal/day or 68% of the infused calories. These results suggest that gut signals generated by concurrent feeding act with intravenous glucose and amino acids to produce a more compensatory reduction in daily food intake.

scholarly journals Glucagon-Like Peptide-1 (GLP-1) in the Integration of Neural and Endocrine Responses to Stress

Nutrients ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3304
Author(s):  
Yolanda Diz-Chaves ◽  
Salvador Herrera-Pérez ◽  
Lucas C. González-Matías ◽  
José Antonio Lamas ◽  
Federico Mallo
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Stress Responses ◽  
Food Motivation ◽  
Hedonic Value ◽  
Central Actions ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Second Messenger Pathways ◽  
The Brain

Glucagon like-peptide 1 (GLP-1) within the brain is produced by a population of preproglucagon neurons located in the caudal nucleus of the solitary tract. These neurons project to the hypothalamus and another forebrain, hindbrain, and mesolimbic brain areas control the autonomic function, feeding, and the motivation to feed or regulate the stress response and the hypothalamic-pituitary-adrenal axis. GLP-1 receptor (GLP-1R) controls both food intake and feeding behavior (hunger-driven feeding, the hedonic value of food, and food motivation). The activation of GLP-1 receptors involves second messenger pathways and ionic events in the autonomic nervous system, which are very relevant to explain the essential central actions of GLP-1 as neuromodulator coordinating food intake in response to a physiological and stress-related stimulus to maintain homeostasis. Alterations in GLP-1 signaling associated with obesity or chronic stress induce the dysregulation of eating behavior. This review summarized the experimental shreds of evidence from studies using GLP-1R agonists to describe the neural and endocrine integration of stress responses and feeding behavior.

scholarly journals Increased Food Intake Leads to Obesity and Insulin Resistance in the Tg2576 Alzheimer’s Disease Mouse Model

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1532-1540 ◽  
Author(s):  
Motoyuki Kohjima ◽  
Yuxiang Sun ◽  
Lawrence Chan
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Food Intake ◽  
Mouse Model ◽  
Feeding Behavior ◽  
Neurotrophic Factor ◽  
Caloric Intake ◽  
Brain Derived Neurotrophic Factor ◽  
Normal Diet ◽  
The Brain

Recent studies suggest that hyperinsulinemia and insulin resistance are linked to Alzheimer’s disease (AD). In this study, we used Tg2576 transgenic (Tg) mice, a widely used transgenic mouse model for AD, to explore the relationship between increased amyloid β-peptide (Aβ) and insulin resistance. When fed a high-fat diet (HFD), Tg mice developed obesity and insulin resistance at 16 wk of age. Furthermore, HFD-fed Tg mice displayed abnormal feeding behavior and increased caloric intake with time. Although caloric intake of HFD-fed Tg mice was similar to that of normal diet-fed Tg or wild-type mice during 4 to 8 wk of age, it increased sharply at 12 wk, and went up further at 16 wk, which paralleled changes in the level of Aβ40 and Aβ42 in the brain of these mice. Limiting food intake in HFD-fed Tg mice by pair-feeding a caloric intake identical with that of normal diet-fed mice completely prevented the obesity and insulin intolerance of HFD-fed Tg mice. The hypothalamus of HFD-fed Tg mice had a significant decrease in the expression of the anorexigenic neuropeptide, brain-derived neurotrophic factor, at both the mRNA and protein levels. These findings suggest that the increased Aβ in the brain of HFD-fed Tg2576 mice is associated with reduced brain-derived neurotrophic factor expression, which led to abnormal feeding behavior and increased food intake, resulting in obesity and insulin resistance in these animals.

Folate transport in the central nervous system

1975 ◽  
Vol 229 (3) ◽  
pp. 777-782 ◽  
Author(s):  
R Spector ◽  
AV Lorenzo
Keyword(s):  
Cerebrospinal Fluid ◽  
Folic Acid ◽  
Transport System ◽  
Plasma Concentrations ◽  
Folate Transport ◽  
Acid Clearance ◽  
Constant Rate ◽  
Intraventricular Injections ◽  
The Central Nervous System ◽  
The Brain

Methyltetrahydrofolic acid or folic acid was infused intravenously at a constant rate into conscious untreated or methotrexate-pretreated rabbits. After 150 min, at equivalent plasma concentrations, folic acid or methyltetrahydrofolic acid readily entered the cerebrospinal fluid and probably brain by a saturable transport system. In contrast, after intraventricular injections, folic acid but not methyltetrahydrofolic acid was cleared from cerebrospinal fluid to blood by a saturable system. Intraventribular injection of folic acid at concentrations that saturated folic acid clearance from cerebrospinal fluid did not affect the transport of methyltetrahydrofolic acid from blood into cerebrospinal fluid. These results suggest that the transport system for mehtyltetrahydrofolic acid, which is about half-saturated at normal plasma concentrations, helps maintain the cerebrospinal fluid and probably brain methyltetrahydrofolic acid concentrations within relatively narrow limits. Moreover, folic acid, which the brain cannot utilize, is transported from cerebrospinal fluid. A possible locus for the systems that transport folic acid from and methyltetrahydrofolic acid into the cerebrospinal fluid is the choroid plexus.

Drug entry into and distribution within brain and cerebrospinal fluid: [14C]urea pharmacokinetics

1982 ◽  
Vol 242 (3) ◽  
pp. R339-R348 ◽  
Author(s):  
S. I. Rapoport ◽  
R. Fitzhugh ◽  
K. D. Pettigrew ◽  
U. Sundaram ◽  
K. Ohno
Keyword(s):  
Cerebrospinal Fluid ◽  
Plasma Concentration ◽  
Plasma Concentrations ◽  
Nonlinear Least Squares ◽  
Compartment Model ◽  
Plasma Distribution ◽  
Urea Uptake ◽  
Cerebral Capillary ◽  
The Brain ◽  
Brain Extracellular Space

A four-compartment model was derived to analyze drug exchange among cerebral capillary plasma, cerebrospinal fluid (CSF), and the brain extracellular and intracellular (or bound) compartments. Equations that were derived incorporated the factor of cerebral blood flow. They were fit by nonlinear least squares to measured brain, plasma, and CSF (when available) concentrations of [14C]urea in the rat, in response to a step increase in plasma concentration, to intravenous infusion, or to a bolus injection of tracer. Best-fit values for the transfer constants were consistent among the three administrative regimens and agreed with published values, when available. Expressions also were derived and numerically evaluated for the lower limit of the brain extracellular space, for half times of brain [14C]urea uptake, and for the steady-state brain/plasma distribution volume. The model should make it possible to use transfer constants obtained for a given drug from one study (e.g., constant plasma concentration) to predict brain concentrations from measured plasma concentrations in other acute or chronic studies.

Intracranial infusion of CCK-8 derivatives suppresses food intake in rats

1986 ◽  
Vol 251 (4) ◽  
pp. R718-R723 ◽  
Author(s):  
T. Mori ◽  
K. Nagai ◽  
H. Nakagawa ◽  
N. Yanaihara
Keyword(s):  
Food Intake ◽  
Dark Period ◽  
Light Period ◽  
Meal Size ◽  
Weight Changes ◽  
Daily Food Intake ◽  
Daily Food ◽  
Male Wistar Rats ◽  
The Brain

The effects of infusions for approximately 1 wk of the synthetic COOH-terminal octapeptide of cholecystokinin (CCK-8) and its derivatives, pyroglutamyl-CCK-8 (pGlu-CCK-8) and glutaryl-CCK-8 (Glt-CCK-8), into the suprachiasmatic nucleus (SCN) of the hypothalamus of male Wistar rats on their feeding behavior under 12:12 light-dark cycle were examined. Infusion of CCK-8 (0.8 pmol/h) did not change the total daily food intake but caused slight decrease in food intake during the 12-h dark period with slight increase in the 12-h light period. Infusions of pGlu-CCK-8 (0.8 pmol/h) and Glt-CCK-8 (0.8 pmol/h) markedly reduced food intake during the 12-h dark period but had little effect in the light period and thus decreased total daily food intake. The reductions in food intake during the 12-h dark period due to infusions of the CCK-8 derivatives were greater than that due to CCK-8 infusion. Body weight changes reflected changes in food intake. CCK-8 derivatives appeared to suppress both meal size and frequency at the early part of the infusion period but reduce only meal size at the later part. Histological examination showed that infusion sites in the brain were widely damaged; however, neurons in the SCN appeared to be intact. These findings suggest that CCK-8 suppresses food intake during the dark period in rats by acting on some site(s) in the brain. The results also support the possibility that CCK-8 is degraded enzymatically in the brain, whereas the two derivatives, pGlu-CCK-8 and Glt-CCK-8, are resistant to degradation.

2,5-anhydro-D-mannitol acts in liver to initiate feeding

1991 ◽  
Vol 261 (2) ◽  
pp. R283-R288 ◽  
Author(s):  
M. G. Tordoff ◽  
N. Rawson ◽  
M. I. Friedman
Keyword(s):  
Food Intake ◽  
Vagus Nerve ◽  
Feeding Behavior ◽  
Low Doses ◽  
Increase Food Intake ◽  
Hepatic Portal ◽  
The Brain

We determined the site at which the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) acts to increase food intake in rats. Rats began eating sooner and ate more food during hepatic portal than during jugular infusions of 2,5-AM (50, 100, or 150 mg/h). After rats were intubated with 2,5-[14C]AM (1.15 microCi in 200 mg/kg), significant quantities of radioactivity were found in liver but not in brain. Hepatic vagotomy prevented the eating response to 200 mg/kg 2,5-AM without altering the effect of the analogue on plasma fuels. These results indicate that low doses of 2,5-AM act in the liver to increase food intake and suggest that the signal for feeding generated in the liver is transmitted to the brain through the hepatic vagus nerve. Taken together, this work provides the strongest evidence to date that a signal initiating feeding behavior originates in the liver.

Sign in / Sign up

Export Citation Format

Share Document