scholarly journals RFRP3 increases food intake in a sex‐dependent manner in the seasonal hamster Phodopus sungorus

2020 ◽  
Vol 32 (5) ◽  
Author(s):  
Fernando Cázarez‐Márquez ◽  
Marie‐Pierre Laran‐Chich ◽  
Paul Klosen ◽  
Andries Kalsbeek ◽  
Valérie Simonneaux
Keyword(s):  
Food Intake ◽  
Phodopus Sungorus ◽  
Dependent Manner

Central glucagon-like peptide 1 receptor-induced anorexia requires glucose metabolism-mediated suppression of AMPK and is impaired by central fructose

2013 ◽  
Vol 304 (7) ◽  
pp. E677-E685 ◽  
Author(s):  
Melissa A. Burmeister ◽  
Jennifer Ayala ◽  
Daniel J. Drucker ◽  
Julio E. Ayala
Keyword(s):  
Food Intake ◽  
Glucose Metabolism ◽  
Dependent Manner ◽  
Anorectic Effect ◽  
Dependent Inhibition ◽  
Glycolytic Inhibitor ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Amp Activated Protein Kinase ◽  
Mediated Reduction

Glucagon-like peptide-1 (GLP-1) suppresses food intake via activation of a central (i.e., brain) GLP-1 receptor (GLP-1R). Central AMP-activated protein kinase (AMPK) is a nutrient-sensitive regulator of food intake that is inhibited by anorectic signals. The anorectic effect elicited by hindbrain GLP-1R activation is attenuated by the AMPK stimulator AICAR. This suggests that central GLP-1R activation suppresses food intake via inhibition of central AMPK. The present studies examined the mechanism(s) by which central GLP-1R activation inhibits AMPK. Supporting previous findings, AICAR attenuated the anorectic effect elicited by intracerebroventricular (icv) administration of the GLP-1R agonist exendin-4 (Ex-4). We demonstrate that Ex-4 stimulates glycolysis and suppresses AMPK phosphorylation in a glucose-dependent manner in hypothalamic GT1-7 cells. This suggests that inhibition of AMPK and food intake by Ex-4 requires central glucose metabolism. Supporting this, the glycolytic inhibitor 2-deoxyglucose (2-DG) attenuated the anorectic effect of Ex-4. However, icv glucose did not enhance the suppression of food intake by Ex-4. AICAR had no effect on Ex-4-mediated reduction in locomotor activity. We also tested whether other carbohydrates affect the anorectic response to Ex-4. Intracerebroventricular pretreatment with the sucrose metabolite fructose, an AMPK activator, attenuated the anorectic effect of Ex-4. This potentially explains the increased food intake observed in sucrose-fed mice. In summary, we propose a model whereby activation of the central GLP-1R reduces food intake via glucose metabolism-dependent inhibition of central AMPK. We also suggest that fructose stimulates food intake by impairing central GLP-1R action. This has significant implications given the correlation between sugar consumption and obesity.

Prolactin stimulates food intake in a dose-dependent manner

1989 ◽  
Vol 256 (1) ◽  
pp. R276-R280 ◽  
Author(s):  
T. Gerardo-Gettens ◽  
B. J. Moore ◽  
J. S. Stern ◽  
B. A. Horwitz
Keyword(s):  
Food Intake ◽  
Female Rats ◽  
High Dose ◽  
Dependent Manner ◽  
Additional Control ◽  
The Mean ◽  
Ovine Prolactin ◽  
Dose Dependent ◽  
Medium Dose ◽  
Cumulative Food Intake

Lactation in the rat is marked by pronounced hyperphagia and suppression of brown fat (BAT) thermogenic capacity. We previously examined the possibility that elevated prolactin levels mediate these changes. The present study evaluated the effect of varying prolactin levels on food intake, BAT mitochondrial GDP binding, and carcass adiposity. Female rats were injected daily for 10 days with ovine prolactin at one of three doses: high = 3.0, medium = 1.0, or low = 0.3 micrograms/g body wt. Controls were injected with 0.9% NaCl. A group of uninjected rats served as an additional control. Cumulative food intake was significantly elevated in a dose-dependent manner in the prolactin-treated animals relative to the saline-injected and uninjected controls. Compared with the saline controls, the mean cumulative food intake was greatest at the high dose (20% increase), intermediate at the medium dose (17%), and smallest at the low dose (12%). Prolactin-treated rats gained significantly more weight during the experiment than did controls. Despite the hyperphagia in the prolactin-treated rats, no significant differences in BAT mitochondrial GDP binding were observed among the five groups. These data indicate that elevated prolactin levels stimulate food intake in a dose-dependent manner and that this hyperphagia is not accompanied by an increase in BAT mitochondrial GDP binding.

Energy intake and fur in summer- and winter-acclimated Siberian hamsters (Phodopus sungorus)

2001 ◽  
Vol 281 (2) ◽  
pp. R519-R527 ◽  
Author(s):  
Alexander S. Kauffman ◽  
Alessandra Cabrera ◽  
Irving Zucker
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Ventral Surface ◽  
Phodopus Sungorus ◽  
Ambient Temperatures ◽  
Siberian Hamsters ◽  
Daily Food ◽  
Brown Adipose ◽  
Wide Range ◽  
The Impact

Few studies have directly addressed the impact of fur on seasonal changes in energy intake. The daily food intake of Siberian hamsters ( Phodopus sungorus) was measured under simulated summer and winter conditions in intact animals and those with varying amounts of pelage removed. Energy intake increased up to 44% above baseline control values for approximately 2–3 wk after complete shaving. Increases in food intake varied with condition and were greater in hamsters housed in short than long day lengths and at low (5°C) than moderate (23°C) ambient temperatures. Removal of 8 cm2 of dorsal fur, equivalent to 30% of the total dorsal fur surface, increased food intake, but removal of 4 cm2 had no effect. An 8-cm2 fur extirpation from the ventral surface did not increase food consumption. Food intake was not influenced differentially by fur removal from above brown adipose tissue hot spots. Fur plays a greater role in energy balance in winter- than summer-acclimated hamsters and conserves energy under a wide range of environmental conditions.

Effects of continuous graded total parenteral nutrition on feeding indexes and metabolic concomitants in rats

1991 ◽  
Vol 260 (1) ◽  
pp. E126-E140 ◽  
Author(s):  
M. M. Meguid ◽  
T. Y. Chen ◽  
Z. J. Yang ◽  
A. C. Campos ◽  
D. C. Hitch ◽  
...  
Keyword(s):  
Amino Acids ◽  
Food Intake ◽  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Consumption Rate ◽  
Hepatic Glycogen ◽  
Free Access ◽  
Dependent Manner ◽  
Whole Brain ◽  
Total Food Intake

The influence of graded amounts of total parenteral nutrition (TPN) on food intake and feeding indexes was investigated in 90 rats housed in Automated Computerized Rat Eater Meter metabolic cages with free access to water and chow. When food intake was stable after catheter placement, 10 control rats continued with the 3 ml/h normal saline used for catheter patency, whereas study rats were given graded TPN continuously for 3 days, amounting to the equivalent of 26% (TPN-26), 53% (TPN-53), 81% (TPN-81), or 114% (TPN-114) of their daily caloric needs. TPN consisted of glucose, fat, and amino acids in the caloric ratio of 50:30:20. In study rats, the graded TPN depressed food intake, meal number, meal size, and eventually food consumption rate, meal sniffs, and intermeal sniffs in a dose- and time-dependent manner. During graded TPN, rats decreased total food intake by eating fewer, smaller, shorter meals at a decreasing consumption rate; sniffing activities were correspondingly curtailed. Stopping TPN led to normalization of feeding indexes. Blood glucose did not change while plasma insulin rose with graded TPN. A decrease in hepatic glycogen and an increase in hepatic triglycerides occurred. Plasma valine, phenylalanine, and methionine rose in a TPN dose-dependent manner. TPN-26 and TPN-53 significantly decreased whole brain amino acids; with TPN-114 no change occurred. Brain influx of tryptophan remained unchanged, but a progressive decrease in brain influx of tyrosine occurred. Whole brain dopamine and serotonin were depressed with TPN-26 and TPN-81 but were normal with TPN-114.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Soy food intake associates with changes in the metabolome and reduced blood pressure in a gut microbiota dependent manner

2020 ◽  
Vol 30 (9) ◽  
pp. 1500-1511
Author(s):  
Rachana D. Shah ◽  
Zheng-Zheng Tang ◽  
Guanhua Chen ◽  
Shi Huang ◽  
Jane F. Ferguson
Keyword(s):  
Blood Pressure ◽  
Food Intake ◽  
Gut Microbiota ◽  
Dependent Manner

Central administration of metformin into the third ventricle of C57BL/6 mice decreases meal size and number and activates hypothalamic S6 kinase

2013 ◽  
Vol 305 (5) ◽  
pp. R499-R505 ◽  
Author(s):  
Hyun-Ju Kim ◽  
Eun-Young Park ◽  
Mi-Jeong Oh ◽  
Sung-Soo Park ◽  
Kyung-Ho Shin ◽  
...  
Keyword(s):  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Third Ventricle ◽  
Meal Size ◽  
Dependent Manner ◽  
Central Administration ◽  
Mediobasal Hypothalamus ◽  
S6 Kinase ◽  
The Third

Administration of metformin is known to reduce both body weight and food intake. Although the hypothalamus is recognized as a critical regulator of energy balance and body weight, there is currently no evidence for an effect of metformin in the hypothalamus. Therefore, we sought to determine the central action of metformin on energy balance and body weight, as well as its potential involvement with key hypothalamic energy sensors, including adenosine monophosphate-activated protein kinase (AMPK) and S6 kinase (S6K). We used meal pattern analysis and a conditioned taste aversion (CTA) test and measured energy expenditure in C56BL/6 mice administered metformin (0, 7.5, 15, or 30 μg) into the third ventricle (I3V). Furthermore, we I3V-administered either control or metformin (30 μg) and compared the phosphorylation of AMPK and S6K in the mouse mediobasal hypothalamus. Compared with the control, I3V administration of metformin decreased body weight and food intake in a dose-dependent manner and did not result in CTA. Furthermore, the reduction in food intake induced by I3V administration of metformin was accomplished by decreases in both nocturnal meal size and number. Compared with the control, I3V administration of metformin significantly increased phosphorylation of S6K at Thr389 and AMPK at Ser485/491 in the mediobasal hypothalamus, while AMPK phosphorylation at Thr172 was not significantly altered. Moreover, I3V rapamycin pretreatment restored the metformin-induced anorexia and weight loss. These results suggest that the reduction in food intake induced by the central administration of metformin in the mice may be mediated by activation of S6K pathway.

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 Sympathetic Activation Induces Skeletal Fgf23 Expression in a Circadian Rhythm-dependent Manner

2013 ◽  
Vol 289 (3) ◽  
pp. 1457-1466 ◽  
Author(s):  
Masanobu Kawai ◽  
Saori Kinoshita ◽  
Shigeki Shimba ◽  
Keiichi Ozono ◽  
Toshimi Michigami
Keyword(s):  
Food Intake ◽  
Circadian Clock ◽  
Sympathetic Tone ◽  
Dark Phase ◽  
Dependent Manner ◽  
Phosphate Metabolism ◽  
Sympathetic Activation ◽  
Clock Network

The circadian clock network is well known to link food intake and metabolic outputs. Phosphorus is a pivotal nutritional factor involved in energy and skeletal metabolisms and possesses a circadian profile in the circulation; however, the precise mechanisms whereby phosphate metabolism is regulated by the circadian clock network remain largely unknown. Because sympathetic tone, which displays a circadian profile, is activated by food intake, we tested the hypothesis that phosphate metabolism was regulated by the circadian clock network through the modification of food intake-associated sympathetic activation. Skeletal Fgf23 expression showed higher expression during the dark phase (DP) associated with elevated circulating FGF23 levels and enhanced phosphate excretion in the urine. The peaks in skeletal Fgf23 expression and urine epinephrine levels, a marker for sympathetic tone, shifted from DP to the light phase (LP) when mice were fed during LP. Interestingly, β-adrenergic agonist, isoproterenol (ISO), induced skeletal Fgf23 expression when administered at ZT12, but this was not observed in Bmal1-deficient mice. In vitro reporter assays revealed that ISO trans-activated Fgf23 promoter through a cAMP responsive element in osteoblastic UMR-106 cells. The mechanism of circadian regulation of Fgf23 induction by ISO in vivo was partly explained by the suppressive effect of Cryptochrome1 (Cry1) on ISO signaling. These results indicate that the regulation of skeletal Fgf23 expression by sympathetic activity is dependent on the circadian clock system and may shed light on new regulatory networks of FGF23 that could be important for understanding the physiology of phosphate metabolism.

scholarly journals A limbic circuit selectively linking active escape to food suppression

2019 ◽  
Author(s):  
Estefania P. Azevedo ◽  
Bowen Tan ◽  
Lisa E. Pomeranz ◽  
Violet Ivan ◽  
Robert N. Fetcho ◽  
...  
Keyword(s):  
Food Intake ◽  
Lateral Septum ◽  
Sexually Dimorphic ◽  
Dependent Manner ◽  
Neural Basis ◽  
Genetic Manipulations ◽  
Glucagon Like Peptide 1 ◽  
Feeding Center ◽  
Cycle Dependent

AbstractStress and anxiety are precipitating factors for eating disorders, but the neural basis linking stress to alterations in feeding is not well understood. Here we describe a novel population of stress-responsive neurons in the lateral septum (LS) of mice that express neurotensin (LSNTS) in a sexually dimorphic, estrous cycle-dependent manner. We used in vivo imaging to show that LSNTS neurons are activated by stressful experiences when flight is a viable option, but not by a stressful experience associated with freezing or immobility. LSNTS activation leads to a decrease of food intake and body weight in mice, without altering locomotion or other behaviors associated with anxiety. Molecular profiling of LSNTS neurons showed that these neurons co-express Glp1r (glucagon-like peptide 1 receptor), and both pharmacologic and genetic manipulations of Glp1r signaling in the LS recapitulates the behavioral effects of LSNTS activation. Finally, we mapped the outputs of LSNTS neurons and show that activation of LSNTS nerve terminals in the lateral hypothalamus (LH), a well-established feeding center, also decrease food intake. Taken together, these results show that LSNTS neurons link stress and anorexia via effects on hypothalamic pathways regulating food intake.

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