scholarly journals Differential effects of glucocorticoids on energy homeostasis in Syrian hamsters

2011 ◽  
Vol 301 (2) ◽  
pp. E307-E316 ◽  
Author(s):  
Matia B. Solomon ◽  
Randall R. Sakai ◽  
Stephen C. Woods ◽  
Michelle T. Foster
Keyword(s):  
Food Intake ◽  
Body Mass ◽  
Energy Homeostasis ◽  
Fat Tissue ◽  
Thymic Involution ◽  
Syrian Hamsters ◽  
Differential Effects ◽  
Body Adiposity ◽  
Increase Food Intake ◽  
Response To Stress

Syrian hamsters, like many humans, increase food intake and body adiposity in response to stress. We hypothesized that glucocorticoids (cortisol and corticosterone) mediate these stress-induced effects on energy homeostasis. Because Syrian hamsters are dual secretors of cortisol and corticosterone, differential effects of each glucocorticoid on energy homeostasis were investigated. First, adrenal intact hamsters were injected with varying physiological concentrations of cortisol, corticosterone, or vehicle to emulate our previously published defeat regimens (i.e., 1 injection/day for 5 days). Neither food intake nor body weight was altered following glucocorticoid injections. Therefore, we investigated the effect of sustained glucocorticoid exposure on energy homeostasis. This was accomplished by implanting hamsters with supraphysiological steady-state pellets of cortisol, corticosterone, or cholesterol as a control. Cortisol, but not corticosterone, significantly decreased food intake, body mass, and lean and fat tissue compared with controls. Despite decreases in body mass and adiposity, cortisol significantly increased circulating free fatty acids, triglyceride, cholesterol, and hepatic triglyceride concentrations. Although corticosterone did not induce alterations in any of the aforementioned metabolic end points, Syrian hamsters were responsive to the effects of corticosterone since glucocorticoids both induced thymic involution and decreased adrenal mass. These findings indicate that cortisol is the more potent glucocorticoid in energy homeostasis in Syrian hamsters. However, the data suggest that cortisol alone does not mediate stress-induced increases in food intake or body mass in this species.

Social defeat and footshock increase body mass and adiposity in male Syrian hamsters

2007 ◽  
Vol 292 (1) ◽  
pp. R283-R290 ◽  
Author(s):  
Matia B. Solomon ◽  
Michelle T. Foster ◽  
Timothy J. Bartness ◽  
Kim L. Huhman
Keyword(s):  
Food Intake ◽  
Body Mass ◽  
Social Stress ◽  
Social Defeat ◽  
Mass Gain ◽  
Syrian Hamsters ◽  
Laboratory Rats ◽  
Footshock Stress ◽  
Lipid Mass ◽  
Increase Food Intake

Obesity is a world-wide epidemic, and many factors, including stress, have been linked to this growing trend. After social stress (i.e., defeat), subordinate laboratory rats and most laboratory mice become hypophagic and, subsequently, lose body mass; the opposite is true of subordinate Syrian hamsters. After social defeat, Syrian hamsters become hyperphagic and gain body mass compared with nonstressed controls. It is unknown whether this increase in body mass and food intake is limited to subordinate hamsters. In experiment 1, we asked, do dominant hamsters increase food intake, body mass, and adiposity after an agonistic encounter? Subordinate hamsters increased food intake and body mass compared with nonstressed controls. Although there was no difference in food intake or absolute body mass between dominant and nonstressed control animals, cumulative body mass gain was significantly higher in dominant than in nonstressed control animals. Total carcass lipid and white adipose tissue (WAT) (i.e., retroperitoneal and epididymal WAT) masses were significantly increased in subordinate, but not dominant, hamsters compared with nonstressed controls. In experiment 2, we asked, does footshock stress increase food intake, body mass, and adiposity. Hamsters exposed to defeat, but not footshock stress, increased food intake relative to nonstressed controls. In animals exposed to defeat or footshock stress, body mass, as well as mesenteric WAT mass, increased compared with nonstressed controls. Collectively, these data demonstrate that social and nonsocial stressors increase body and lipid mass in male hamsters, suggesting that this species may prove useful for studying the physiology of stress-induced obesity in some humans.

Social defeat increases food intake, body mass, and adiposity in Syrian hamsters

2006 ◽  
Vol 290 (5) ◽  
pp. R1284-R1293 ◽  
Author(s):  
Michelle T. Foster ◽  
Matia B. Solomon ◽  
Kim L. Huhman ◽  
Timothy J. Bartness
Keyword(s):  
Food Intake ◽  
Body Mass ◽  
Interaction Model ◽  
Social Defeat ◽  
Syrian Hamsters ◽  
Laboratory Rats ◽  
Increase Food Intake ◽  
Human Stress ◽  
Natural Stressor ◽  
Resident Intruder

Overeating and increases in body and fat mass are the most common responses to day-to-day stress in humans, whereas stressed laboratory rats and mice respond oppositely. Group housing of Syrian hamsters increases body mass, adiposity, and food intake, perhaps due to social confrontation-induced stress. In experiment 1 we asked, Does repeated social defeat increase food intake, body mass, and white adipose tissue (WAT) mass in Syrian hamsters? Male hamsters subjected to the resident-intruder social interaction model and defeated intermittently 15 times over 34 days for 7-min sessions significantly increased their food intake, body mass, and most WAT masses compared with nondefeated controls. Defeat significantly increased terminal adrenal norepinephrine, but not epinephrine, content. In experiment 2 we asked, Are 15 intermittent resident-intruder interactions necessary to increase body mass and food intake? Body mass and food intake of subordinate hamsters defeated only once were similar to those of nondefeated controls, but four or eight defeats similarly and significantly increased these responses. In experiment 3 we asked, Do intermittent defeats increase adiposity and food intake more than consecutive defeats? Four intermittent or consecutive defeats similarly and significantly increased food intake and body mass compared with nondefeated controls, but only intermittent defeats significantly increased all WAT masses. Consecutive defeats significantly increased mesenteric and inguinal WAT masses. Plasma leptin, but not insulin, concentrations were similarly and significantly increased compared with nondefeated controls. Collectively, social defeat, a natural stressor, significantly increased food intake, body mass, and adiposity in Syrian hamsters and may prove useful in determining mechanisms underlying human stress-induced obesity.

Effects of the fructose analog, 2,5-anhydro-D-mannitol, on food intake and estrous cyclicity in Syrian hamsters

1997 ◽  
Vol 272 (3) ◽  
pp. R935-R939
Author(s):  
J. E. Schneider
Keyword(s):  
Food Intake ◽  
Plasma Glucose ◽  
Acid Oxidation ◽  
Estrous Cycles ◽  
Syrian Hamsters ◽  
Glucose Levels ◽  
Fuel Metabolism ◽  
Increase Food Intake ◽  
Estrous Cyclicity ◽  
Estrous Cycling

Hyperphagia and anovulation are both triggered by prior food deprivation or other treatments that decrease intracellular availability of metabolic fuels in most species studied. Syrian hamsters fail to show compensatory hyperphagia, but do show anestrus in response to these energetic challenges. In the present experiments, we examined food intake, plasma glucose levels, and estrous cyclicity in Syrian hamsters in response to 2,5-anhydro-D-mannitol (2,5-AM), a fructose analog that is thought to trigger eating in rats by depleting intracellular levels of ATP. In experiment 1, female estrous cycling hamsters were treated with 100, 200, 400, or 800 mg/kg 2,5-AM or the vehicle by intraperitoneal injection. Food intake was measured 1, 2, 4, 8, and 24 h after treatment. There were no statistically significant increases in food intake in response to any dose of 2,5-AM. In experiment 2, blood samples were drawn at 0, 1, 3, 5, 7, and 25 h after hamsters were treated with 0 or 400 mg/kg 2,5-AM. 2,5-AM treatment resulted in a mild but significant decrease in plasma glucose levels similar to those seen in 2,5-AM-treated rats, suggesting that 2,5-AM has similar effects on fuel metabolism in rats and hamsters. In experiment 3, hamsters received 2,5-AM, 2,5-AM plus the fatty acid oxidation inhibitor methyl palmoxirate, or vehicle every 6 h over the first 48 h of the estrous cycle and were tested for indexes of estrous cyclicity at the end of the cycle. All hamsters showed normal estrous cycles, regardless of treatment. If 2,5-AM has similar metabolic consequences in rats and hamsters, the present results suggest that decreased intracellular levels of ATP and mild hypoglycemia do not increase food intake or inhibit estrous cyclicity in Syrian hamsters.

scholarly journals Genetic architecture drives seasonal onset of hibernation in the 13-lined ground squirrel

2017 ◽  
Author(s):  
Katharine R. Grabek ◽  
Thomas F. Cooke ◽  
L. Elaine Epperson ◽  
Kaitlyn K. Spees ◽  
Gleyce F. Cabral ◽  
...  
Keyword(s):  
Food Intake ◽  
Body Mass ◽  
Genetic Architecture ◽  
Energy Homeostasis ◽  
Muscarinic Acetylcholine Receptor ◽  
Ground Squirrels ◽  
Eqtl Analysis ◽  
A Genome ◽  
Prohormone Convertase 2 ◽  
Genotype By Sequencing

AbstractHibernation is a highly dynamic phenotype whose timing, for many mammals, is controlled by a circannual clock and accompanied by rhythms in body mass and food intake. When housed in an animal facility, 13-lined ground squirrels exhibit individual variation in the seasonal onset of hibernation, which is not explained by environmental or biological factors, such as body mass and sex. We hypothesized that underlying genetic architecture instead drives variation in this timing. After first increasing the contiguity of the genome assembly, we therefore employed a genotype-by-sequencing approach to characterize genetic variation in 153 13-lined ground squirrels. Combining this with datalogger records, we estimated high heritability (61-100%) for the seasonal onset of hibernation. After applying a genome-wide scan with 46,996 variants, we also identified 21 loci significantly associated with hibernation immergence, which alone accounted for 54% of the variance in the phenotype. The most significant marker (SNP 15, p=3.81×10−6) was located near prolactin-releasing hormone receptor (PRLHR), a gene that regulates food intake and energy homeostasis. Other significant loci were located near genes functionally related to hibernation physiology, including muscarinic acetylcholine receptor M2 (CHRM2), involved in the control of heart rate, exocyst complex component 4 (EXOC4) and prohormone convertase 2 (PCSK2), both of which are involved in insulin signaling and processing. Finally, we applied an expression quantitative loci (eQTL) analysis using existing transcriptome datasets, and we identified significant (q<0.1) associations for 9/21 variants. Our results highlight the power of applying a genetic mapping strategy to hibernation and present new insight into the genetics driving its seasonal onset.

scholarly journals Cold-induced hyperphagia requires AgRP-neuron activation in mice

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Jennifer Deem ◽  
Chelsea L Faber ◽  
Christian Pedersen ◽  
Bao Anh Phan ◽  
Sarah A Larsen ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Cold Environment ◽  
Energy Demands ◽  
Acute Cold Exposure ◽  
Neuron Activation ◽  
Increase Food Intake

To maintain energy homeostasis during cold exposure, the increased energy demands of thermogenesis must be counterbalanced by increased energy intake. To investigate the neurobiological mechanisms underlying this cold-induced hyperphagia, we asked whether agouti-related peptide (AgRP) neurons are activated when animals are placed in a cold environment and, if so, whether this response is required for the associated hyperphagia. We report that AgRP-neuron activation occurs rapidly upon acute cold exposure, as do increases of both energy expenditure and energy intake, suggesting the mere perception of cold is sufficient to engage each of these responses. We further report that silencing of AgRP neurons selectively blocks the effect of cold exposure to increase food intake but has no effect on energy expenditure. Together, these findings establish a physiologically important role for AgRP neurons in the hyperphagic response to cold exposure.

scholarly journals Deficiency of Irx5 protects mice from diet-induced obesity and associated metabolic abnormalities

2021 ◽  
Author(s):  
Joe Son ◽  
Kyoung-Han Kim ◽  
Chi-chung Hui
Keyword(s):  
Food Intake ◽  
Body Mass ◽  
Energy Homeostasis ◽  
Caloric Intake ◽  
Mass Composition ◽  
Metabolic Abnormalities ◽  
Diet Induced Obesity ◽  
Body Mass Composition ◽  
Polygenic Obesity

Obesity, a leading cause of several metabolic abnormalities, is mainly due to an imbalance of energy homeostasis. IRX3 and IRX5 have been suggested as determinants of obesity in connection with the intronic variants of FTO, the strongest genetic risk factor of polygenic obesity in humans. Although the causal effects of Irx3 on obesity and its related metabolic consequences have been demonstrated in vivo, the metabolic function of Irx5 remains unclear. In this study, using mice homozygous for an Irx5-knockout (Irx5KO) allele, we show a direct link between Irx5 expression and regulation of body mass/composition and energy homeostasis. Irx5KO mice are leaner and resistant to diet-induced obesity and associated metabolic abnormalities, primarily through the loss of adiposity with an increase in basal metabolic rate with adipose thermogenesis and lower food intake. Furthermore, our long-term feeding analysis found that Irx3 mutant mouse lines also have less food intake, indicating that lower caloric intake also contributes to their lean phenotype. Together, these results demonstrate that Irx5 is critical for energy homeostasis and regulation of body mass/composition and suggest that it likely acts in other tissues beyond adipocytes.

Food hoarding is increased by food deprivation and decreased by leptin treatment in Syrian hamsters

2003 ◽  
Vol 285 (5) ◽  
pp. R1021-R1029 ◽  
Author(s):  
Carolyn A. Buckley ◽  
Jill E. Schneider
Keyword(s):  
Food Intake ◽  
Food Deprivation ◽  
Syrian Hamsters ◽  
Laboratory Rats ◽  
Hoarding Behavior ◽  
Increase Food Intake ◽  
Ad Libitum ◽  
Access To Food ◽  
Plasma Leptin ◽  
Rats And Mice

Compensatory increases in food intake are commonly observed after a period of food deprivation in many species, including laboratory rats and mice. Thus it is interesting that Syrian hamsters fail to increase food intake after a period of food deprivation, despite a fall in plasma leptin concentrations similar to those seen in food-deprived rats and mice. In previous laboratory studies, food-deprived Syrian hamsters increased the amount of food hoarded. We hypothesized that leptin treatment during food deprivation would attenuate food-deprivation-induced increases in hoarding. Baseline levels of hoarding were bimodally distributed, with no hamsters showing intermediate levels of hoarding. Both high (HH) and low hoarding (LH) hamsters were included in each experimental group. Fifty-six male hamsters were either food deprived or given ad libitum access to food for 48 h. One-half of each group received intraperitoneal injections of leptin (4 mg/kg) or vehicle every 12 h during the food-deprivation period. Within the HH group, the hoarding score increased significantly in food-deprived but not fed hamsters ( P < 0.05). Leptin treatment significantly decreased hoarding in the food-deprived HH hamsters ( P < 0.05). The LH hamsters did not increase hoarding regardless of whether they were food deprived or had ad libitum access to food. These results are consistent with the idea that HH hamsters respond to energetic challenges at least in part by changing their hoarding behavior and that leptin might be one factor that mediates this response.

scholarly journals Cold-induced hyperphagia requires AgRP neuron activation in mice

2020 ◽  
Author(s):  
Jennifer D. Deem ◽  
Chelsea L. Faber ◽  
Christian Pedersen ◽  
Bao Anh Phan ◽  
Sarah A. Larsen ◽  
...  
Keyword(s):  
Food Intake ◽  
Energy Expenditure ◽  
Energy Intake ◽  
Cold Exposure ◽  
Energy Homeostasis ◽  
Cold Environment ◽  
Energy Demands ◽  
Acute Cold Exposure ◽  
Neuron Activation ◽  
Increase Food Intake

ABSTRACTTo maintain energy homeostasis during cold exposure, the increased energy demands of thermogenesis must be counterbalanced by increased energy intake. To investigate the neurobiological mechanisms underlying this cold-induced hyperphagia, we asked whether agouti-related peptide (AgRP) neurons are activated when animals are placed in a cold environment and, if so, whether this response is required for the associated hyperphagia. We report that AgRP-neuron activation occurs rapidly upon acute cold exposure, as do increases of both energy expenditure and energy intake, suggesting the mere perception of cold is sufficient to engage each of these responses. We further report that silencing of AgRP neurons selectively blocks the effect of cold exposure to increase food intake. Together, these findings establish a physiologically important role for AgRP neurons in the hyperphagic response to cold exposure.

Obesity and adiposity: the culprit of dietary protein efficacy

2020 ◽  
Vol 134 (4) ◽  
pp. 389-401
Author(s):  
Carla El-Mallah ◽  
Omar Obeid
Keyword(s):  
Food Intake ◽  
Behavioural Change ◽  
Physiological Mechanism ◽  
Short Term ◽  
The Past ◽  
Body Adiposity ◽  
Reduce Sugar ◽  
Eye Opening ◽  
Potential Strategy ◽  
Limitations And Exceptions

Abstract Obesity and increased body adiposity have been alarmingly increasing over the past decades and have been linked to a rise in food intake. Many dietary restrictive approaches aiming at reducing weight have resulted in contradictory results. Additionally, some policies to reduce sugar or fat intake were not able to decrease the surge of obesity. This suggests that food intake is controlled by a physiological mechanism and that any behavioural change only leads to a short-term success. Several hypotheses have been postulated, and many of them have been rejected due to some limitations and exceptions. The present review aims at presenting a new theory behind the regulation of energy intake, therefore providing an eye-opening field for energy balance and a potential strategy for obesity management.

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