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.

Insulin-induced anestrus in Syrian hamsters

1991 ◽  
Vol 260 (1) ◽  
pp. R148-R152 ◽  
Author(s):  
G. N. Wade ◽  
J. E. Schneider ◽  
M. I. Friedman
Keyword(s):  
Food Intake ◽  
Body Fat ◽  
Significant Inhibition ◽  
Acid Oxidation ◽  
Estrous Cycles ◽  
Syrian Hamsters ◽  
Metabolic Fuel ◽  
Energy Demands ◽  
Estrous Cyclicity ◽  
Ad Libitum

In Syrian hamsters, reproduction is sensitive to the availability of metabolic fuels. Estrous cycles can be interrupted by brief periods of food deprivation, by pharmacological inhibition of glycolysis and fatty acid oxidation, or by increasing energy demands for thermoregulation. We predicted that manipulations that divert an excessive portion of the metabolic fuel supply into storage also should inhibit reproduction. Redirection of metabolic fuels from oxidation to storage was accomplished by treatment with protamine zinc insulin suspension (PZI). Syrian hamsters treated with PZI and fed ad libitum increased their food intake by approximately equal to 40% and body fat stores, but there was no effect on estrous cycles. When PZI-treated hamsters were limited to approximately equal to 110% of their preinjection food intake, they still fattened, and there was a significant inhibition of estrous cyclicity. Thus, in the absence of overeating, PZI-enhanced energy storage may lead to a shortage of oxidizable metabolic fuels with the result that reproduction is inhibited in favor of processes essential for survival (e.g., cellular maintenance, thermoregulation). It is unlikely that insulin-induced anestrus is due to actions of PZI unrelated to metabolic fuel partitioning, because the hormone had no effects on estrous cyclicity in ad libitum-fed hamsters. These findings are inconsistent with the hypothesis that nutritional infertility is due to the failure to maintain a minimum body fat content and raise the possibility that the infertility associated with some types of obesity could be due in part to a disorder of macronutrient partitioning.

scholarly journals Interactive effects of central leptin and peripheral fuel oxidation on estrous cyclicity

1999 ◽  
Vol 277 (4) ◽  
pp. R1020-R1024 ◽  
Author(s):  
Jill E. Schneider ◽  
Dan Zhou
Keyword(s):  
Systemic Treatment ◽  
Chain Fatty Acid ◽  
Interactive Effects ◽  
Acid Oxidation ◽  
Long Chain Fatty Acid ◽  
Fasting Period ◽  
Fuel Oxidation ◽  
Estrous Cycles ◽  
Fuel Metabolism ◽  
Estrous Cyclicity

A 48-h period of fasting inhibits estrous cycles in Syrian hamsters, and fasting-induced anestrus can be prevented by intracerebroventricular treatment with leptin during the fasting period. In the present experiment, the effects of intracerebroventricular leptin were blocked by systemic treatment with inhibitors of metabolic fuel oxidation. Leptin was infused continuously into the lateral ventricles (1 μg/day) during fasting on days 1 and 2 of the estrous cycle. Intraperitoneal injection of 2-deoxy-d-glucose (2DG) was used to block both central and peripheral glucose oxidation, and intragastric treatment with methyl palmoxirate (MP) was used to inhibit peripheral long-chain fatty acid oxidation during the fasting and leptin-treatment period. 2DG or MP were administered at doses that did not induce anestrus in ad libitum-fed hamsters. Despite elevated central levels of leptin, fasting-induced anestrus occurred in hamsters treated with either 2DG or MP. Thus an elevated intracerebroventricular leptin concentration is not a sufficient condition for normal estrous cycles when fuel oxidation is inhibited. These results raise the possibility that central leptin influences reproduction by indirect effects on peripheral fuel metabolism.

Central vs. peripheral metabolic control of estrous cycles in Syrian hamsters. I. Lipoprivation

1997 ◽  
Vol 272 (1) ◽  
pp. R400-R405 ◽  
Author(s):  
J. E. Schneider ◽  
A. J. Hall ◽  
G. N. Wade
Keyword(s):  
Fatty Acid ◽  
Metabolic Control ◽  
Metabolic Energy ◽  
Acid Oxidation ◽  
Inhibitory Effects ◽  
Critical Signal ◽  
Estrous Cycles ◽  
Syrian Hamsters ◽  
Sham Surgery ◽  
Circulating Levels

Metabolic energy availability has profound effects on reproduction in a wide variety of species. We have been studying the effects of fasting on estrous cycles in Syrian hamsters as a model system for metabolic control of reproduction. In previous experiments, a 48-h period of fasting inhibited estrous cycles in lean, but not fat, hamsters. In fat hamsters the effects of fasting may have been offset by the presence of high circulating levels of free fatty acids mobilized from lipids in adipose tissue. Consistent with this idea fat hamsters treated with the inhibitor of fatty acid oxidation methyl palmoxirate (MP) showed fasting-induced anestrus. Experiment 1 was designed to examine whether vagally transmitted signals are critical for the inhibitory effects of fasting and MP treatment. Lean or fat hamsters that had received bilateral subdiaphragmatic vagotomy or sham surgery were fasted and treated with MP or vehicle. In vagotomized and sham-operated hamsters, estrous cycles were inhibited in lean fasted hamsters and in fat fasted hamsters treated with MP, but not in fat fasted hamsters treated with vehicle. Thus the results of experiment 1 indicated that vagally transmitted signals about peripheral fatty acid availability are not critical for the effects of these particular metabolic challenges on estrous cycles in Syrian hamsters. In experiment 2, hamsters without food were allowed to ingest pure glucose or fructose solutions or vegetable shortening. One-half of each group was treated with an inhibitor of glucose utilization, 2-deoxy-D-glucose (2-DG), or vehicle. If ingestion of fructose or shortening, but not glucose, had protected hamsters from 2-DG-induced anestrus, this might have indicated that peripheral fuel availability is critical for anestrus. On the contrary, 2-DG treatment induced anestrus regardless of the type of fuel ingested. Neither experiment yielded results that implicated changes in peripheral fuel availability as a critical signal in metabolic control of estrous cycles.

2,5-anhydro-D-mannitol: a fructose analogue that increases food intake in rats

1988 ◽  
Vol 254 (1) ◽  
pp. R150-R153 ◽  
Author(s):  
M. G. Tordoff ◽  
R. Rafka ◽  
M. J. DiNovi ◽  
M. I. Friedman
Keyword(s):  
Fatty Acids ◽  
Food Intake ◽  
Free Fatty Acids ◽  
Plasma Glucose ◽  
Ketone Bodies ◽  
Diabetic Rats ◽  
Substrate Analogues ◽  
Increase Food Intake ◽  
Related Increase

We examined the effects on food intake and plasma fuels of 2,5-anhydro-D-mannitol (2,5-AM; 2-deoxy-D-fructose), a fructose analogue that inhibits hepatocyte gluconeogenesis and glycogenolysis in vitro. 2,5-AM (50-800 mg/kg po) given to rats during the diurnal fast produced a dose-related increase in food intake during the 2 h after administration. A 200-mg/kg dose of 2,5-AM decreased plasma glucose, increased plasma ketone bodies, free fatty acids, and glycerol, and had no effect on triglycerides. Normal and diabetic rats given 2,5-AM (200 mg/kg ip) increased food intake to the same extent. These results suggest that, unlike other substrate analogues that increase food intake, 2,5-AM increases feeding by creating a metabolic state that resembles fasting.

scholarly journals Hourly analysis of cerebrospinal fluid glucose shows large diurnal fluctuations

2016 ◽  
Vol 36 (5) ◽  
pp. 899-902 ◽  
Author(s):  
Marcel M Verbeek ◽  
Wilhelmina G Leen ◽  
Michèl A Willemsen ◽  
Diane Slats ◽  
Jurgen A Claassen
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Plasma Glucose ◽  
Enzymatic Reactions ◽  
Glucose Levels ◽  
Fluid Analysis ◽  
Glucose Ratio ◽  
Influence Of Food ◽  
Energy Formation ◽  
Adult Volunteers

Cerebrospinal fluid analysis is important in the diagnostics of many neurological disorders. Since the influence of food intake on the cerebrospinal fluid glucose concentration and the cerebrospinal fluid/plasma glucose ratio is largely unknown, we studied fluctuations in these parameters in healthy adult volunteers during a period of 36 h. Our observations show large physiological fluctuations of cerebrospinal fluid glucose and the cerebrospinal fluid/plasma glucose ratio, and their relation to food intake. These findings provide novel insights into the physiology of cerebral processes dependent on glucose levels such as energy formation (e.g. glycolysis), enzymatic reactions (e.g. glycosylation), and non-enzymatic reactions (e.g. advanced endproduct glycation).

Role of fatty acid oxidation in food intake and hunger motivation in Syrian hamsters

1988 ◽  
Vol 43 (5) ◽  
pp. 617-623 ◽  
Author(s):  
Jill E. Schneider ◽  
Sandra J. Lazzarini ◽  
Mark I. Friedman ◽  
George N. Wade
Keyword(s):  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Syrian Hamsters ◽  
Hunger Motivation

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.

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.

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