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.

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.

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.

Metabolic response to a specific lipid-depleting factor in parabiotic rats

1986 ◽  
Vol 250 (2) ◽  
pp. R276-R286 ◽  
Author(s):  
R. B. Harris ◽  
R. J. Martin
Keyword(s):  
Fatty Acid ◽  
Body Fat ◽  
Metabolic Response ◽  
Tube Feeding ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Body Protein ◽  
Obese Rats ◽  
Ad Libitum

Parabiosis has been used as a technique for demonstrating the existence of a humoral factor in the control of body fat. The timing and metabolic basis for specific loss of fat from parabiotic partners of obese rats were examined. One member of a pair received 200% control intake, by stomach tube, for 8, 23, 39, or 57 days. Their partners ate 9.8 +/- 0.1 g/day. Members of ad libitum-fed pairs ate 9.6 +/- 0.1 g/day. All rats received the same diet. After 39 days, body fat in partners of obese rats was 6 +/- 1 g/rat compared with 17 +/- 1 g/rat in members of ad libitum pairs. Body protein was not different. In vitro hepatic fatty acid synthesis (FAS) and esterification (FAE) and inguinal FAS, FAE, and glycerol release suggested that fat loss was due to inhibition of adipose FAE. Partners of overfed rats and members of ad libitum pairs were then compared after 27 days of tube feeding when loss of fat was expected to be most rapid. Hepatic FAS, FAE, and fatty acid oxidation were the same for both groups. Inguinal FAS and FAE were decreased in partners of obese rats. An unidentified "lipid-depleting" agent, originating in obese rats, appears to inhibit adipose FAS and FAE in their partners independently of changes in feeding.

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

Diabesity: A Polygenic Model of Dietary-Induced Obesity from Ad Libitum Overfeeding of Sprague–Dawley Rats and Its Modulation by Moderate and Marked Dietary Restriction

2005 ◽  
Vol 33 (6) ◽  
pp. 650-674 ◽  
Author(s):  
Kevin P. Keenan ◽  
Chao-Min Hoe ◽  
Lori Mixson ◽  
Carol L. Mccoy ◽  
John B. Coleman ◽  
...  
Keyword(s):  
Body Fat ◽  
Dietary Restriction ◽  
Reproductive Organs ◽  
Multiple Organ ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Age Related ◽  
Organ Systems ◽  
Estrous Cyclicity ◽  
Ad Libitum

This study compared the effects of ad libitum (AL) overfeeding and moderate or marked dietary restriction (DR) on the pathogenesis of a metabolic syndrome of diabesity comprised of age-related degenerative diseases and obesity in a outbred stock of Sprague–Dawley (SD) rats [Crl:CD (SD) IGS BR]. SD rats were fed Purina Certified Rodent Diet AL (group 1), DR at 72–79% of AL (group 2), DR at 68–72% of AL (group 3) or DR at 47–48% of AL (group 4) for 106 weeks. Interim necropsies were performed at 13, 26, and 53 weeks, after a 7-day 5-bromo-2-deoxyuridine (BrdU)-filled minipump implantation. Body weights, organ weights, carcass analysis, in-life data including estrous cyclicity, and histopathology were determined. At 6–7 weeks of age SD rats had 6% body fat. AL-feeding resulted in hypertriglyceridemia, hypercholesterolemia, and dietary-induced obesity (DIO) by study week 14, with 25% body fat that progressed to 36–42% body fat by 106 weeks. As early as 14 weeks, key biomarkers developed for spontaneous nephropathy, cardiomyopathy, and degenerative changes in multiple organ systems. Early endocrine disruption was indicated by changes in metabolic and endocrine profiles and the early development and progression of lesions in the pituitary, pancreatic islets, adrenals, thyroids, parathyroids, liver, kidneys, and other tissues. Reproductive senescence was seen by 9 months with declines in estrous cyclicity and pathological changes in the reproductive organs of both sexes fed AL or moderate DR, but not marked DR. The diabesity syndrome in AL-fed, DIO SD rats was readily modulated or prevented by moderate to marked DR. Moderate DR of balanced diets resulted in a better toxicology model by significantly improving survival, controlling adult body weight and obesity, reducing the onset, severity, and morbidity of age-related renal, endocrine, metabolic, and cardiac diseases. Moderate DR feeding reduces study-to-study variability, increases treatment exposure time, and increases the ability to distinguish true treatment effects from spontaneous aging. The structural and metabolic differences between the phenotypes of DIO and DR SD rats indicated changes of polygenic expression over time in this outbred stock. AL-overfeeding of SD rats produces a needed model of DIO and diabesity that needs further study of its patterns of polygenic expression and phenotype.

scholarly journals Dietary thylakoids reduce visceral fat mass and increase expression of genes involved in intestinal fatty acid oxidation in high-fat fed rats

2016 ◽  
Vol 311 (3) ◽  
pp. R618-R627 ◽  
Author(s):  
Eva-Lena Stenblom ◽  
Emil Egecioglu ◽  
Caroline Montelius ◽  
Deepti Ramachandran ◽  
Britta Bonn ◽  
...  
Keyword(s):  
Body Weight ◽  
Fatty Acid ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Dietary Fat ◽  
Visceral Fat ◽  
Acid Oxidation ◽  
High Fat ◽  
Fat Accumulation

Thylakoids reduce body weight gain and body fat accumulation in rodents. This study investigated whether an enhanced oxidation of dietary fat-derived fatty acids in the intestine contributes to the thylakoid effects. Male Sprague-Dawley rats were fed a high-fat diet with ( n = 8) or without thylakoids ( n = 8) for 2 wk. Body weight, food intake, and body fat were measured, and intestinal mucosa was collected and analyzed. Quantitative real-time PCR was used to measure gene expression levels of key enzymes involved in fatty acid transport, fatty acid oxidation, and ketogenesis. Another set of thylakoid-treated ( n = 10) and control rats ( n = 10) went through indirect calorimetry. In the first experiment, thylakoid-treated rats ( n = 8) accumulated 25% less visceral fat than controls. Furthermore, fatty acid translocase ( Fat/Cd36), carnitine palmitoyltransferase 1a ( Cpt1a), and mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 ( Hmgcs2) genes were upregulated in the jejunum of the thylakoid-treated group. In the second experiment, thylakoid-treated rats ( n = 10) gained 17.5% less weight compared with controls and their respiratory quotient was lower, 0.86 compared with 0.91. Thylakoid-intake resulted in decreased food intake and did not cause steatorrhea. These results suggest that thylakoids stimulated intestinal fatty acid oxidation and ketogenesis, resulting in an increased ability of the intestine to handle dietary fat. The increased fatty acid oxidation and the resulting reduction in food intake may contribute to the reduced fat accumulation in thylakoid-treated animals.

Energy balance and brown adipose tissue thermogenesis during pregnancy in Syrian hamsters

1986 ◽  
Vol 250 (5) ◽  
pp. R845-R850 ◽  
Author(s):  
G. N. Wade ◽  
G. Jennings ◽  
P. Trayhurn
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Interscapular Brown Adipose Tissue ◽  
Estrous Cycles ◽  
Syrian Hamsters ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Circulating Levels

Energy balance and brown adipose tissue thermogenesis were examined during pregnancy in Syrian hamsters (Mesocricetus auratus). Neither estrous cycles nor pregnancy had any effect on food intake, but both were accompanied by significant changes in body weight. Despite their substantial weight gains (attributable to growth of fetuses and placentas), pregnant hamsters actually lost a mean of 48 kJ in carcass energy, whereas unmated controls gained 98 kJ over the same 15 days. During pregnancy hamsters exhibited an increase in protein deposition (almost entirely in the fetuses and placentas), but they lost nearly 40% of their body lipid. An apparent increase in energy expenditure occurred despite a highly significant decrease in brown adipose tissue thermogenesis during pregnancy. By day 15 of pregnancy (within 13 h of expected parturition) there were substantial decreases in interscapular brown adipose tissue weight (-59%), protein content (-54%), and cytochrome-c oxidase activity (-69%). These changes in brown adipose tissue were evident by day 4 of pregnancy and persisted through lactation. It is suggested that this suppression of brown adipose tissue function is due to increased circulating levels of prolactin and subsequently to the nutritional stress of conceptus growth in the absence of an increase in food intake.

Changes in environmental temperature influence leptin responsiveness in low- and high-fat-fed mice

2007 ◽  
Vol 293 (1) ◽  
pp. R106-R115 ◽  
Author(s):  
Ruth B. S. Harris ◽  
Tiffany D. Mitchell ◽  
Emily W. Kelso ◽  
W. P. Flatt
Keyword(s):  
Fatty Acid ◽  
Food Intake ◽  
Energy Expenditure ◽  
Fatty Acid Oxidation ◽  
Body Fat ◽  
Leptin Resistance ◽  
Positive Energy ◽  
Acid Oxidation ◽  
High Fat ◽  
Hot Environment

Loss of body fat in leptin-treated animals has been attributed to reduced energy intake, increased thermogenesis, and preferential fatty acid oxidation. Leptin does not decrease food intake or body fat in leptin-resistant high-fat (HF)-fed mice, possibly due to a failure of leptin to activate hypothalamic receptors. We measured energy expenditure of male C57BL/6 mice adapted to low-fat (LF) or HF diet and infused them for 13 days with PBS or 10 μg leptin/day from an intraperitoneal miniosmotic pump to test whether leptin resistance prevented leptin-induced increases in energy expenditure and fatty acid oxidation. There was no effect of low-dose leptin infusions on either of these measures in LF-fed or HF-fed mice, even though LF-fed mice lost body fat. Experiment 2 tested leptin responsiveness in LF-fed and HF-fed mice housed at different temperatures (18°C, 23°C, 27°C), assuming that the cold would increase and the hot environment would inhibit food intake and thermogenesis, which could potentially interfere with leptin action. LF-fed mice housed at 23°C were the only mice that lost body fat during leptin infusion, suggesting that an ability to modify energy expenditure is essential to the maintenance of leptin responsiveness. HF-fed mice in cold or warm environments did not respond to leptin. HF-fed mice in the hot environment were fatter than other HF-fed mice, and, surprisingly, leptin caused a further increase in body fat, demonstrating that the mice were not totally leptin resistant and that partial leptin resistance in a hot environment favors positive energy balance and fat deposition.

Specific depletion of body fat in parabiotic partners of tube-fed obese rats

1984 ◽  
Vol 247 (2) ◽  
pp. R380-R386 ◽  
Author(s):  
R. B. Harris ◽  
R. J. Martin
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Food Intake ◽  
Body Fat ◽  
Blood Samples ◽  
Reverse Triiodothyronine ◽  
Obese Rats ◽  
Ad Libitum ◽  
Beta Hydroxybutyrate ◽  
Normal Food

One member in each of 15 parabiosed pairs of rats was fed twice its normal food intake as four tube-fed meals per day. Seven other pairs ate ad libitum. Partners of overfed rats ate approximately 90% of the intake of individual members of ad libitum pairs. After 46 days of overfeeding, blood samples were taken and the rats were killed for carcass analysis. Tube-fed parabiotic rats had gained a considerable amount of fat and some protein. Their partners had a normal lean body mass but very little fat. Serum corticosterone, reverse triiodothyronine, free fatty acids, and beta-hydroxybutyrate were the same in all parabionts. Serum triiodothyronine and insulin were increased and growth hormone was decreased in obese rats. Serum thyroxine and triiodothyronine were increased and glucose was decreased in their parabiotic partners. The results are discussed as evidence for a humoral factor that crossed the parabiotic union and acted as a "lipid-depleting" agent in the partners of overfed rats.

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