Effect of exercise training on energy balance of orchidectomized rats

1989 ◽  
Vol 257 (3) ◽  
pp. R550-R555 ◽  
Author(s):  
S. Rivest ◽  
J. Landry ◽  
D. Richard

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and testosterone on energy balance. Male rats were divided into sedentary and exercise-trained groups. Each group formed was further divided into a sham-operated group, an orchidectomized group, or an orchidectomized group treated with testosterone. Rats were exercised on a motor-driven treadmill for 1 h/day over 28 consecutive days, after which rats were killed. Energy balance measurements, body composition analyses, and serum testosterone assay were then performed. The weight, protein content, and cytochrome-c oxidase activity of interscapular brown adipose tissue (IBAT) were also measured. Results indicate that total food intake, final body weight, and body weight gain were generally lower in exercise-trained rats than in sedentary animals. In orchidectomized rats treated with testosterone, gains of both fat and protein were lower in exercise-trained than in sedentary animals. There was no difference in metabolizable energy intake and body energy gain between trained and sedentary rats that underwent orchidectomy without replacement therapy. In orchidectomized groups of rats, energy gain was lower in trained rats that were treated with testosterone than in those that did not receive any treatment. Furthermore, in trained orchidectomized rats treated with testosterone, both energetic efficiency and energy density of body weight gain were lower than those of trained orchidectomized rats that were not treated. Finally, a significant reduction in IBAT weight was observed in exercise-trained animals, whereas neither exercise nor the various hormonal manipulations affected IBAT protein content and cytochrome-c oxidase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

2020 ◽  
Vol 5 (2) ◽  
pp. 40-47
Author(s):  
I. Irmawaty ◽  
Tuti Widjastuti ◽  
Asep Anang ◽  
Muhammad Nur Hidayat

This experiment shows performance chickens of Kedu, Arab, and Poncin with Giffen different protein content.  This experiment uses chickens of Kedu, Arab, and Poncin (a crossbreed of male Arab and female Kedu) that each breed consists of 40 Day Old Chicken. Each species was randomly placed in 8 units of experiment cage, and every experiment cage consists of 5 Day Old Chicken.  Treatment dietary is used 15% (R1) dan 18% (R2).  The experiment's design is used a completely random design 2x3 factorial, that i two treatments of dietary and three breeds of chickens. Every treatment is replayed four times, and the show used 24 units of experiment cage.  The parameter is limited watch on dietary Consumption, body weight gain, and feed conversion. The result showed that Poncin chickens gave better growth performance when compared to Arab and Kedu chickens. Simultaneously, the ration protein content of 18 % resulted in better growth performance compared to 15% ration protein.


Author(s):  
Lauren M. Stein ◽  
Lauren E McGrath ◽  
Rinzin Lhamo ◽  
Kieran Koch-Laskowski ◽  
Samantha M. Fortin ◽  
...  

The peptide hormone amylin reduces food intake and body weight, and is an attractive candidate target for novel pharmacotherapies to treat obesity. However, the short half-life of native amylin and amylin analogs like pramlintide limits these compounds' potential utility in promoting sustained negative energy balance. Here, we evaluate the ability of the novel long-acting amylin/calcitonin receptor agonist ZP5461 to reduce feeding and body weight in rats, and also test the role of calcitonin receptors (CTRs) in the dorsal vagal complex (DVC) of the hindbrain in the energy balance effects of chronic ZP5461 administration. Acute dose-response studies indicate that systemic ZP5461 (0.5-3 nmol/kg) robustly suppresses energy intake and body weight gain in chow- and high-fat diet (HFD)-fed rats. When HFD-fed rats received chronic systemic administration of ZP5461 (1-2 nmol/kg), the compound initially produced reductions in energy intake and weight gain, but failed to produce sustained suppression of intake and body weight. Using virally-mediated knockdown of DVC CTRs, the ability of chronic systemic ZP5461 to promote early reductions in intake and body weight gain was determined to be mediated in part by activation of DVC CTRs, implicating the DVC as a central site of action for ZP5461. Future studies should address other dosing regimens of ZP5461 to determine whether an alternative dose/frequency of administration would produce more sustained body weight suppression.


1987 ◽  
Vol 253 (5) ◽  
pp. R740-R745 ◽  
Author(s):  
D. Richard ◽  
L. Rochon ◽  
Y. Deshaies ◽  
R. Denis

The purpose of the present study was to investigate both the respective and interactive roles of exercise training and ovarian hormones on the regulation of energy balance. Female rats were divided into sedentary and exercise-trained groups. Each group thus formed was further divided into a sham-operated group, an ovariectomized group, or ovariectomized estradiol-treated group. Rats were exercise trained on a rodent motor-driven treadmill. After 33 days of treatment, rats were killed and the energy contents of carcasses, feces, and food were determined. Brown adipose tissue (BAT) thermogenesis was assessed through mitochondrial GDP binding. The results show that ovariectomy led to increases in food intake, body weight, and protein gains, whereas estradiol treatment abolished these effects. The results also show that exercise training reduced fat gain. Exercise training interacted with ovariectomy on energy gain; in sedentary rats ovariectomy enhanced the energy gain, an effect that disappeared in exercise-trained rats. However, exercise training was found to alter neither body weight and protein gains nor energy intake. Ovariectomy did not affect energy expenditure when the results are expressed in relative terms (kJ.kg body wt-0.67.day-1). Similarly, exercise training did not modify energy expenditure (kJ.kg body wt-0.67.day-1) once the cost of the training program was subtracted. BAT mitochondrial GDP binding was not affected by any of the experimental treatments. The present results therefore suggest that neither ovariectomy nor exercise training affect energy expenditure through regulatory forms of BAT-mediated thermogenesis.


Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4246-4255 ◽  
Author(s):  
Roxanne Dutia ◽  
Kana Meece ◽  
Shveta Dighe ◽  
Andrea J. Kim ◽  
Sharon L. Wardlaw

Proopiomelanocortin (POMC) is posttranslationally processed to several peptides including α-MSH, a primary regulator of energy balance that inhibits food intake and stimulates energy expenditure. However, another POMC-derived peptide, β-endorphin (β-EP), has been shown to stimulate food intake. In this study we examined the effects of intracerebroventricular (icv) β-EP on food intake and its ability to antagonize the negative effects of α-MSH on energy balance in male rats. A single icv injection of β-EP stimulated food intake over a 2- to 6-h period during both the light and dark cycles. This effect was, however, not sustained with chronic icv β-EP infusion. In the next study, a subthreshold dose of β-EP was injected together with Nle4, d-Phe7 (NDP)-MSH after a 16-h fast, and the negative effects of NDP-MSH on refeeding and body weight gain were partially reversed. Finally, peptide interactions were studied in a chronic icv infusion model. Weight gain and food intake were significantly suppressed in the NDP-MSH group during the entire study. A subthreshold dose of β-EP antagonized these suppressive effects on food intake and weight gain for the first 3 d. However on d 4–7, β-EP no longer blocked these effects. Of note, the stimulatory effect of β-EP on feeding and its ability to antagonize MSH were specific for β-EP1–31 and were not observed with β-EP1–27. This study highlights the importance of understanding how the balance between α-MSH and β-EP is maintained and the potential role of differential POMC processing in regulating energy balance.


2002 ◽  
Vol 9 (4) ◽  
pp. 771-776 ◽  
Author(s):  
Frédéric Picard ◽  
Denis Arsenijevic ◽  
Denis Richard ◽  
Yves Deshaies

ABSTRACT Infection of male Swiss Webster mice with Toxoplasma gondii or Neospora caninum leads to long-term alterations in energy balance. Following an initial 20 to 30% weight loss in all T. gondii-infected mice, half of the animals regain most of the lost weight (gainers), whereas the others maintain their low body weight (nongainers). Infection with N. caninum does not elicit weight loss. Lipoprotein lipase (LPL), the enzyme responsible for plasma triglyceride (TG) clearance and partitioning among tissues, is under tissue-specific modulation associated with energy balance. It is also a major determinant of infection-induced hypertriglyceridemia. This study aimed to assess the long-term modulation of adipose and muscle LPL activity in mice infected with T. gondii or N. caninum, to evaluate the effects of subsequent acute lipopolysaccharide (LPS) administration, and to relate LPL modulation in these conditions with infection-related changes in body weight gain. Twenty-eight days after infection, LPL activity in muscle of both gainer and nongainer T. gondii-infected mice was reduced by 40 to 50% compared with the levels in controls and N. caninum-infected mice, whereas LPL activity in adipose depots remained unchanged in all infected groups compared to the level in controls. LPS (from Escherichia coli, 100 ng/kg) injection induced a global reduction in adipose LPL in all groups, as assessed 90 min later. In both T. gondii-infected subgroups, muscle LPL was not further reduced by LPS treatment, whereas it was decreased by 40 to 50% in muscles of control and N. caninum-infected mice. Pre-LPS TG levels in plasma were similar in all groups. LPS greatly increased TG levels in plasma in both control and N. caninum-infected animals, whereas it did not alter those of T. gondii-infected gainer or nongainer animals. These results show that (i) independently of the extent of postinfection weight gain, long-term infection with T. gondii chronically reduces muscle LPL, which becomes unresponsive to acute endotoxemia; (ii) modulation of tissue LPL activity during chronic T. gondii infection favors TG partitioning towards adipose tissue; and (iii) skeletal muscle LPL is a key determinant of the acute response of triglyceridemia to LPS.


1989 ◽  
Vol 66 (4) ◽  
pp. 1970-1975 ◽  
Author(s):  
J. Arnold ◽  
R. A. Little ◽  
N. J. Rothwell

The effects of continuously administered endotoxin on 7-day energy balance were investigated in male rats. Three groups of rats were implanted with osmotic pumps; two groups received saline-filled pumps, whereas the third received endotoxin. One of the saline groups was pair fed to match the food intake of the endotoxemic rats. After 7 days, body energy and protein and fat contents of rats were determined together with the energy content of food and feces. Endotoxin infusion not only induced fever, but it also suppressed appetite and significantly decreased body weight gain. Metabolizable energy intake was reduced by approximately 20% in infected rats. Although protein and fat gains were lowest in the endotoxin group, there appeared to be a selective loss of protein when considered as percent of body weight. Percent body fat was unaltered between the groups. Energy expenditure considered in absolute (kJ) or body weight-independent (kJ/kg0.67) terms yielded similar patterns of results; expenditure (kJ) was 10 and 20% (P less than 0.05, P less than 0.01) lower in the endotoxemic and pair-fed rats, respectively, compared with controls. Hence, compared with pair-fed rats, endotoxin-infused animals had a 10% rise in their expenditure. Brown adipose tissue thermogenesis was assessed by mitochondrial binding of guanosine 5′-diphosphate, and results showed that binding was greatest in endotoxemic rats and lowest in the pair-fed animals. The present results suggest that in this endotoxemic model appetite suppression exacerbates changes in energy balance. However, the reduction in body weight gain is also dependent on a decrease in metabolic efficiency and an increase in total energy expenditure.(ABSTRACT TRUNCATED AT 250 WORDS)


1990 ◽  
Vol 68 (2) ◽  
pp. 520-526 ◽  
Author(s):  
C. B. Dolkas ◽  
K. J. Rodnick ◽  
C. E. Mondon

The objectives of this study were to determine how long increased insulin sensitivity, elicited by exercise training, persists after the end of training and what the effect of weight gain is on this retention. Exercise-trained (ET) rats ran voluntarily in freely rotating wheel cages, and insulin sensitivity was assessed by oral glucose tolerance tests (OGTT) and insulin suppression tests (IST). After training, ET rats were retired for 1, 3, or 7 days (R1, R3, or R7). Initial OGTT and IST studies indicated that sensitivity to insulin-induced glucose uptake was increased in ET rats compared with sedentary control (C) rats and was progressively lost with retirement: ET greater than R1 and R3 greater than R7 and C rats, and this reaction was generally associated with a rapid gain in body weight. Subsequent IST tests were performed on C and R7 rats fed laboratory chow or a hypocaloric diet consisting of equal parts of cellulose and chow for 7 days before the test. The results of these tests showed that steady-state serum glucose (SSSG) levels averaged 165 +/- 12 mg/dl for chow-fed C rats and 172 +/- 11 mg/dl for chow-fed R7 rats that gained body weight at rates twice those of C rats. Chow-fed R7 rats, gaining weight at rates comparable to C rats, had SSSG levels of 104 +/- 6 mg/dl. C and R7 rats fed the hypocaloric diet had SSSG values of 102 +/- 6 and 59 +/- 4 mg/dl, respectively. Muscle glycogen levels were comparable in all groups, and liver glycogen was lower in C and R7 rats fed the hypocaloric diet.(ABSTRACT TRUNCATED AT 250 WORDS)


1977 ◽  
Vol 232 (5) ◽  
pp. E510
Author(s):  
K A Houpt ◽  
T R Houpt ◽  
W G Pond

The energy balance of suckling Yorkshire pigs 1 day to 2 wk old was challenged by: food deprivation, glucoprivation, and caloric and noncaloric gastric loads delivered by intubation. tafter 2--4 h fasts, food intake greatly increased over nonfasted control intake during a 3-h refeeding period. This response occurred both when body weight gain was used as a measure of intake for pigs nursing on the sow and when intake was measured directly in bottle-fed pigs. Glucoprivation produced by 0.5--2 U/kg insulin did not stimulate food intake although plasma glucose fell to a mean of 49 mg/100 ml (43% of control) after 1 U/kg insulin. Gastric loads of water or 3% NACl depressed intake after 3-h fast, but 0.9% NaCl did not. All the caloric gastric loads depressed intake; in order of increasing effectiveness, they were: heavy cream, protein hydrolysate, corn oil, milk, 5% glucose, and 5% lactose. The carbohydrate loads were most effective, a result which indicates that the response was not to calories alone but to some specific nutrient, possibly glucose.


1982 ◽  
Vol 52 (3) ◽  
pp. 556-561 ◽  
Author(s):  
J. Leblanc ◽  
J. Dussault ◽  
D. Lupien ◽  
D. Richard

Male and female rats were fed standard laboratory chow or a highly palatable diet (cafeteria diet) for 10 wk. The cafeteria diet caused an increase in caloric intake and in body weight, and it induced thermogenesis that was associated with elevated plasma triiodothyronine (T3) levels, increased brown adipose tissue size, and enhanced metabolic response to norepinephrine. For a comparable caloric intake, body-weight gain was significantly greater in female than in male rats possibly because of difference in thermogenesis as suggested by the response to norepinephrine. Exercise training (swimming 2 h/day for 10 wk) reduced food intake and body-weight gain and failed to increase norepinephrine-induced thermogenesis in rats fed laboratory chow. In animals fed the cafeteria diet, food intake and body-weight gain were also reduced by exercise training, which at the same time diminished the diet-induced thermogenesis as evidenced by the diminution of 1) brown fat hypertrophy, 2) the elevation of plasma T3, and 3) the hyperthermic response to injected norepinephrine. It is suggested that the thyroid hormone and catecholamines through their actions on the brown adipose tissue are the important regulatory of thermogenesis. Exercise training would reduce the diet-induced thermogenesis by preventing increased T3 production. Enhanced thermogenesis may be considered an adaptive reaction as it serves to reduce fat deposition in animals fed cafeteria diet and to promote nonshivering heat production in the cold. On the other hand, exercise training reduces thermogenesis and thus prevents energy wasting.


1988 ◽  
Vol 60 (2) ◽  
pp. 355-360 ◽  
Author(s):  
Nancy J. Rothwell ◽  
Michael J. Stock

1. Daily injection of the β2-adrenergic agonist clenbuterol (1 mg/kg body-weight) increased weight gain by 12% in young (35 d) male rats and by 18% in castrated rats, but had no effect on energy intake, expenditure or efficiency in either group.2. Body fat content was not affected by clenbuterol or castration, but water and protein content were significantly increased by clenbuterol treatment in both intact and castrated rats. The ratio, body protein:fat was increased by 13 and 16% in these two groups compared with their respective, untreated controls.3. Bilateral surgical adrenalectomy (ADX) of young (45 d) male rats significantly reduced body-weight, and energy intake, expenditure and efficiency. Carcass energy and fat contents were also reduced in ADX rats compared with age-matched controls.4. Clenbuterol injections stimulated weight gain (% increase: intact 15, ADX 35), and increased body protein content (% increase: intact 12, ADX 8) and the ratio, carcass protein:fat (% increase: intact 34, ADX 23).5. These findings demonstrate that the effects of clenbuterol on body-weight gain and composition in male rats occur in the absence of either gonadal or adrenal hormones. Together with other studies, these results provide further evidence to suggest that clenbuterol probably exerts its effects by a direct action on lean body mass.


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