Effects of exercise training on energy balance of ovariectomized rats

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.

1986 ◽  
Vol 60 (3) ◽  
pp. 1054-1059 ◽  
Author(s):  
D. Richard ◽  
J. Arnold ◽  
J. Leblanc

The present study was carried out to investigate the effects of exercise training on energy balance in male rats acclimated at two different environmental temperatures. Sedimentary and exercised rats were housed and trained at either 24 or 4 degrees C, with the training program consisting of running on a motor-driven treadmill within their respective environments. After 45 days, energy, protein, and fat contents of rats were determined together with the energy content of food and feces. The results show that metabolizable energy intake was reduced by 10% in exercise-trained groups. Substantial differences in energy gains were observed between sedentary and trained rats; sedentary rats showed almost three times more energy gain than trained rats. Carcass analysis revealed the energy gain differences to be mainly due to varied amounts of fat deposition. Energy expenditure (kJ) excluding the cost of exercise training was corrected for metabolic body size (BW 0.75), which in turn showed no significant differences between trained rats and their respective sedentary controls. The present results suggested that exercise training in rats leads to neither increase nor decrease in energy expenditure through components additional to physical activity. The present results also indicated that brown adipose tissue thermogenesis, as assessed through mitochondrial guanosine 5′-diphosphate binding, was not significantly modified by exercise training, regardless of the temperature at which the rats were housed and trained.


1989 ◽  
Vol 67 (4) ◽  
pp. 402-409 ◽  
Author(s):  
Denis Richard ◽  
Serge Rivest

The role of exercise training in energy balance has been reviewed. Recent well-conducted studies showed that exercise may increase energy expenditure not only during the period of exercise itself but during the postexercise period as well. This notion of excess postexercise oxygen consumption (EPOC), which has been a controversial issue for many years, is now becoming a generally well-accepted concept, the consensus being that EPOC takes place following prolonged and strenuous exercise bouts. Besides, the role of EPOC in long-term energy balance remains to be determined. Long-term energy balance studies carried out in rats show that exercise affects energy balance by altering food intake and promoting energy expenditure. In male rats exercise causes a marked decrease in energy intake which contributes, in association with the expenditure of exercise itself, to retard lean and fat tissue growth. From the suppressed deposition of lean body mass, decreases in basal metabolic rate can be predicted in males. In female rats, exercise does not affect food intake; the lower energy gain of exercise-trained females results from the elevated expenditure rate associated with exercise itself. In both male and female rats, there is no evidence that exercise training affects energy expenditure other than during exercise itself unless the habitual feeding pattern of the rats is radically modified. The interactive effects of diet and exercise, which have to be further investigated in long-term energy balance, emerge as a promising area of research.Key words: exercise training, nutritional energetics, brown adipose tissue, diet-induced thermogenesis, body composition.


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)


1986 ◽  
Vol 250 (2) ◽  
pp. R245-R249 ◽  
Author(s):  
D. Richard

This study was carried out to investigate the nutritional energetics of ovariectomized rats with or without ovarian hormone replacement. Rats were divided into five groups: 1) sham operated, 2) ovariectomized, 3) ovariectomized and treated with progesterone, 4) ovariectomized and treated with estradiol, or 5) ovariectomized and treated with estradiol and progesterone. After 36 days of treatment, energy contents of all five groups were determined together with energy content of food and feces. Brown adipose tissue thermogenesis was assessed through mitochondrial GDP binding assay. Results show that ovariectomy leads to a 16% increase in metabolizable energy intake. This increase was accompanied by a twofold increase in body energy gain. Progesterone did not further affect energy intake and gain in ovariectomized rats. However, increases in both food intake and energy gain were prevented by the estradiol replacement therapy. There was no difference in energy expenditure between sham-operated and ovariectomized rats in the absence of estradiol. In estradiol-treated animals, energy expenditure (kJ.kg body wt-0.75 . day-1) showed a slight increase. There was no difference in protein content of interscapular brown adipose tissue between all five groups. GDP binding was slightly reduced in ovariectomized estradiol-treated rats. It is concluded from this study that ovarian hormones produce their effects on energy balance mainly by altering food intake.


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)


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.


1989 ◽  
Vol 67 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Jean Himms-Hagen

Obligatory thermogenesis is a necessary accompaniment of all metabolic processes involved in maintenance of the body in the living state, and occurs in ail organs. It includes energy expenditure involved in ingesting, digesting, and processing food (thermic effect of food (TEF)). At certain life stages extra energy expenditure for growth, pregnancy, or lactation would also be obligatory. Facultative thermogenesis is superimposed on obligatory thermogenesis and can be rapidly switched on and rapidly suppressed by the nervous system. Facultative thermogenesis is important in both thermal balance, in which control of thermoregulatory thermogenesis (shivering in muscle, nonshivering in brown adipose tissue (BAT)) balances neural control of heat loss mechanisms, and in energy balance, in which control of facultative thermogenesis (exercise-induced in muscle, diet-induced thermogenesis (DIT) in BAT) balances control of energy intake. Thermal balance (i.e., body temperature) is much more stringently controlled than energy balance (i.e., body energy stores). Reduced energy expenditure for thermogenesis is important in two types of obesity in laboratory animals. In the first type, deficient DIT in BAT is a prominent feature of altered energy balance. It may or may not be associated with hyperphagia. In a second type, reduced cold-induced thermogenesis in BAT as well as in other organs is a prominent feature of altered thermal balance. This in turn results in altered energy balance and obesity, exacerbated in some examples by hyperphagia. In some of the hyperphagic obese animals it is likely that the exaggerated obligatory thermic effect of food so alters thermal balance that BAT thermogenesis is suppressed. In all obese animals, deficient hypothalamic control of facultative thermogenesis and (or) food intake is implicated.Key words: thermogenesis, brown adipose tissue, energy balance, obesity, cold, thermoregulation, diet.


2014 ◽  
Vol 221 (3) ◽  
pp. 381-390 ◽  
Author(s):  
Gustavo W Fernandes ◽  
Cintia B Ueta ◽  
Tatiane L Fonseca ◽  
Cecilia H A Gouveia ◽  
Carmen L Lancellotti ◽  
...  

Three types of beta adrenergic receptors (ARβ1–3) mediate the sympathetic activation of brown adipose tissue (BAT), the key thermogenic site for mice which is also present in adult humans. In this study, we evaluated adaptive thermogenesis and metabolic profile of a mouse withArβ2knockout (ARβ2KO). At room temperature, ARβ2KO mice have normal core temperature and, upon acute cold exposure (4 °C for 4 h), ARβ2KO mice accelerate energy expenditure normally and attempt to maintain body temperature. ARβ2KO mice also exhibited normal interscapular BAT thermal profiles during a 30-min infusion of norepinephrine or dobutamine, possibly due to marked elevation of interscapular BAT (iBAT) and ofArβ1, andArβ3mRNA levels. In addition, ARβ2KO mice exhibit similar body weight, adiposity, fasting plasma glucose, cholesterol, and triglycerides when compared with WT controls, but exhibit marked fasting hyperinsulinemia and elevation in hepaticPepck(Pck1) mRNA levels. The animals were fed a high-fat diet (40% fat) for 6 weeks, ARβ2KO mice doubled their caloric intake, accelerated energy expenditure, and inducedUcp1expression in a manner similar to WT controls, exhibiting a similar body weight gain and increase in the size of white adipocytes to the WT controls. However, ARβ2KO mice maintain fasting hyperglycemia as compared with WT controls despite very elevated insulin levels, but similar degrees of liver steatosis and hyperlipidemia. In conclusion, inactivation of the ARβ2KO pathway preserves cold- and diet-induced adaptive thermogenesis but disrupts glucose homeostasis possibly by accelerating hepatic glucose production and insulin secretion. Feeding on a high-fat diet worsens the metabolic imbalance, with significant fasting hyperglycemia but similar liver structure and lipid profile to the WT controls.


2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  

Loss of body weight and fat mass is one of the nonmotor symptoms of Parkinson’s disease (PD). Weight loss is due primarily to reduced energy intake and increased energy expenditure. Whereas inadequate energy intake in PD patients is caused mainly by appetite loss and impaired gastrointestinal absorption, the underlying mechanisms for increased energy expenditure remain largely unknown. Brown adipose tissue (BAT), a key thermogenic tissue in humans and other mammals, plays an important role in thermoregulation and energy metabolism; however, it has not been tested whether BAT is involved in the negative energy balance in PD. Here, using the 6-hydroxydopamine (6-OHDA) rat model of PD, we found that the activity of sympathetic nerve (SN), the expression of Ucp1 in BAT, and thermogenesis were increased in PD rats. BAT sympathetic denervation blocked sympathetic activity and decreased UCP1 expression in BAT and attenuated the loss of body weight in PD rats. Interestingly, sympathetic denervation of BAT was associated with decreased sympathetic tone and lipolysis in retroperitoneal and epididymal white adipose tissue. Our data suggeste that BAT-mediated thermogenesis may contribute to weight loss in PD.


2016 ◽  
Vol 11 (1) ◽  
pp. 212 ◽  
Author(s):  
Saudy Saret Pablo-Pérez ◽  
María Mirian Estévez-Carmona ◽  
María Estela Meléndez-Camargo

<p class="Abstract">The aim of this study was to evaluate the diuretic activity of <em>Eysenhardtia polystachya</em> bark aqueous extract at different doses in a rat model. Different doses of <em>E. polystachya</em> (125, 250, 500 and 750 mg/kg body weight), furosemide (4 mg/kg) and vehicle were administered per os to female rats (n=6 animals per group). After 6 hours in metabolic cages, the effect on urinary flow, glomerular filtration rate and electrolyte balance of sodium and potassium were assessed in all animals. <em>E. polystachya</em> at the doses of 500 and 750 mg/kg induced diuretic activity, since markedly increased (p&lt;0.05) the urinary flow rate, similar to that of furosemide treated group. Only the dose of 750 mg/kg produced an increment in urinary excretion of sodium but not of potassium compared with control group. These findings indicate that<em> E. polystachya</em> bark-induced diuretic activity, providing evidence for its folkloric use.</p><p> </p>


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