Energy expenditure and locomotor activity in mice selected for food intake adjusted for body weight

1990 ◽  
Vol 79 (1) ◽  
pp. 131-136 ◽  
Author(s):  
S. M. Moruppa
2008 ◽  
Vol 295 (2) ◽  
pp. E350-E355 ◽  
Author(s):  
Frank Isken ◽  
Andreas F. H. Pfeiffer ◽  
Rubén Nogueiras ◽  
Martin A. Osterhoff ◽  
Michael Ristow ◽  
...  

Menopause and premature gonadal steroid deficiency are associated with increases in fat mass and body weight. Ovariectomized (OVX) mice also show reduced locomotor activity. Glucose-dependent-insulinotropic-polypeptide (GIP) is known to play an important role both in fat metabolism and locomotor activity. Therefore, we hypothesized that the effects of estrogen on the regulation of body weight, fat mass, and spontaneous physical activity could be mediated in part by GIP signaling. To test this hypothesis, C57BL/6 mice and GIP-receptor knockout mice (Gipr−/−) were exposed to OVX or sham operation ( n = 10 per group). The effects on body composition, markers of insulin resistance, energy expenditure, locomotor activity, and expression of hypothalamic anorexigenic and orexigenic factors were investigated over 26 wk in all four groups of mice. OVX wild-type mice developed obesity, increased fat mass, and elevated markers of insulin resistance as expected. This was completely prevented in OVX Gipr−/− animals, even though their energy expenditure and spontaneous locomotor activity levels did not significantly differ from those of OVX wild-type mice. Cumulative food intake in OVX Gipr−/− animals was significantly reduced and associated with significantly lower hypothalamic mRNA expression of the orexigenic neuropeptide Y (NPY) but not of cocaine-amphetamine-related transcript (CART), melanocortin receptors (MCR-3 and MCR-4), or thyrotropin-releasing hormone (TRH). GIP receptors thus interact with estrogens in the hypothalamic regulation of food intake in mice, and their blockade may carry promising potential for the prevention of obesity in gonadal steroid deficiency.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A56-A56
Author(s):  
Karina Prins ◽  
Patric J Delhanty ◽  
Martin Huisman ◽  
Rosinda Mies ◽  
Anke McLuskey ◽  
...  

Abstract Ghrelin, a peptide hormone secreted by the stomach, stimulates both appetite and reward signalling. Its deletion in mice results in poor recovery from metabolic challenges, like starvation, but does not affect food intake or body weight. While sex differences in appetite and feeding behavior have been reported, little is known about the role of ghrelin herein. To investigate this, we used a metabolic cage system to continuously monitor responses of ghrelin-deficient (GKO) and wildtype (WT) mice to three different diets. Male and female mice (5 weeks old) were housed individually in a Promethion system (Sable Systems, USA) and provided one of three diets for 9 weeks: RA, continuous chow with restricted access to a Western-style diet (WD; 2h access, 3d/week) in the light phase; CA, continuous access to both diets; CC, continuous chow. Glucose tolerance was assessed at week 7 by IPGTT; food intake (kcal/g bodyweight), energy expenditure and locomotor activity at week 8; body weight and body composition (EchoMRI, USA) at week 9. On access days, RA mice ate up to 60% of their 24h intake during the WD access period. Following WD access GKO RA mice ate less chow than WT RA mice. Intriguingly, this compensatory reduction in food intake by GKO mice occurred at different times for males and females. GKO RA males ate 45% less chow in the dark phase immediately after WD access (p < 0.001). In contrast, this reduction in food intake (30% less) did not occur until the following, non-access, day in GKO RA females (genotype-sex: p < 0.05). Depending on diet, GKO mice showed differential regulation of energy expenditure in the light phase. Energy expenditure was 6–17% higher in GKO than WT mice in the RA group on access days and in the CA group. On non-access days, however, GKO mice in the RA group expended 13% less energy than WT RA mice (p < 0.005). Regardless of diet, locomotor activity in females was greater than in males (p < 0.001). However, GKO females in the RA and CC groups showed a marked 30% reduction in locomotor activity compared to WTs (genotype-sex: p < 0.05). After nine weeks, neither sex nor genotype effects were seen in body weight gain and composition of RA animals. CA females gained 17% more body weight and had a 6.1% higher fat percentage than CA males (both p < 0.001). In the CC group body weight gain did not differ, but GKO females had 3.1% more fat than WT females (genotype-sex: p < 0.01). Glucose tolerance (AUC) was similar in all groups. In conclusion, we demonstrated that ghrelin deficiency changes the response to the three diets in a sex-dependent manner. Especially, restricted access to WD differentially affected food intake timing and locomotor activity of male and female GKO mice. These results add to the growing body of evidence that ghrelin signalling is sexually dimorphic.


2007 ◽  
Vol 293 (5) ◽  
pp. R1855-R1863 ◽  
Author(s):  
Christine Mack ◽  
Julie Wilson ◽  
Jennifer Athanacio ◽  
James Reynolds ◽  
Kevin Laugero ◽  
...  

The ability of amylin to reduce acute food intake in rodents is well established. Longer-term administration in rats (up to 24 days) shows a concomitant reduction in body weight, suggesting energy intake plays a significant role in mediating amylin-induced weight loss. The current set of experiments further explores the long-term effects of amylin (4–11 wk) on food preference, energy expenditure, and body weight and composition. Furthermore, we describe the acute effect of amylin on locomotor activity and kaolin consumption to test for possible nonhomeostatic mechanisms that could affect food intake. Four-week subcutaneous amylin infusion of high-fat fed rats (3–300 μg·kg−1·day−1) dose dependently reduced food intake and body weight gain (ED50for body weight gain = 16.5 μg·kg−1·day−1). The effect of amylin on body weight gain was durable for up to 11 wks and was associated with a specific loss of fat mass and increased metabolic rate. The body weight of rats withdrawn from amylin (100 μg·kg−1·day−1) after 4 wks of infusion returned to control levels 2 wks after treatment cessation, but did not rebound above control levels. When self-selecting calories from a low- or high-fat diet during 11 wks of infusion, amylin-treated rats (300 μg·kg−1·day−1) consistently chose a larger percentage of calories from the low-fat diet vs. controls. Amylin acutely had no effect on locomotor activity or kaolin consumption at doses that decreased food intake. These results demonstrate pharmacological actions of amylin in long-term body weight regulation in part through appetitive-related mechanisms and possibly via changes in food preference and energy expenditure.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Joanna Moro ◽  
Catherine Chaumontet ◽  
Patrick C. Even ◽  
Anne Blais ◽  
Julien Piedcoq ◽  
...  

AbstractTo study, in young growing rats, the consequences of different levels of dietary protein deficiency on food intake, body weight, body composition, and energy balance and to assess the role of FGF21 in the adaptation to a low protein diet. Thirty-six weanling rats were fed diets containing 3%, 5%, 8%, 12%, 15% and 20% protein for three weeks. Body weight, food intake, energy expenditure and metabolic parameters were followed throughout this period. The very low-protein diets (3% and 5%) induced a large decrease in body weight gain and an increase in energy intake relative to body mass. No gain in fat mass was observed because energy expenditure increased in proportion to energy intake. As expected, Fgf21 expression in the liver and plasma FGF21 increased with low-protein diets, but Fgf21 expression in the hypothalamus decreased. Under low protein diets (3% and 5%), the increase in liver Fgf21 and the decrease of Fgf21 in the hypothalamus induced an increase in energy expenditure and the decrease in the satiety signal responsible for hyperphagia. Our results highlight that when dietary protein decreases below 8%, the liver detects the low protein diet and responds by activating synthesis and secretion of FGF21 in order to activate an endocrine signal that induces metabolic adaptation. The hypothalamus, in comparison, responds to protein deficiency when dietary protein decreases below 5%.


2010 ◽  
Vol 298 (5) ◽  
pp. R1409-R1416 ◽  
Author(s):  
Amy Warner ◽  
Preeti H. Jethwa ◽  
Catherine A. Wyse ◽  
Helen I'Anson ◽  
John M. Brameld ◽  
...  

The objective of this study was to determine whether the previously observed effects of photoperiod on body weight in Siberian hamsters were due to changes in the daily patterns of locomotor activity, energy expenditure, and/or feeding behavior. Adult males were monitored through a seasonal cycle using an automated comprehensive laboratory animal monitoring system (CLAMS). Exposure to a short-day photoperiod (SD; 8:16-h light-dark cycle) induced a significant decline in body weight, and oxygen consumption (V̇o2), carbon dioxide production (V̇co2), and heat production all decreased reaching a nadir by 16 wk of SD. Clear daily rhythms in locomotor activity, V̇o2, and V̇co2 were observed at the start of the study, but these all progressively diminished after prolonged exposure to SD. Rhythms in feeding behavior were also detected initially, reflecting an increase in meal frequency but not duration during the dark phase. This rhythm was lost by 8 wk of SD exposure such that food intake was relatively constant across dark and light phases. After 18 wk in SD, hamsters were transferred to a long-day photoperiod (LD; 16:8-h light-dark cycle), which induced significant weight gain. This was associated with an increase in energy intake within 2 wk, while V̇o2, V̇co2, and heat production all increased back to basal levels. Rhythmicity was reestablished within 4 wk of reexposure to long days. These results demonstrate that photoperiod impacts on body weight via complex changes in locomotor activity, energy expenditure, and feeding behavior, with a striking loss of daily rhythms during SD exposure.


2021 ◽  
Author(s):  
Sebastian Dieckmann ◽  
Akim Strohmeyer ◽  
Monja Willershaeuser ◽  
Stefanie Maurer ◽  
Wolfgang Wurst ◽  
...  

Objective Activation of uncoupling protein 1 (UCP1) in brown adipose tissue (BAT) upon cold stimulation leads to substantial increase in energy expenditure to defend body temperature. Increases in energy expenditure after a high caloric food intake, termed diet-induced thermogenesis, are also attributed to BAT. These properties render BAT a potential target to combat diet-induced obesity. However, studies investigating the role of UCP1 to protect against diet-induced obesity are controversial and rely on the phenotyping of a single constitutive UCP1-knockout model. To address this issue, we generated a novel UCP1-knockout model by Cre-mediated deletion of Exon 2 in the UCP1 gene. We studied the effect of constitutive UCP1 knockout on metabolism and the development of diet-induced obesity. Methods UCP1 knockout and wildtype mice were housed at 30°C and fed a control diet for 4-weeks followed by 8-weeks of high-fat diet. Body weight and food intake were monitored continuously over the course of the study and indirect calorimetry was used to determine energy expenditure during both feeding periods. Results Based on Western blot analysis, thermal imaging and noradrenaline test, we confirmed the lack of functional UCP1 in knockout mice. However, body weight gain, food intake and energy expenditure were not affected by deletion of UCP1 gene function during both feeding periods. Conclusion Conclusively, we show that UCP1 does not protect against diet-induced obesity at thermoneutrality. Further we introduce a novel UCP1-KO mouse enabling the generation of conditional UCP1-knockout mice to scrutinize the contribution of UCP1 to energy metabolism in different cell types or life stages.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Irene Cimino ◽  
Debra Rimmington ◽  
Y. C. Loraine Tung ◽  
Katherine Lawler ◽  
Pierre Larraufie ◽  
...  

AbstractNeuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.


1988 ◽  
Vol 255 (4) ◽  
pp. R616-R621 ◽  
Author(s):  
J. O. Hill ◽  
J. C. Anderson ◽  
D. Lin ◽  
F. Yakubu

The effects of differences in meal frequency on body weight, body composition, and energy expenditure were studied in mildly food-restricted male rats. Two groups were fed approximately 80% of usual food intake (as periodically determined in a group of ad libitum fed controls) for 131 days. One group received all of its food in 2 meals/day and the other received all of its food in 10-12 meals/day. The two groups did not differ in food intake, body weight, body composition, food efficiency (carcass energy gain per amount of food eaten), or energy expenditure at any time during the study. Both food-restricted groups had a lower food intake, body weight gain, and energy expenditure than a group of ad libitum-fed controls. In conclusion, these results suggest that amount of food eaten, but not the pattern with which it is ingested, has a major influence on energy balance during mild food restriction.


Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5855-5864 ◽  
Author(s):  
Jonathan D. Roth ◽  
Heather Hughes ◽  
Eric Kendall ◽  
Alain D. Baron ◽  
Christen M. Anderson

Effects of amylin and pair feeding (PF) on body weight and metabolic parameters were characterized in diet-induced obesity-prone rats. Peripherally administered rat amylin (300 μg/kg·d, 22d) reduced food intake and slowed weight gain: approximately 10% (P < 0.05), similar to PF. Fat loss was 3-fold greater in amylin-treated rats vs. PF (P < 0.05). Whereas PF decreased lean tissue (P < 0.05 vs. vehicle controls; VEH), amylin did not. During wk 1, amylin and PF reduced 24-h respiratory quotient (mean ± se, 0.82 ± 0.0, 0.81 ± 0.0, respectively; P < 0.05) similar to VEH (0.84 ± 0.01). Energy expenditure (EE mean ± se) tended to be reduced by PF (5.67 ± 0.1 kcal/h·kg) and maintained by amylin (5.86 ± 0.1 kcal/h·kg) relative to VEH (5.77 ± 0.0 kcal/h·kg). By wk 3, respiratory quotient no longer differed; however, EE increased with amylin treatment (5.74 ± 0.09 kcal/·kg; P < 0.05) relative to VEH (5.49 ± 0.06) and PF (5.38 ± 0.07 kcal/h·kg). Differences in EE, attributed to differences in lean mass, argued against specific amylin-induced thermogenesis. Weight loss in amylin and pair-fed rats was accompanied by similar increases arcuate neuropeptide Y mRNA (P < 0.05). Amylin treatment, but not PF, increased proopiomelanocortin mRNA levels (P < 0.05 vs. VEH). In a rodent model of obesity, amylin reduced body weight and body fat, with relative preservation of lean tissue, through anorexigenic and specific metabolic effects.


1964 ◽  
Vol 15 (6) ◽  
pp. 969 ◽  
Author(s):  
N McCGraham

The energy costs of standing, of rumination, of eating prepared meals, and of grazing were determined in laboratory experiments by indirect calorimetry. Sheep with body weights ranging from 30 to 110 kg were used. Energy expenditure due to standing amounted to 0.34 ± 0.02 kcal/hr/kg body weight. The energy cost of rumination was 0.24 ± 0.03 kcal/hr/kg. Rate of food intake varied from 60 g dry matter/hr with sheep grazing a poor sward to 800 g/hr with sheep eating hay, but in general this did not affect energy expenditure appreciably. The cost of eating prepared meals of either fresh herbage or hay was 0.54 ± 0.05 kcal/hr/kg body weight. It tended to be greatest when rate of food intake was greatest. Energy expenditure due to grazing was also 0.54 ± 0.05 kcal/hr/kg, irrespective of the type of sward and associated grazing behaviour. It is estimated that muscular work, mainly standing and eating, could account for nearly 40% of the daily energy expenditure of a sheep at maintenance, grazing a poor but level pasture, with drinking water available, and only 10% of that of a caged animal. Such a grazing animal could thus have requirements over 40% greater than those of a caged one. With sheep on hilly pasture or a long way from water, the cost of walking could become a major item.


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