Energy expenditure is reduced in preobese 2-day Zucker fa/fa rats

1985 ◽  
Vol 249 (2) ◽  
pp. R262-R265 ◽  
Author(s):  
B. J. Moore ◽  
S. J. Armbruster ◽  
B. A. Horwitz ◽  
J. S. Stern
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Body Size ◽  
Energy Expenditure ◽  
Body Mass ◽  
Early Age ◽  
Ambient Temperatures ◽  
Consumption Data ◽  
Brown Adipose ◽  
Rate Of Oxygen Consumption

The rate of oxygen consumption was measured in 2-day Zucker preobese (fa/fa), homozygous (Fa/Fa) lean, and lean rats of unknown genotype (Fa/?) over the ambient temperature range of 26-35 degrees C. Significant differences in body mass were found among the three groups at this early age, the preobese pups having the greatest body mass. To account for body mass differences, the oxygen consumption data were expressed in terms of metabolic body size (ml O2 consumed X g body mass-2/3 X h-1). This mass-independent rate of oxygen consumption was significantly lower in the preobese pups than in the homozygous lean (Fa/Fa) pups at both thermoneutral (33-34 degrees C) and cold (26-27 degrees C) ambient temperatures at which, respectively, minimal and maximal rates of oxygen consumption were observed. This reduction in energy expenditure occurs before the establishment of hyperphagia or decreased levels of activity in the preobese pups. These data support the view that attenuated energy expenditure is a significant contributor to the early development of obesity in the Zucker fatty rat and point to the possibility of defective brown adipose tissue-mediated thermogenesis in the preobese pup.

scholarly journals Effects of Chronic Intracerebroventricular Infusion of RFamide-Related Peptide-3 on Energy Metabolism in Male Mice

2020 ◽  
Vol 21 (22) ◽  
pp. 8606
Author(s):  
Shogo Moriwaki ◽  
Yuki Narimatsu ◽  
Keisuke Fukumura ◽  
Eiko Iwakoshi-Ukena ◽  
Megumi Furumitsu ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Food Intake ◽  
Energy Expenditure ◽  
Body Mass ◽  
The Other ◽  
Related Peptide ◽  
Intracerebroventricular Infusion ◽  
Brown Adipose ◽  
The Masses

RFamide-related peptide-3 (RFRP-3), the mammalian ortholog of avian gonadotropin-inhibitory hormone (GnIH), plays a crucial role in reproduction. In the present study, we explored the other functions of RFRP-3 by investigating the effects of chronic intracerebroventricular infusion of RFRP-3 (6 nmol/day) for 13 days on energy homeostasis in lean male C57BL/6J mice. The infusion of RFRP-3 increased cumulative food intake and body mass. In addition, the masses of brown adipose tissue (BAT) and the liver were increased by the administration of RFRP-3, although the mass of white adipose tissue was unchanged. On the other hand, RFRP-3 decreased O2 consumption, CO2 production, energy expenditure, and core body temperature during a short time period in the dark phase. These results suggest that the increase in food intake and the decrease in energy expenditure contributed to the gain of body mass, including the masses of BAT and the liver. The present study shows that RFRP-3 regulates not only reproductive function, but also energy metabolism, in mice.

scholarly journals Gqα/G11α deficiency in dorsomedial hypothalamus leads to obesity resulting from decreased energy expenditure and impaired sympathetic nerve activity

2020 ◽  
Author(s):  
Eric A. Wilson ◽  
Hui Sun ◽  
Zhenzhong Cui ◽  
Marshal T. Jahnke ◽  
Mritunjay Pandey ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Expenditure ◽  
Energy Homeostasis ◽  
Dorsomedial Hypothalamus ◽  
Ambient Temperatures ◽  
Brown Adipose ◽  
Inhibit Food Intake ◽  
Specific Deletion

The G protein subunits Gqα and G11α (Gq/11α) couple receptors to phospholipase C, leading to increased intracellular calcium. In this study we investigated the consequences of Gq/11α deficiency in the dorsomedial hypothalamus (DMH), a critical site for the control of energy homeostasis. Mice with DMH-specific deletion of Gq/11α (DMHGq/11KO) were generated by stereotaxic injection of AAV-Cre-GFP into the DMH of Gqαflox/flox:G11α-/- mice. Compared to control mice that received DMH injection of AAV-GFP, DMHGq/11KO mice developed obesity associated with reduced energy expenditure without significant changes in food intake or physical activity. DMHGq/11KO mice showed no defects in the ability of the melanocortin agonist melanotan II to acutely stimulate energy expenditure or to inhibit food intake. At room temperature (22oC) DMHGq/11KO mice showed reduced sympathetic nervous system activity in brown adipose tissue (BAT) and heart, accompanied with decreased basal BAT Ucp1 gene expression and lower heart rates. These mice were cold intolerant when acutely exposed to cold (6oC for 5 hours) and had decreased cold-stimulated BAT Ucp1 gene expression. DMHGq/11KO mice also failed to adapt to gradually declining ambient temperatures and to develop adipocyte browning in inguinal white adipose tissue although their BAT Ucp1 was proportionally stimulated. Consistent with impaired cold-induced thermogenesis, the onset of obesity in DMHGq/11KO mice was significantly delayed when housed under thermoneutral conditions (30ºC). Thus, our results show that Gqα and G11α in the DMH are required for the control of energy homeostasis by stimulating energy expenditure and thermoregulation.

EFFECT OF TEMPERATURE ON METABOLIC RATES OF LIVER AND BROWN FAT HOMOGENATES

1967 ◽  
Vol 45 (11) ◽  
pp. 1763-1771 ◽  
Author(s):  
Jane C. Roberts ◽  
Robert E. Smith
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Brown Fat ◽  
Effect Of Temperature ◽  
Metabolic Rates ◽  
Brown Adipose ◽  
Rate Of Oxygen Consumption ◽  
Effects Of Temperature

The effects of temperature in vitro upon metabolic rates of homogenates of brown fat and liver from control and cold-acclimated rats have been examined over the range 10–37 °C. At all temperatures, brown adipose tissue exhibits a higher rate of oxygen consumption [Formula: see text] than does liver, α-ketoglutarate being used as substrate. At 10 °C, brown adipose tissue retains a larger percentage (36–38%) of its 37 °C metabolic rate than does liver (22–24%).Q10 values and energies of activation (Ea) have been determined and compared with other data reported for these tissues. At 20 °C, breaks appear in the Arrhenius plots for liver from both control and cold-acclimated rats and also for brown fat from control rats, but not for the brown fat from cold-acclimated rats. Thus brown adipose tissue from cold-acclimated rats retains relatively higher levels of respiration at temperatures below the 20 °C breaking point than does brown fat from control rats.In view of previously reported cold-induced increases in mass, vascularity, and [Formula: see text] of brown fat, this decreased temperature sensitivity in the cold-acclimated rats appears wholly consonant with the adaptive behavior of brown fat in its role as a thermogenic effector.

Thermoregulatory responses of dystrophic hamsters to changes in ambient temperatures

1985 ◽  
Vol 63 (9) ◽  
pp. 1145-1150 ◽  
Author(s):  
M. Desautels ◽  
R. A. Dulos ◽  
J. A. Thornhill
Keyword(s):  
Carbon Dioxide ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Body Temperature ◽  
Metabolic Activity ◽  
Carbon Dioxide Production ◽  
Ambient Temperatures ◽  
Brown Adipose ◽  
Lower Temperature ◽  
Do So

The ability of dystrophic hamsters to maintain their body temperature despite abnormal muscle and brown adipose tissue, two organs involved in thermoregulation, was evaluated. Dystrophic hamsters (CHF 146) between the ages of 30 and 160 days kept at 21 °C had core (rectal) temperatures (TR) that were 0.5–1.5 °C lower than Golden Syrian controls. The reduced core temperatures of dystrophic hamsters were unlikely the result of an incapacity to generate heat since the dystrophic hamsters were able to maintain their TRs during 3 h of acute cold stress (4 °C) and to adapt to prolonged cold exposure. However, TRs of cold-acclimated dystrophic hamsters were still 1 °C below TRs of cold-acclimated control animals. By contrast, increasing the ambient temperature raised TRs of both normal and dystrophic hamsters. When kept at 32 °C overnight, the TRs of dystrophic hamsters remained significantly below those of control animals. When heat-exposed dystrophic hamsters were returned to 21 °C, their TRs returned to values significantly lower than those of control hamsters. Thus, dystrophic hamsters showed a capacity to thermoregulate, like control hamsters, but appeared to do so at a lower temperature. The reduced core temperatures of dystrophic hamsters kept at 21 °C cannot be explained by a reduction in metabolic activity since newborns and 30- and 140-day-old dystrophic hamsters had rates of oxygen consumption [Formula: see text] and carbon dioxide production [Formula: see text] that were similar to those of controls. These results suggest that the thermoregulatory set point may be altered in dystrophic hamsters.

scholarly journals Eicosapentaenoic Acid Regulates Brown Adipose Tissue Function, Independently of UCP1 (FS11-01-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Mandana Pahlavani ◽  
Latha Ramalingam ◽  
Emily Miller ◽  
Kalhara Menikdiwela ◽  
Shane Scoggin ◽  
...  
Keyword(s):  
Mitochondrial Dna ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Expenditure ◽  
Eicosapentaenoic Acid ◽  
Brown Adipose Tissue ◽  
Metabolic Effects ◽  
High Fat ◽  
Protein Levels ◽  
Brown Adipose

Abstract Objectives Brown adipose tissue (BAT) is a critical tissue in energy expenditure through its specific uncoupling protein 1 (UCP1). We previously reported that mice fed high fat (HF) diet supplemented with eicosapentaenoic acid (EPA) reduced body weight, adiposity, and insulin resistance, and increased UCP1 protein and mRNA levels of other thermogenic markers in BAT at ambient temperature. Hence, we hypothesized that these metabolic effects of EPA on BAT are in part mediated by UCP1. Methods To determine the role of UCP1 in obesity and BAT regulation by EPA, wild type (WT) and UCP1 knockout (KO) B6 male mice were housed at thermoneutral conditions (30°C), previously reported to induce obesity in the KO mice. Mice were fed a high-fat diet (HF, 45% kcal fat) or HF diet supplemented with 36 g/kg of AlaskOmega EPA-enriched fish oil (800 mg/g), kindly provided by Organic Technologies, for up to 14 weeks. We metabolically phenotyped these mice and investigated metabolic and molecular changes in their interscapular BAT. Specifically, we determined effects of UCP1 deficiency and EPA on BAT thermogenic and mitochondrial markers. Results The previously reported beneficial metabolic effects of EPA in WT mice at ambient, including increased UCP1 expression, were attenuated or lost at thermoneutral temperature. EPA reduced weight gain and adiposity, and improved glucose tolerance in KO mice. In both diets (HF and EPA), BAT triglyceride content was increased, while mitochondrial UCP1, COX I and COX IV protein levels were decreased in the KO compared to the WT genotype (P < 0.05). EPA also increased (P < 0.05) mitochondrial DNA/nuclear DNA ratio in the KO mice. Finally, BAT PGC1α at both gene and protein levels along with whole-body oxygen consumption were increased (P < 0.05) by EPA in KO mice. EPA did not alter the calcium cycling-related markers such as sarcoplasmic/endoplasmic reticulum calcium ATPase 2b (Serca2b) and transient receptor potential vanilloid 2 (Trpv2) in any of the genotypes. Conclusions EPA effects on BAT and mitochondrial function are independent of UCP1, and include increased mitochondrial DNA and oxygen consumption, which may be in part relate to increased PGC1α. Additional studies are required to determine fuel or mitochondrial mechanisms by which energy expenditure is increased independently of UCP1. Funding Sources NIH/NCCIH grant # R15AT008879-01A1.

Leptin increases uncoupling protein expression and energy expenditure

1997 ◽  
Vol 273 (1) ◽  
pp. E226-E230 ◽  
Author(s):  
P. J. Scarpace ◽  
M. Matheny ◽  
B. H. Pollock ◽  
N. Tumer
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Food Consumption ◽  
Uncoupling Protein ◽  
Mrna Levels ◽  
Sympathetic Outflow ◽  
Brown Adipose ◽  
Ad Libitum

In ob/ob mice, leptin increases energy expenditure and sympathetic outflow to brown adipose tissue (BAT). To test whether the mechanism of increased energy expenditure may involve increased thermogenesis in BAT, we acclimated normal rats to thermoneutrality for 2 wk followed by leptin administration for 1 wk. Some rats were food restricted for 1 wk to the level of food consumption in the leptin-treated ad libitum-fed rats, and the same rats were both food restricted and administered leptin for a second week. We examined oxygen consumption and uncoupling protein (UCP) expression in BAT. Leptin increased oxygen consumption after the 5th and 6th days in ad libitum-fed rats and after the 4th, 5th, and 6th days in food-restricted rats. Leptin increased BAT UCP mRNA levels greater than twofold in both ad libitum-fed and food-restricted rats. These data demonstrate a leptin-induced increase in energy expenditure in nonmutant rodents and suggest that one mechanism by which leptin increases energy expenditure is through increased thermogenesis in BAT, including increased expression of UCP.

scholarly journals The effect of mirabegron on energy expenditure and brown adipose tissue in healthy lean South Asian and Europid men

2020 ◽  
Vol 22 (11) ◽  
pp. 2032-2044 ◽  
Author(s):  
Kimberly J. Nahon ◽  
Laura G. M. Janssen ◽  
Aashley S. D. Sardjoe Mishre ◽  
Manu P. Bilsen ◽  
Jari A. Eijk ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
South Asian ◽  
Brown Adipose

W1854 Roux-en-Y Gastric Bypass Activates Brown Adipose Tissue and Increases Energy Expenditure in Obese Mice

2010 ◽  
Vol 138 (5) ◽  
pp. S-754 ◽  
Author(s):  
Nicholas Stylopoulos ◽  
Xiao B. Zhang ◽  
Anna-Liisa Brownell ◽  
Lee M. Kaplan
Keyword(s):  
Gastric Bypass ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Obese Mice ◽  
Brown Adipose
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