scholarly journals Detraining of exercise-trained rats: effects on energetic efficiency and brown adipose tissue thermogenesis

1987 ◽  
Vol 57 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Jeff Arnold ◽  
Denis Richard
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
The Body ◽  
Metabolizable Energy ◽  
Treadmill Running ◽  
Energetic Efficiency ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

1. Complete energy balance measurements were made in exercise-trained (treadmill running) rats subjected to 27 d of exercise detraining.2. The 20% difference in body-weight that existed at the end of the training period between sedentary and trained rats was negated by detraining. Detrained rats had twice the body-weight gain of their untrained controls.3. An elevation (12%) in metabolizable energy (ME) intake (relative to body-weight) was observed in detrained rats while their gross energetic efficiency was augmented by 60%.4. Energy expenditure, excluding the estimated costs of fat and protein storage, was similar for detrained and untrained rats. Complementing the latter was the finding that thermogenesis in brown adipose tissue, a known energy buffering process, was also similar.5. Elevated ME intake (relative to body-weight) largely contributed to the increased energetic efficiency of detrained rats.

Energy balance and brown adipose tissue thermogenesis during chronic endotoxemia in rats

1989 ◽  
Vol 66 (4) ◽  
pp. 1970-1975 ◽  
Author(s):  
J. Arnold ◽  
R. A. Little ◽  
N. J. Rothwell
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Male Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

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)

scholarly journals Nicotine Improves Obesity and Hepatic Steatosis and ER Stress in Diet-Induced Obese Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1679-1689 ◽  
Author(s):  
Patricia Seoane-Collazo ◽  
Pablo B. Martínez de Morentin ◽  
Johan Fernø ◽  
Carlos Diéguez ◽  
Rubén Nogueiras ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Balance ◽  
Protein Kinase ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Amp Activated Protein Kinase

Nicotine, the main addictive component of tobacco, promotes body weight reduction in humans and rodents. Recent evidence has suggested that nicotine acts in the central nervous system to modulate energy balance. Specifically, nicotine modulates hypothalamic AMP-activated protein kinase to decrease feeding and to increase brown adipose tissue thermogenesis through the sympathetic nervous system, leading to weight loss. Of note, most of this evidence has been obtained in animal models fed with normal diet or low-fat diet (LFD). However, its effectiveness in obese models remains elusive. Because obesity causes resistance towards many factors involved in energy homeostasis, the aim of this study has been to compare the effect of nicotine in a diet-induced obese (DIO) model, namely rats fed a high-fat diet, with rats fed a LFD. Our data show that chronic peripheral nicotine treatment reduced body weight by decreasing food intake and increasing brown adipose tissue thermogenesis in both LFD and DIO rats. This overall negative energy balance was associated to decreased activation of hypothalamic AMP-activated protein kinase in both models. Furthermore, nicotine improved serum lipid profile, decreased insulin serum levels, as well as reduced steatosis, inflammation, and endoplasmic reticulum stress in the liver of DIO rats but not in LFD rats. Overall, this evidence suggests that nicotine diminishes body weight and improves metabolic disorders linked to DIO and might offer a clear-cut strategy to develop new therapeutic approaches against obesity and its metabolic complications.

Brown adipose tissue thermogenesis in testosterone-treated rats

1992 ◽  
Vol 126 (5) ◽  
pp. 434-437 ◽  
Author(s):  
María Abelenda ◽  
Maria Paz Nava ◽  
Alberto Fernández ◽  
María Luisa Puerta
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Male Rats ◽  
Weight Regulation ◽  
Body Weight Regulation ◽  
Sexual Hormones ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

The participation of sexual hormones in body weight regulation is partly accomplished by altering food intake. Nonetheless, female sexual hormones also alter brown adipose tissue thermogenesis in females. This study was aimed to find out if male hormones could alter brown adipose tissue thermogenesis in male rats. Testosterone was administered by means of Silastic capsules in adult male rats acclimated either at 28°C (thermoneutrality) or at 6°C (cold), treatment lasting 15 days. Food intake and body weight gain were reduced by hormonal treatment. However, brown adipose tissue mass, protein content, mitochondrial mass and GDP-binding were unchanged at both environmental temperatures. Accordingly, testosterone participation in body weight regulation is thought to be carried out without altering brown adipose tissue thermogenesis. A reduction in the weight of the sex accessory glands was also observed after cold acclimation.

Energy balance following sympathetic denervation of brown adipose tissue

1984 ◽  
Vol 62 (2) ◽  
pp. 235-240 ◽  
Author(s):  
A. G. Dulloo ◽  
D. S. Miller
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Energy Balance ◽  
Brown Adipose Tissue ◽  
Body Fat ◽  
Metabolizable Energy ◽  
Energetic Efficiency ◽  
Interscapular Brown Adipose Tissue ◽  
Body Protein ◽  
Brown Adipose

The effects of sham, bilateral surgical denervation or excision of interscapular brown adipose tissue on body composition and energetic efficiency were studied in young CFLP mice kept at 25 °C and fed a laboratory stock diet. A preliminary experiment showed that 15 weeks following surgery, total body fat was increased by 42% in the denervated group and by 72% in the excised group while body protein was unchanged. In another 7-week energy balance experiment, body fat was also significantly higher by 15 and 18% in the denervated and excised group, respectively, but metabolizable energy intake was slightly lower than that of sham controls. Determination of energy expenditure both by the comparative carcass slaughter technique and by measurement of daily oxygen consumption showed that the metabolic rate was reduced in the denervated and excised groups. The capacity for thermogenesis, as measured by an increase in oxygen consumption following injections of noradrenaline (600 μg/kg body weight) was similar in all groups. These studies show that denervation or excision of interscapular brown adipose tissue causes an elevation in energetic efficiency, and indicates an important role of the sympathetic nervous system in the regulation of animal heat production by brown adipose tissue and in the overall control of thermogenesis.

Increased sensitivity of the genetically obese mouse to corticosterone

1987 ◽  
Vol 252 (2) ◽  
pp. E202-E208 ◽  
Author(s):  
K. Tokuyama ◽  
J. Himms-Hagen
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Brown Adipose Tissue ◽  
Body Weight Gain ◽  
Serum Insulin ◽  
Obese Mouse ◽  
Serum Corticosterone ◽  
Brown Adipose

Adrenalectomy normalizes many abnormalities of the obese (ob/ob) mouse. The high corticosterone concentration in blood may account in part for development of obesity and other abnormalities in the ob/ob mouse. Our objective was to determine dose-response relationships for the effect of corticosterone on the obesity. Lean and ob/ob mice were adrenalectomized or sham-operated at 4.5 wk of age. Adrenalectomized mice received 100 mg implants of cholesterol containing corticosterone (0, 2, 5, 20, or 50 mg) at 8.5 wk of age and were killed at 10.5 wk of age. In ob/ob mice, but not in lean mice, low physiological levels of serum corticosterone (up to 10 micrograms/dl) markedly increased body weight gain, food intake, and serum insulin. They also increased white and brown adipose tissue weights and decreased brown adipose tissue mitochondrial GDP binding. Higher levels of corticosterone (12-22 micrograms/dl) increased body weight gain, white and brown adipose tissue weights, and serum insulin and suppressed brown adipose tissue mitochondrial GDP binding in lean mice also, although in most cases to a lesser extent than in ob/ob mice, but were still without effect on food intake. Only very high levels of corticosterone (approximately 30 micrograms/dl) increased food intake in lean mice. Hyperglycemia was induced in ob/ob, but not lean, mice only at concentrations of corticosterone greater than 17 micrograms/dl. Thermoregulation was unaffected by serum corticosterone at levels from 0 to 30 micrograms/dl in both ob/ob and lean mice. Thus the ob/ob mouse is excessively sensitive and responsive to an effect of physiological levels of corticosterone that results in hyperphagia, hyperinsulinemia, and increased weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Leptin: Is It Thermogenic?

2019 ◽  
Vol 41 (2) ◽  
pp. 232-260 ◽  
Author(s):  
Alexander W Fischer ◽  
Barbara Cannon ◽  
Jan Nedergaard
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Sympathetic Nerve Activity ◽  
Leptin Receptor ◽  
The Body ◽  
Nerve Activity ◽  
Brown Adipose ◽  
Intact Organism

Abstract Animals that lack the hormone leptin become grossly obese, purportedly for 2 reasons: increased food intake and decreased energy expenditure (thermogenesis). This review examines the experimental evidence for the thermogenesis component. Analysis of the data available led us to conclude that the reports indicating hypometabolism in the leptin-deficient ob/ob mice (as well as in the leptin-receptor-deficient db/db mice and fa/fa rats) derive from a misleading calculation artefact resulting from expression of energy expenditure per gram of body weight and not per intact organism. Correspondingly, the body weight-reducing effects of leptin are not augmented by enhanced thermogenesis. Congruent with this, there is no evidence that the ob/ob mouse demonstrates atrophied brown adipose tissue or diminished levels of total UCP1 mRNA or protein when the ob mutation is studied on the inbred C57BL/6 mouse background, but a reduced sympathetic nerve activity is observed. On the outbred “Aston” mouse background, brown adipose tissue atrophy is seen, but whether this is of quantitative significance for the development of obesity has not been demonstrated. We conclude that leptin is not a thermogenic hormone. Rather, leptin has effects on body temperature regulation, by opposing torpor bouts and by shifting thermoregulatory thresholds. The central pathways behind these effects are largely unexplored.

scholarly journals Male and Female Animals Respond Differently to High-Fat Diet and Regular Exercise Training in a Mouse Model of Hyperlipidemia

2021 ◽  
Vol 22 (8) ◽  
pp. 4198
Author(s):  
Melinda E. Tóth ◽  
Brigitta Dukay ◽  
Mária Péter ◽  
Gábor Balogh ◽  
Gergő Szűcs ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
The Body ◽  
Treadmill Running ◽  
Cardiometabolic Health ◽  
Regular Exercise ◽  
High Fat ◽  
Brown Adipose

Inappropriate nutrition and a sedentary lifestyle can lead to obesity, one of the most common risk factors for several chronic diseases. Although regular physical exercise is an efficient approach to improve cardiometabolic health, the exact cellular processes are still not fully understood. We aimed to analyze the morphological, gene expression, and lipidomic patterns in the liver and adipose tissues in response to regular exercise. Healthy (wild type on a normal diet) and hyperlipidemic, high-fat diet-fed (HFD-fed) apolipoprotein B-100 (APOB-100)-overexpressing mice were trained by treadmill running for 7 months. The serum concentrations of triglyceride and tumor necrosis factor α (TNFα), as well as the level of lipid accumulation in the liver, were significantly higher in HFD-fed APOB-100 males compared to females. However, regular exercise almost completely abolished lipid accumulation in the liver of hyperlipidemic animals. The expression level of the thermogenesis marker, uncoupling protein-1 (Ucp1), was significantly higher in the subcutaneous white adipose tissue of healthy females, as well as in the brown adipose tissue of HFD-fed APOB-100 females, compared to males. Lipidomic analyses revealed that hyperlipidemia essentially remodeled the lipidome of brown adipose tissue, affecting both the membrane and storage lipid fractions, which was partially restored by exercise in both sexes. Our results revealed more severe metabolic disturbances in HFD-fed APOB-100 males compared to females. However, exercise efficiently reduced the body weight, serum triglyceride levels, expression of pro-inflammatory factors, and hepatic lipid accumulation in our model.

scholarly journals Cranberry Polyphenolic Extract Exhibits an Antiobesity Effect on High-Fat Diet–Fed Mice through Increased Thermogenesis

2020 ◽  
Vol 150 (8) ◽  
pp. 2131-2138 ◽  
Author(s):  
Fang Zhou ◽  
Jielong Guo ◽  
Xue Han ◽  
Yunxiao Gao ◽  
Qimin Chen ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Uncoupling Protein ◽  
The Body ◽  
High Fat ◽  
Uncoupling Protein 1 ◽  
Polyphenolic Extract ◽  
Brown Adipose

ABSTRACT Background Although polyphenol-rich cranberry extracts reportedly have an antiobesity effect, the exact reason for this remains unclear. Objectives In light of the reported health benefits of the polyphenolic compounds in cranberry, we investigated the effects and mechanism of a cranberry polyphenolic extract (CPE) in high-fat diet (HFD)–fed obese mice. Methods The distributions of individual CPE compounds were characterized by HPLC fingerprinting. Male C57BL/6J mice (4 wk old) were fed for 16 wk normal diet (ND, 10% fat energy) or HFD (60% fat energy) with or without 0.75% CPE in drinking water (HFD + CPE). Body and adipose depot weights, indices of glucose metabolism, energy expenditure (EE), and expression of genes related to brown adipose tissue (BAT) thermogenesis, and inguinal/epididymal white adipose tissue (iWAT/eWAT) browning were measured. Results After 16 wk, the body weight was 22.5% lower in the CPE-treated mice than in the HFD group but remained 17.9% higher than in the ND group. CPE treatment significantly increased EE compared with that of the ND and HFD groups. The elevated EE was linked with BAT thermogenesis, and iWAT/eWAT browning, shown by the induction of thermogenic genes, especially uncoupling protein 1 (Ucp1), and browning-related genes, including Cd137, a member of the tumor necrosis factor receptor superfamily (Tnfrsf9). The mRNA expression and abundance of uncoupling protein 1 in BAT of CPE-fed mice were 5.78 and 1.47 times higher than in the HFD group, and 0.61 and 1.12 times higher than in the ND group, respectively. Cd137 gene expression in iWAT and eWAT of CPE-fed mice were 2.35 and 3.13 times higher than in the HFD group, and 0.84 and 1.39 times higher than in the ND group, respectively. Conclusions Dietary CPE reduced but did not normalize HFD-induced body weight gain in male C57BL/6J mice, possibly by affecting energy metabolism.

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