Brown adipose tissue activation in a rat model of Parkinson’s disease

2017 ◽  
Vol 313 (6) ◽  
pp. E731-E736 ◽  
Author(s):  
Wenjuan Wang ◽  
Xiangzhi Meng ◽  
Chun Yang ◽  
Dongliang Fang ◽  
Xuemeng Wang ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Energy Intake ◽  
Rat Model ◽  
Sympathetic Denervation ◽  
Brown Adipose

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.

scholarly journals Weight loss and brown adipose tissue reduction in rat model of sleep apnea

2008 ◽  
Vol 7 (1) ◽  
pp. 26 ◽  
Author(s):  
Denis Martinez ◽  
Luiz FT Vasconcellos ◽  
Patricia G de Oliveira ◽  
Signorá P Konrad
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Sleep Apnea ◽  
Brown Adipose Tissue ◽  
Rat Model ◽  
Brown Adipose ◽  
Tissue Reduction

Relationship between cold-induced thermoregulation and spontaneous rapid body weight loss of aging F344 rats

1996 ◽  
Vol 271 (5) ◽  
pp. R1115-R1122 ◽  
Author(s):  
R. B. McDonald ◽  
M. Florez-Duquet ◽  
C. Murtagh-Mark ◽  
B. A. Horwitz
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Physiological State ◽  
Rapid Weight Loss ◽  
Acute Cold Exposure ◽  
Brown Adipose ◽  
F344 Rats

We previously showed that, although cold-induced thermoregulation is attenuated in 26-mo-old male Fischer 344 (F344) rats, not all rats this age exhibit the same degree of cold-exposed hypothermia or diminished brown adipose tissue nonshivering thermogenic capacity. Examination of this heterogeneity suggested the hypothesis that it was associated with a difference in the physiological state between aged rats that were maintaining stable body weight versus those showing the rapid weight loss often occurring near the end of the rat's natural life span. To test this, we acutely exposed male F344 rats to cold (4 h at 6 degrees C) beginning at 24 mo of age. This exposure was weekly for the first 2 wk and then on alternate weeks as long as the rat's body weight was stable. If body weight progressively declined for 3-5 consecutive days, the rat's response to the acute cold exposure was again measured, as was that of two additional rats not displaying this rapid loss in body weight. If body temperature decreased during the cold exposure to intraperitoneal temperatures < or = 32.5 degrees C, the rat was killed with pentobarbital sodium and interscapular brown adipose tissue was removed. One of the age-matched controls was also killed at this time. The age at which body weight showed a spontaneous rapid decline ranged from 24.5 to 29 mos. All eight rats displaying spontaneous rapid weight loss had significant hypothermia during the acute cold exposure, whereas none of the eight weight-stable rats did. The development of hypothermia in the spontaneous rapid weight loss group was not, in general, observed before their weight loss. The weight loss and hypothermia were associated with lower levels of brown fat uncoupling protein and significant changes in body fat and protein. These data suggest that the development of senescence-related hypothermia occurs rapidly and is not a simple function of chronological age or the median life span of the animals. Furthermore, these data imply that the rate of aging in terms of maintenance of thermoregulatory homeostasis has both a gradual and rapid component, the latter being associated with a different physiological state than the former.

Effects of ovarian hormones on energy balance and brown adipose tissue thermogenesis

1986 ◽  
Vol 250 (2) ◽  
pp. R245-R249 ◽  
Author(s):  
D. Richard
Keyword(s):  
Adipose Tissue ◽  
Energy Balance ◽  
Food Intake ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Energy Intake ◽  
Ovarian Hormones ◽  
Ovariectomized Rats ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis

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.

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.

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 Chronic Hindbrain Administration of Oxytocin Elicits Weight Loss in Male Diet-Induced Obese Mice

2021 ◽  
Author(s):  
Melise Marie Edwards ◽  
Ha Khanh Nguyen ◽  
Adam Jay Herbertson ◽  
Andrew Dale Dodson ◽  
Tomasz Wietecha ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Adipose Tissue ◽  
Food Intake ◽  
Energy Intake ◽  
Uncoupling Protein ◽  
Post Injection ◽  
Reduced Body ◽  
Brown Adipose ◽  
Pre Treatment

Previous studies indicate that oxytocin (OT) administration reduces body weight in high fat diet (HFD)-induced obese (DIO) rodents through both reductions in food intake and increases in energy expenditure. We recently demonstrated that chronic hindbrain [fourth ventricular (4V)] infusions of OT evoke weight loss in DIO rats. Based on these findings, we hypothesized that chronic 4V OT would elicit weight loss in DIO mice. We assessed the effects of 4V infusions of OT (16 nmol/day) or vehicle over 28 days on body weight, food intake and body composition. OT reduced body weight by approximately 4.5±1.4% in DIO mice relative to OT pre-treatment body weight (P<0.05). These effects were associated with reduced adiposity and adipocyte size (inguinal white adipose tissue (IWAT)] (P<0.05) and attributed, in part, to reduced energy intake (P<0.05) at a dose that did not increase kaolin intake (P=NS). OT tended to increase uncoupling protein-1 expression in IWAT (0.05<P<0.1) suggesting that OT stimulates browning of WAT. To assess OT-elicited changes in brown adipose tissue (BAT) thermogenesis, we examined the effects of 4V OT on interscapular BAT temperature (TIBAT). 4V OT (1 μg) elevated TIBAT at 0.75 (P=0.08), 1, and 1.25 h (P<0.05) post-injection; a higher dose (5 μg) elevated TIBAT at 0.75, 1, 1.25, 1.5, 1.75 (P<0.05), and 2-h (0.05<P<0.1) post-injection. Together, these findings support the hypothesis that chronic hindbrain OT treatment evokes sustained weight loss in DIO mice by reducing energy intake and increasing BAT thermogenesis at a dose that is not associated with evidence of visceral illness.

Gentisic acid prevents diet-induced obesity in mice by accelerating the thermogenesis of brown adipose tissue

2021 ◽  
Author(s):  
Xue Han ◽  
Jielong Guo ◽  
Yunxiao Gao ◽  
Weidong Huang ◽  
Jicheng Zhan ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Energy Intake ◽  
Effective Strategy ◽  
Gentisic Acid ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Obesity In Mice

Since obesity occurs when energy intake is higher than energy expenditure, increasing energy expenditure is an effective strategy to prevent or treat obesity. Brown adipose tissue (BAT) is a classic...

scholarly journals Reducing Adiposity in a Critical Developmental Window Has Lasting Benefits in Mice

Endocrinology ◽  
2015 ◽  
Vol 157 (2) ◽  
pp. 666-678 ◽  
Author(s):  
Jaclyn S. Lerea ◽  
Laurence E. Ring ◽  
Rim Hassouna ◽  
Angie C. N. Chong ◽  
Klara Szigeti-Buck ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Early Onset ◽  
Weight Regain ◽  
Time Window ◽  
Dietary Interventions ◽  
Brown Adipose ◽  
And Function

Abstract Although most adults can lose weight by dieting, a well-characterized compensatory decrease in energy expenditure promotes weight regain more than 90% of the time. Using mice with impaired hypothalamic leptin signaling as a model of early-onset hyperphagia and obesity, we explored whether this unfavorable response to weight loss could be circumvented by early intervention. Early-onset obesity was associated with impairments in the structure and function of brown adipose tissue mitochondria, which were ameliorated by weight loss at any age. Although decreased sympathetic tone in weight-reduced adults resulted in net reductions in brown adipose tissue thermogenesis and energy expenditure that promoted rapid weight regain, this was not the case when dietary interventions were initiated at weaning. Enhanced energy expenditure persisted even after mice were allowed to resume overeating, leading to lasting reductions in adiposity. These findings reveal a time window when dietary interventions can produce metabolic improvements that are stably maintained.

scholarly journals Signalling in body-weight homeostasis: neuroendocrine efferent signals

2000 ◽  
Vol 59 (3) ◽  
pp. 397-404 ◽  
Author(s):  
Jonathan Webber ◽  
Ian A. Macdonald
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Energy Expenditure ◽  
Brown Adipose Tissue ◽  
Resting Energy Expenditure ◽  
Excess Energy ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

Whilst a number of neuroendocrine afferent signals are implicated in body-weight homeostasis, the major efferent pathway is the sympathetic nervous system (SNS), which affects both energy expenditure and substrate utilization. Thyroid hormones and their interactions with the SNS may also have a role to play. Some of the variability in resting energy expenditure can be explained by differences in SNS activity, and β-blockade can reduce energy expenditure and diet-induced thermogenesis in Caucasians. Excess energy intake leads to SNS activation and increased diet-induced thermogenesis. A relationship has also been demonstrated between spontaneous physical activity and SNS activity. In many animal models the SNS activates brown adipose tissue thermogenesis, hence increasing diet-induced thermogenesis and dissipating excess energy as heat. This effect is mediated via β3-adrenoceptors and activation of an uncoupling protein unique to brown adipose tissue. Homologous proteins have been identified in human tissues and may play a role in human energy expenditure. How the SNS is implicated in this process is unclear at present. β3-Adrenoceptor polymorphism has been associated both with lower resting energy expenditure in some populations and with reduced autonomic nervous system activity. SNS effects on substrate cycling may also play a role. In the development of obesity the effects of the SNS in promoting lipolysis and fat oxidation are likely to be at least as important as its effects on thermogenesis. β-Blockade has relatively small effects on energy expenditure, but more pronounced effects on reducing lipid oxidation, so tending to favour fat storage and weight gain. Low lipid oxidation is a risk factor for weight gain, and there is some evidence that low basal sympathetic nerve activity in muscle is associated with this process. Overall, the relationship between SNS activity and obesity is complex, with evidence of low SNS activity occurring in some, but not all, studies.

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