Fat-depleted CLA-treated mice enter torpor after a short period of fasting

Bouthegourd, Jean-Christophe; Martin, Jean-Charles; Gripois, D.; Roseau, Suzanne; Tomé, Daniel; Even, Patrick C.

doi:10.1016/j.appet.2003.07.003

Cited by 9 publications

(3 citation statements)

References 20 publications

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“…Under acute food deprivation and cool ambient temperature (T a ), laboratory mice allow their body temperature to fall to near ambient temperature, with a minimum body temperature around 20°C and a concomitant reduction in metabolic rate [1]–[6]. This heterothermic response contrasts with true hibernators, like ground squirrels, that can achieve a minimum body temperature at or below freezing for weeks at a time [7].…”

Section: Introductionmentioning

confidence: 99%

Norepinephrine Controls Both Torpor Initiation and Emergence via Distinct Mechanisms in the Mouse

Swoap

2008

PLoS ONE

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Some mammals, including laboratory mice, enter torpor in response to food deprivation, and leptin can attenuate these bouts of torpor. We previously showed that dopamine β-hydroxylase knockout (Dbh −/−) mice, which lack norepinephrine (NE), do not reduce circulating leptin upon fasting nor do they enter torpor. To test whether the onset of torpor in mice during a fast requires a NE-mediated reduction in circulating leptin, double mutant mice deficient in both leptin (ob/ob) and DBH (DBL MUT) were generated. Upon fasting, control and ob/ob mice entered torpor as assessed by telemetric core Tb acquisition. While fasting failed to induce torpor in Dbh −/− mice, leptin deficiency bypassed the requirement for NE, as DBL MUT mice readily entered torpor upon fasting. These data indicate that sympathetic activation of white fat and suppression of leptin is required for the onset of torpor in the mouse. Emergence from torpor was severely retarded in DBL MUT mice, revealing a novel, leptin-independent role for NE in torpor recovery. This phenotype was mimicked by administration of a β3 adrenergic receptor antagonist to control mice during a torpor bout. Hence, NE signaling via β3 adrenergic receptors presumably in brown fat is the first neurotransmitter-receptor system identified that is required for normal recovery from torpor.

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Section: Introductionmentioning

confidence: 99%

Norepinephrine Controls Both Torpor Initiation and Emergence via Distinct Mechanisms in the Mouse

Swoap

2008

PLoS ONE

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“…Some small endotherms have the ability to hibernate, using multiday bouts of lowered body temperature (T b ), as low as 5°C, that are separated by brief arousal periods (Lyman et al, 1982;Heldmaier et al, 1993;Geiser and Ruf, 1995;Geiser, 2004). Other species, including Mus musculus, exhibit a shallower minimum T b (17-31°C) with bouts of shorter duration, typically ranging from 2 to 20 h (Hudson and Scott, 1979;Webb et al, 1982;Himms-Hagen, 1985a;Swoap, 2001;Bae et al, 2003;Bouthegourd et al, 2004). The regulation of T b is maintained during torpor and not merely a function of heat lost to the environment after thermoregulation has been abandoned (Carey et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

The Full Expression of Fasting-Induced Torpor Requires β3-Adrenergic Receptor Signaling

Swoap

Gutilla²,

Liles³

et al. 2006

J. Neurosci.

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Torpor, a controlled rapid drop in metabolic rate and body temperature (T b ), is a hypometabolic adaptation to stressful environmental conditions, which occurs in many small mammals, marsupials, and birds. To date, signaling pathways required for torpor have not been identified. We examined the role of the sympathetic nervous system (SNS) in mediating the torpor adaptation to fasting by telemetrically monitoring the T b of dopamine ␤-hydroxylase knock-out (Dbh؊/؊) mice, which lack the ability to produce the SNS transmitters, norepinephrine (NE), and epinephrine. Control (Dbh؉/؊) mice readily reduced serum leptin levels and entered torpor after a fast in a cool environment. In contrast, Dbh؊/؊ mice failed to reduce serum leptin and enter torpor under fasting conditions, whereas restoration of peripheral but not central NE lowered serum leptin levels and rescued the torpor response. Torpor was expressed in fasted Dbh؊/؊ mice immediately after administration of either the nonselective ␤-adrenergic receptor agonist isoproterenol or the ␤3-

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“…The total uptake attributed to each organ was expressed as the radioactivity recovered in that organ over the total radioactivity injected. Assuming that epididymal adipose tissue contributes to one-fifth of total adipose tissue, 19 and reflects the metabolic behavior of all adipose tissue, the total [ 3 H] cholesteryl oleyl ether uptake attributed to total fat was calculated and expressed as percent of injected dose. …”

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confidence: 99%

In Vivo Evidence for a Role of Adipose Tissue SR-BI in the Nutritional and Hormonal Regulation of Adiposity and Cholesterol Homeostasis

Yvan‐Charvet

Bobard

Bossard

et al. 2007

ATVB

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Objectives-This study examines the role of insulin and angiotensin II in high-density lipoprotein (HDL) metabolism by focusing on the regulation and function of scavenger receptor type-BI (SR-BI) in adipose tissue. Methods and Results-Insulin or angiotensin II injection in wild-type mice induced a decrease in circulating HDL and it was associated with the translocation of SR-BI from intracellular sites to the plasma membrane of adipose tissue. Refeeding upregulated adipose HDL selective cholesteryl esters uptake and SR-BI proteins through transcriptional and posttranscriptional mechanisms. This occurred along with a decrease in serum HDL and an increase in adipose cholesterol content. Similar results were obtained with transgenic mice overexpressing locally angiotensinogen in adipose tissue. In adipose 3T3-L1 cell line, HDL induced lipogenesis by increasing liver X receptor binding activity. This mechanism was dependent of insulin and angiotensin II. Key Words: adipose tissue Ⅲ angiotensin II Ⅲ high-density lipoprotein Ⅲ insulin A dipose tissue has a central role in the energy metabolism adaptation to the nutritional environment because of its ability to store energy as triglycerides. Besides its role in triglyceride storage, adipose tissue is also the body's largest pool of cholesterol store, representing Ϸ25% of whole-body cholesterol in human. 1 A particular interest of adipocytes is that these cells accumulate cholesterol proportionally to triglycerides. Because of an extremely low cholesterol de novo synthesis, 2 adipocytes must acquire cholesterol from exogenous sources. Interestingly, clinical observations have found a correlation between obesity and low levels of high-density lipoprotein (HDL) cholesterol, 3 which is the reflect of an increased incidence of atherosclerosis. 4 There is also growing evidence that altered insulin sensitivity or increased angiotensin II concentrations, which occur along with obesity, play a crucial role in the acceleration of atherosclerosis but mechanisms are not yet fully deciphered. 5,6 The scavenger receptor type-BI (SR-BI) has been identified as a membrane transporter involved in the selective cholesteryl esters (CEs) uptake from HDL. 7 The pivotal role of SR-BI in lipoprotein metabolism and cholesterol transport in steroidogenic tissues and liver has been well-established. 8 SR-BI is also expressed in adipocytes, but little is known about its function and regulation in these cells. 9 Recently, studies from our laboratory have reported that SR-BI provide an important source of cholesterol from HDL in adipose cell lines and that insulin and angiotensin II induce the translocation of this receptor leading to an increase in cholesterol influx and storage. 10,11 However, the nutritional and hormonal regulation of this translocation and its potential consequences on plasma HDL have not been yet explored in vivo. Conclusions-OurBecause cholesterol plays a role in the regulation of signal transduction and gene expression, we further investigated the consequence of the cho...

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Fat-depleted CLA-treated mice enter torpor after a short period of fasting

Cited by 9 publications

References 20 publications

Norepinephrine Controls Both Torpor Initiation and Emergence via Distinct Mechanisms in the Mouse

Norepinephrine Controls Both Torpor Initiation and Emergence via Distinct Mechanisms in the Mouse

The Full Expression of Fasting-Induced Torpor Requires β3-Adrenergic Receptor Signaling

In Vivo Evidence for a Role of Adipose Tissue SR-BI in the Nutritional and Hormonal Regulation of Adiposity and Cholesterol Homeostasis

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