Energy Metabolism During Cold Exposure

Vallerand, A. L.; Jacobs, Ira

doi:10.1055/s-2007-1024636

Cited by 27 publications

(11 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cold exposure has been reported to improve glucose tolerance in rats (29,30). To test whether this holds true in mice and whether the effect is influenced by rapamycin treatment, we performed glucose tolerance tests after 72 h of cold challenge.…”

Section: Resultsmentioning

confidence: 99%

Rapamycin Blocks Induction of the Thermogenic Program in White Adipose Tissue

Tran

Mukherjee

et al. 2016

Diabetes

View full text Add to dashboard Cite

Rapamycin extends life span in mice, yet paradoxically causes lipid dysregulation and glucose intolerance through mechanisms that remain incompletely understood. Whole-body energy balance can be influenced by beige/brite adipocytes, which are inducible by cold and other stimuli via β-adrenergic signaling in white adipose depots. Induction of beige adipocytes is considered a promising strategy to combat obesity because of their ability to metabolize glucose and lipids, dissipating the resulting energy as heat through uncoupling protein 1. Here, we report that rapamycin blocks the ability of β-adrenergic signaling to induce beige adipocytes and expression of thermogenic genes in white adipose depots. Rapamycin enhanced transcriptional negative feedback on the β3-adrenergic receptor. However, thermogenic gene expression remained impaired even when the receptor was bypassed with a cell-permeable cAMP analog, revealing the existence of a second inhibitory mechanism. Accordingly, rapamycin-treated mice are cold intolerant, failing to maintain body temperature and weight when shifted to 4°C. Adipocyte-specific deletion of the mTORC1 subunit Raptor recapitulated the block in β-adrenergic signaling. Our findings demonstrate a positive role for mTORC1 in the recruitment of beige adipocytes and suggest that inhibition of β-adrenergic signaling by rapamycin may contribute to its physiological effects.

show abstract

Section: Resultsmentioning

confidence: 99%

Rapamycin Blocks Induction of the Thermogenic Program in White Adipose Tissue

Tran

Mukherjee

et al. 2016

Diabetes

View full text Add to dashboard Cite

show abstract

“…Higher levels of cold stress at HA may be responsible for the difference in antioxidant and redox status between SOJ 1 and SOJ 2 at HA. Cold might act as a potential cause of free radical generation in ubiquinone-coenzyme Q juncture of mitochondrial electron transport chain (Askew 1995;Rauen et al 1998;Venditti et al 2007) by inducing rapid increase in energy expenditure as well as metabolic rate (Vallerand and Jacobs 1992;Hoyt et al 1994). Almost 10% higher resting oxygen consumption was also noted in SOJ 1 which is attributed to the higher REE in SOJ 1 as compared to SOJ 2 at HA (our unpublished observation with the same volunteers).…”

Section: Discussionmentioning

confidence: 98%

Antioxidant and oxidative stress responses of sojourners at high altitude in different climatic temperatures

et al. 2009

View full text Add to dashboard Cite

High altitude (HA) is a multi-stressor environment comprising hypobaric hypoxia and cold. Climatic temperature varies with seasonal variation at HA. The present study was undertaken to investigate the effect of ambient temperature on antioxidant profile among sojourners at HA. The study was conducted on sojourners exposed to an altitude of 4,560 m in two different seasons and categorized into two groups (SOJ 1, n=63, ambient temp. at HA: -6 degree to +10degreeC; SOJ 2, n=81, ambient temp. at HA: 3degree-22degreeC). Blood was collected at sea level (SL) and after 4 weeks of HA exposure. Antioxidant enzymes showed significant upregulation in SOJ 2 at HA. In SOJ 1, superoxide dismutase and glutathione peroxidase showed significant upregulation but catalase and glutathione reductase showed significant decrease at HA. Non-enzymatic antioxidants showed significant reduction in SOJ 1 whereas a sustained antioxidant profile was observed in SOJ 2 at HA. Oxidative stress markers showed higher levels in SOJ 1 than SOJ 2 at HA. Differences observed between SOJ 1 and SOJ 2 at HA may be the consequence of different environmental temperatures. Cold stress was higher in SOJ 1 as evidenced from the significantly lower oral temperature in SOJ 1 as compared to SOJ 2. Cold- and hypoxia-induced increase in energy expenditure was significantly high in SOJ 1 than SOJ 2. To conclude, chronic exposure to hypoxia in moderate climatic temperature has a potential preconditioning effect on antioxidant system, but exposure to both cold and hypoxia causes greater oxidative stress due to altered metabolic rate.

show abstract

“…Cold exposure of homeothermic animals leads to improved glucose uptake in spite of an apparent resistance to insulin action [8,29,30]. During cold exposure, a high adrenergic tonus stimulates lipolysis in white adipose tissue and thermogenesis in brown adipose tissue (BAT) [7,15,20,28]. The adrenergic signals generated during cold exposure may also participate in the control of glucose flow by modulating insulin action and perhaps activating insulin-independent mechanisms of glucose uptake [4,13,17,23].…”

Section: Introductionmentioning

confidence: 98%

β3-Adrenergic-dependent and -independent mechanisms participate in cold-induced modulation of insulin signal transduction in brown adipose tissue of rats

Gasparetti

Alvarez-Rojas

Araújo

et al. 2004

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

During cold exposure, homeothermic animals mobilize glucose with higher efficiency than at thermoneutrality. An interaction between the insulin signal transduction machinery and high sympathetic tonus is thought to play an important role in this phenomenon. In the present study, rats were exposed to cold during 8 days and treated, or not, with a beta3-adrenergic agonist, BRL37344 sodium 4-2-2-(3-chlorophenyl)-2-hydroxyethyl amino propyl phenoxy-acetic acid sodium (BRL37344), or antagonist, SR59230A 3-(2-ethylphenoxy)-[(1S)-1,2,3,4-tetrahydronaphth-1-ylamino]-(2S)-2-propanol oxalate (SR59230A), to evaluate the cross-talk between insulin and beta3-adrenergic intracellular signaling in brown adipose tissue. The drugs did not modify food ingestion, body temperature, and body weight in control and cold-exposed rats. Treatment of control rats with BRL37344 led to higher insulin-induced tyrosine phosphorylation of the insulin receptors, insulin receptor substrate (IRS)-1 and ERK, higher insulin-induced IRS-1/PI3-kinase association, and higher [Ser(473)] phosphorylation of Akt. Cold exposure alone promoted higher insulin-induced tyrosine phosphorylation of the insulin receptors, IRS-1, IRS-2, and ERK, and higher insulin-induced IRS-1 and IRS-2/PI3-kinase association. Except for the regulation of ERK, SR59230A abolished all the cold-induced effects upon the insulin signal transduction pathway. However, this antagonist only partially inhibited the cold-induced increase of glucose uptake. Thus, the sympathetic tonus generated during cold-exposure acts, in brown adipose tissue, through the beta3-adrenergic receptor and modulates insulin signal transduction, with the exception of ERK. However, insulin-independent mechanisms other than beta3-adrenergic activation participate in cold-induced glucose uptake in brown adipose tissue of rats.

show abstract

Energy Metabolism During Cold Exposure

Cited by 27 publications

References 5 publications

Rapamycin Blocks Induction of the Thermogenic Program in White Adipose Tissue

Rapamycin Blocks Induction of the Thermogenic Program in White Adipose Tissue

Antioxidant and oxidative stress responses of sojourners at high altitude in different climatic temperatures

β3-Adrenergic-dependent and -independent mechanisms participate in cold-induced modulation of insulin signal transduction in brown adipose tissue of rats

Contact Info

Product

Resources

About