Interactions of cold exposure and starvation on glucose tolerance and insulin response

Vallerand, A. L.; Lupien, J.; Bukowiecki, L. J.

doi:10.1152/ajpendo.1983.245.6.e575

Cited by 35 publications

(45 citation statements)

References 18 publications

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“…1). This is quite different from the response to cold exposure, in which blood glucose levels in response to glucose administration are similar or slightly decreased compared to mice kept in the control environment, although insulin levels are decreased in both cold-and cool temperature-exposed mice [6,22,23].…”

Section: Resultscontrasting

confidence: 58%

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Metabolic adaptation of mice in a cool environment

Uchida

Shiuchi

Inada

et al. 2010

Pflugers Arch - Eur J Physiol

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Homeothermic animals, including humans, live by adapting to changes in ambient temperature. Numerous studies have demonstrated cold exposure (at approximately 5 degrees C) improves glucose tolerance despite reducing insulin secretion and increasing energy expenditure. To determine the effects of a small reduction in ambient temperature on energy metabolism, we compared two groups of mice; one exposed to a cool environment (20 degrees C) and the other maintained in a near-thermoneutral environment (25 degrees C) for 10 days. Both glucose-induced insulin secretion and glucose response were significantly impaired in mice exposed to a cool environment. In the cool temperature-exposed mice, skin temperatures were reduced, and plasma norepinephrine levels were increased, suggesting that impairment of insulin secretion was facilitated by induction of sympathetic nervous activity due to skin cooling. In addition, expression of GLUT4 mRNA was increased significantly in inguinal subcutaneous adipose tissue (IWAT) but not in epididymal or brown adipose tissue or skeletal muscle in these mice. Moreover, expression of Dok1, a molecule linked to activation of insulin receptors in adipocyte hypertrophy, and Cd36, a molecule related to NEFA uptake, were also increased at mRNA and/or protein levels only in IWAT of the cool temperature-exposed mice. Fatty acid synthesis was also facilitated, and fat weights were increased only in IWAT from mice kept at 20 degrees C. These results suggest that a small reduction in ambient temperature can affect glucose homeostasis through regulation of insulin secretion and preferentially enhances fat storage in IWAT. These adaptations can be interpreted as preparation for a further reduction in ambient temperature.

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Section: Resultscontrasting

confidence: 58%

“…After cold exposure, glucose clearance rates are improved, and blood insulin concentrations are reduced in both rodents and humans [18,21,22]. In addition, lipolysis is accelerated in humans after cold exposure [24].…”

Section: Introductionmentioning

confidence: 99%

Metabolic adaptation of mice in a cool environment

Uchida

Shiuchi

Inada

et al. 2010

Pflugers Arch - Eur J Physiol

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“…Through a decreased j3-adrenergic sensitivity, insulin could diminish UCP biosynthesis and thus play a role in the impaired brown adipose tissue thermogenesis usually associated with hyperinsulinemia in animal models of obesity (15). Otherwise, cold-adapted rats have an increased thermogenesis associated with suppressed plasma insulin levels (21). These observations suggest a negative correlation between insulin and thermogenesis.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional down-regulation by insulin of the beta 3-adrenergic receptor expression in 3T3-F442A adipocytes: a mechanism for repressing the cAMP signaling pathway.

Fève

Elhadri

Quignard‐Boulangé

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Modulation of the three -adrenergic receptor subtypes (1&ARs) by Insulin was investigated in mouse 3T3-F442A adipocytes. Saturation and competition experiments measuring binding of 12I-abeled (-)-cyanopindolol to adipocyte membranes demonstrated that cell exposure to insulin for 4 days caused a 3.5-fold decrease in the density of the major P-AR component of the adipocyte, the #3-AR, while 1i-AR sites remained unchanged and P2-ARs were undetectable. This correlated with a lower potency of the 13-ARselective agonists CGP12177, IC1201651, and BRL37344 in stimulating adenylate cyclase. Northern blotting analysis indicated that insulin induced a rapid and sharp decrease in 13-AR mRNA levels. This effect was detectable at low insulin concentrations (EC5o = 3 nM) and was not observed in the presence of insulin-like growth factor I, sugging an insulin receptormediated phenomenon. Reverse transcriptase-PCR analysis showed that, in contrast to Its dramatic down-regulatory effect on (3-AR mRNA, insulin did not modify the levels of JR,-and SE-AR transcripts. As as d by nuclear run-on assays, insulin inhibited the 13-AR gene transcription rate by 90% within 30 min. mRNA turnover experiments showed that the half-life of P3-AR mRNA was short (90 min) and remained unaffected by insulin. These findings demonstrate the genetic control of a 3-AR subtype expression by insulin and reveal a mechanism for the regulation by this hormone of cAMPdependent biological processes in adipocytes.

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“…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].…”

Section: Introductionmentioning

confidence: 99%

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

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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.

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Interactions of cold exposure and starvation on glucose tolerance and insulin response

Cited by 35 publications

References 18 publications

Metabolic adaptation of mice in a cool environment

Metabolic adaptation of mice in a cool environment

Transcriptional down-regulation by insulin of the beta 3-adrenergic receptor expression in 3T3-F442A adipocytes: a mechanism for repressing the cAMP signaling pathway.

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

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