Influence of ambient temperature on excretion of catecholamines and metabolites

Shum, Andrew Yau‐Chik; Jin, G.; Flattery, K. V.

doi:10.1152/ajplegacy.1969.216.5.1164

Cited by 47 publications

(14 citation statements)

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“…One possible explanation for this discrepancy might be that the contribution of inflammation to insulin resistance is limited to animals that are metabolically stressed. For example, housing of mice at T a of 20–22°C imposes significant cold stress, resulting in the secretion of glucocorticoids and the activation of sympathetic nervous system (Gordon, 1993; Leduc, 1961; Shum et al, 1969; Yahata and Kuroshima, 1987). Because both glucocorticoids and catecholamines are catabolic, they interfere with the normal anabolic actions of insulin (Hall, 2010).…”

Section: Discussionmentioning

confidence: 99%

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

et al. 2016

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SUMMARY Chronic, low-grade inflammation triggered by excess intake of dietary lipids has been proposed to contribute to the pathogenesis of metabolic disorders, such as obesity, insulin resistance, type 2 diabetes, and atherosclerosis. Although considerable evidence supports a causal association between inflammation and metabolic diseases, most tests of this link have been performed in cold-stressed mice that are housed below their thermoneutral zone. We report here that thermoneutral housing of mice has a profound effect on the development of metabolic inflammation, insulin resistance, and atherosclerosis. Mice housed at thermoneutrality develop metabolic inflammation in adipose tissue and in the vasculature at an accelerated rate. Unexpectedly, this increased inflammatory response contributes to the progression of atherosclerosis but not insulin resistance. These findings not only suggest that metabolic inflammation can be uncoupled from obesity-associated insulin resistance, but also point to how thermal stress might limit our ability to faithfully model human diseases in mice.

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Section: Discussionmentioning

confidence: 99%

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

et al. 2016

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“…Changes in rates of excretion of noradrenaline (Eeduc 1961 ) and its metabolites (Shum et al 1969), in tissue content of noradrenaline (Leduc 196 1 ) , in rate of synthesis of noradrenaline in tissues (Cordon et al 1946), in rate of renewal of noradrenaline (Costa et al 1969) and in tissue levels of tyrosine 3-hydroxylase (EC 1.14.1 6.2) (Gibson et al 1969) are early examples of methods used to detect increased SWS activity during cold exposure. These methods, however, are not useful for detecting acute changes in SNS activity in intact animals.…”

Section: Inkpodueticanmentioning

confidence: 99%

Dopamine β-Hydroxylase in Rat Serum and Lymph: Changes with Age and Effect of Cold Exposure

Behrens¹,

Depocas²

1975

Can. J. Physiol. Pharmacol.

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The pH optimum for rat serum dopamine beta-hydroxylase (DBH) (3,4-dihydroxyphenylethylamine, ascorbate:oxygen oxidoreductase (beta-hydroxylating)(EC 1.14.17.1) was 4.0 in acetate buffer; other requirements were as reported by others. DBH activity in serum of 20-day-old fetuses is slightly higher than in that of their mothers. Levels of the enzyme in blood a few hours after birth are almost five times greater than in the adult, remain high during the suckling period, then drop rapidly during the 4th week after birth to about three times the adult level, which is then slowly reached over the next few weeks. These fluctuations in serum DBH activity coincide with the period of intense development and maturation of the sympathetic nervous system. There was not significant effect of cold exposure on blood DBH activity when newborn, suckling, weanling or adult warm- and cold-acclimated rats were exposed to cold. Similarly, exposure to cold that elicited two- to three-fold increases in O2 consumption failed to increase DBH activity in thoracic duct lymph. Therefore serum and lymph DBH activities are not sensitive indices of sympathetic secretory activity in the intact rat.

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“…The suggestion that cold exposure causes increased activation of the peripheral sympathetic nervous system rests on two sources of evidence: an increase in the turnover rate of noradrenaline in organs with a sympathetic innervation (Spector, Gordon, Sjoerdsma & Udenfriend, 1967;Costa, Neff & Ngai, 1969;Bralet, Beley & Lallemant, 1972) and an increase in the noradrenaline excretion in the urine (Leduc, 1961;Shum, Johnson & Flattery, 1969;Bibbiani & Viola-Magni, 1971;Konzett, Hortnagl, Hortnagl & Winkler, 1971).…”

Section: Introductionmentioning

confidence: 99%

Noradrenaline Release in Rats During Prolonged Cold‐stress and Repeated Swim‐stress

Benedict

Fillenz²,

Stanford³

1979

British J Pharmacology

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Plasma noradrenaline concentration in rats was measured during prolonged cold‐stress and repeated swim‐stress. Cold exposure for 6 h caused a rise in plasma noradrenaline which reached a peak at 4 h. Administration of desmethylimipramine and normetanephrine to block neuronal and extraneuronal uptake of noradrenaline raised plasma noradrenaline concentration without changing the pattern of the response to cold exposure. Repeated cold exposure on subsequent days produced no change in the pattern of plasma noradrenaline concentration. Five successive 1‐min swims at 30‐min intervals caused a rise in plasma noradrenaline concentration which was maximal after the third swim. It is suggested that prolonged and repeated activation of sympathetic nerve terminals leads to a decline in noradrenaline release.

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Influence of ambient temperature on excretion of catecholamines and metabolites

Cited by 47 publications

References 0 publications

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

Thermoneutral Housing Accelerates Metabolic Inflammation to Potentiate Atherosclerosis but Not Insulin Resistance

Dopamine β-Hydroxylase in Rat Serum and Lymph: Changes with Age and Effect of Cold Exposure

Noradrenaline Release in Rats During Prolonged Cold‐stress and Repeated Swim‐stress

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