Rapid rise in plasma glucagon induced by acute cold exposure in man and rat

Seitz, Hans; Krone, Wilhelm; Wilke, H; Tarnowski, W.; Carsten, D.; Dunkelmann, B.; Harneit, Angelika

doi:10.1007/bf00582100

Cited by 58 publications

(32 citation statements)

References 25 publications

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“…S). The hyperglycemic effect of cold stress is similar to that reported by Larkin et al (1992) in 26-mo-old male rats that were cold-stressed at 5°C for 4 h. The hyperglycaemic effect may be related to the diminished ability to oxidise carbohydrates in the cold and the mechanisms can be attributed to the increased plasma glucose levels in cold-stressed rats due to increased plasma glucagon leading to elevated hepatic gluconeogenesis and ketogenesis (Seitz et al, 1981) and this may not be the case in the old rats since the uptake and metabolism of glucose is reduced with age.…”

Section: Discussionsupporting

confidence: 80%

Intermittent cold-induced hippocampal oxidative stress is associated with changes in the plasma lipid composition and is modifiable by vitamins C and E in old rats

Devi

Manjula

2014

Neurochemistry International

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a b s t r a c tThis study primarily investigated the effects of intermittent cold exposure (ICE) on oxidative stress (OS) in the hippocampus(HC) and plasma lipid profile of old male rats. Secondly, it evaluated structural changes in the hippocampus region of the rat's brain. Thirdly, it attempted an evaluation of the effectiveness of the combined supplement of vitamins C and E in alleviating cold stress in terms of these biochemical parameters. Thirty male rats aged 24 months were divided into groups of five each: control (CON), cold-exposed at 10°C (C10), cold-exposed at 5°C (C5), supplemented control (CON+S), and supplemented cold-exposed at either 5°C (C5+S) or 10°C (C10+S). The rats were on a daily supplement of vitamin C and vitamin E. Cold exposure lasted 2 h/day for 4 weeks. Rats showed increased levels of hydrogen peroxide (H 2 O 2 ), and thiobarbituric acid reactive substances (TBARS) in the HC at 10°C with further increase at 5°C. Cold also induced neuronal loss in the hippocampus with concomitant elevations in total cholesterol (TCH), triglycerides (TG) and low-density lipoproteins (LDL-C) levels, and a depletion in high-density lipoprotein (HDL-C). A notable feature was the hyperglycaemic effects of ICE and depleted levels of vitamins C and E in the hippocampus and plasma while supplementation increased their levels. More importantly, a positive correlation was observed between plasmatic LDL-C, TCH and TG and hippocampal TBARS and H 2 O 2 levels. Further, intensity of cold emerged as a significant factor impacting the responses to vitamin C and E supplementation. These results suggest that cold-induced changes in the plasma lipid profile correlate with OS in the hippocampus, and that vitamin C and E together are effective in protecting from metabolic and possible cognitive consequences in the old under cold exposures.

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Section: Discussionsupporting

confidence: 80%

Intermittent cold-induced hippocampal oxidative stress is associated with changes in the plasma lipid composition and is modifiable by vitamins C and E in old rats

Devi

Manjula

2014

Neurochemistry International

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“…Effect of cold acclimation. Plasma glucagon level has been reported to increase by about 100 to 1,000pg/ml (about 3 x 10-11 to 3 x 10-10 M) during cold exposure and cold acclimation (KUROSHIMA and Doi,1976;KUROSHIMA et al, 1978KUROSHIMA et al, , 1981SEITZ et al, 1981). Glucagon binding in the present assay was 0.5 to 2 x i0' -5 mol/105 cells for these levels of glucagon (Fig.…”

Section: Discussionsupporting

confidence: 48%

Effect of cold acclimation on glucagon receptors of rat white adipocytes.

1986

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In order to determine the role of glucagon in cold acclimation, the changes in glucagon receptor were investigated in white adipocytes from cold-acclimated rats by establishing a glucagon radioreceptor assay method for isolated white adipocytes. The following conditions were found to be appropriate for specific glucagon receptor binding assay; cell concentration of about 1 x 105 cells/ml, 15 min preincubation with glucagon and 30 mm-reaction at 25°C in the presence of bacitracin (1 mg/ml). Cold acclimation decreased the size and increased the number of epididymal white adipocytes. Cold acclimation increased the number of glucagon receptors of white adipocytes, resulting in 140% in terms of unit cell, and 260% increase per unit surface area and 210% increase per whole tissue. However, the affinity of the binding site for glucagon was not affected. The results suggested that an enhanced metabolic response of cold-acclimated rats to glucagon could be partly explained by the increased number of glucagon receptor in white adipocytes.

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“…The primary action of glucagon on BAT has been considered to be lipolytic; while BAT sensitivity to glucagon, reflected by EC50, is higher, responsiveness is lower than to noradrenaline (reviewed in [S]). Plasma glucagon increases in both acute [9] and chronic [lo] cold exposure and glucagon secretion is increased, and insulin secretion reduced, from the arginine-stimulated isolated perfused rat pancreas during cold acclimation [I 11 and plasma insulin levels are also reduced in chronic cold exposure [12]. It has been suggested that glucagon may act in BAT to promote postlipolytic events as indicated by enhanced retention, and presumably utilization, of free fatty acids in BAT fragments [13].…”

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confidence: 98%

Modulation by insulin and glucagon of noradrenaline-induced activation of isolated brown adipocytes from the rat

Howland

Bond

1987

Eur J Biochem

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1. The effects of insulin (2 nM and 4 nM) upon oxygen consumption ( VoJ, lipolysis rates and indirectly derived rates of fatty acid utilization, by isolated brown adipocytes from warm-acclimated (W cells) and cold-acclimated (C cells) animals, induced by noradrenaline and glucagon separately and conjointly, are reported.2. Changes in interrelationships (coupling) between the parameters under different treatment regimes were assessed using bivariate regression analyses.3. Administration of glucagon with noradrenaline increased lipolysis/fatty acid utilization coupling without concomitant increase of Vo2 suggesting that glucagon may increase re-esterification through glycogenolytic generation of glycerol 3-phosphate, trapping intracellular fatty acid in excess of the capacity of disposal mechanisms, thus conserving respiratory substrate.4. W cells were unresponsive to glucagon in terms of lipolysis and po2'; C cells responded to glucagon with parallel increases in lipolysis rate and Both cell types responded to noradrenaline alone and conjointly with glucagon; C cells-were more sensitive to these agonists than W cells.5. Lipolysis/ Vo, coupling was reduced in C cells suggesting that in cold acclimation, noradrenaline-induced lipolysis rates are in excess of the capacity of cellular oxidation/re-esterification mechanisms.6. Insulin inhibited noradrenaline and glucagon-induced lipolysis, simultaneously increasing po2, supporting the hypothesis that glucose may be a thermogenic substrate in brown adipase tissue, permitting concurrent thermogenesis and lipogenesis. C cells were more insulin-sensitive than W cells.7. The data indicate that insulin may mediate its effects (additively with noradrenaline) by activation of pyruvate dehydrogenase, generating glycolytic flux and, in the presence of noradrenaline-inhibited lipogenesis, generate additional oxaloacetate, permitting increased P-oxidation.In homeotherms, non-shivering thermogenesis is mediated primarily by brown adipose tissue (BAT) [l]. The principal mechanism of activation is by means of increased sympathetic activity with liberation of noradrenaline from the dense adrenergic terminals with which the tissue is invested, and consequent activation of P-adrenergically mediated lipolysis leading to the liberation of free fatty acids from intracellular triacylglycerols. Subsequent P-oxidation of free fatty acids, associated with increased mitochondrial proton conductance induced by increased free fatty acid concentrations [2], leads to enhanced heat production by dissipation of the mitochondrial proton gradient [3]. A second effect attributed to noradrenaline release in chronic cold exposure is increased synthesis of mitochondrial protonophore [4].While noradrenaline appears to be the prime mediator of BAT thermogenesis [5], there is evidence that non-adrenergic factors such as glucagon [6, 71 may have permissive or

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Rapid rise in plasma glucagon induced by acute cold exposure in man and rat

Cited by 58 publications

References 25 publications

Intermittent cold-induced hippocampal oxidative stress is associated with changes in the plasma lipid composition and is modifiable by vitamins C and E in old rats

Intermittent cold-induced hippocampal oxidative stress is associated with changes in the plasma lipid composition and is modifiable by vitamins C and E in old rats

Effect of cold acclimation on glucagon receptors of rat white adipocytes.

Modulation by insulin and glucagon of noradrenaline-induced activation of isolated brown adipocytes from the rat

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