Some changes in carbohydrate metabolism during acclimation to moderate hyperthermic environment in rats

Miova, Biljana; Dinevska-Ќovkarovska, Suzana; Mitev, Slavco

doi:10.1515/jbcpp.2008.19.1.65

Cited by 6 publications

(8 citation statements)

References 38 publications

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“…Besides the well-known hepatic glycogenolysis in the STHA [6][7][8], we also observed intensive glycogenolysis at the level of heart Glk stores (Fig. 1).…”

Section: Short-term Heat Acclimationsupporting

confidence: 63%

“…In this sense, there is an enhancement of the metabolic machinery to elevate the energy potential of heat-acclimated organism which is accompanied by a decrease of the rate of the whole body metabolism [4,5]. Metabolic changes which are most evident during heat acclimation are: energy sparing, which is manifested as a rebound of liver glycogen (Glk) in rats [6][7][8] and hamsters [9] (as a result of increased activity of enzymes involved in a direct Glk synthesis), and decreased glucose (Glu) production [6][7][8]. As is the case with the liver, heat acclimation produces favorable adaptations in mechanical and metabolic aspects of the heart performance, such as: twofold greater heart Glk level, increased b-adrenergic sensibility, lowered heart rate and greater stroke volume.…”

Section: Introductionmentioning

confidence: 99%

“…It consists of an early transient, ''inefficient'' acclimation phase [short-term heat acclimation (STHA), up to the 2nd day of heat exposure] to an ''efficient'' state after acclimation homeostasis has been reached [long-term heat acclimation (LTHA), after the 2nd day of heat exposure] [2,3]. The time-dependent changes of the hepatic carbohydrate metabolism have already been described [7], but little is known about time-dependent acclimatory changes of heart Glk metabolism in the direction of the elevation of the energy potential of the heat-acclimated organism.…”

Section: Introductionmentioning

confidence: 99%

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Heat acclimation-induced changes in heart glycogen/glucose metabolism in rats

et al. 2011

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Based on the observation that heat acclimation is a slowly developing response, evoked by continuous exposure to moderate heat, we investigated the time-dependent acclimatory changes of heart glycogen metabolism. Cardiac levels of key carbohydrate-related enzymes and substrates were studied in the function of the duration of short-term (STHA; 6, 12, 24 and 48 h) and long-term heat acclimation (LTHA; 7, 14, 21 and 30 days) to high environmental temperature (35 ± 1°C). The changes in heart glycogen metabolism during STHA could be separated in two phases: up to 12 h exposure, where significant decrease of the heart glycogen (Glk), glucose-6-phosphate (G6P), hexokinase (HK) activity as well as increase of heart glucose was observed; and from 24 to 48 h exposure, manifested with elevation of Glk, Glu, glycogen phosphorylase a (GPa), phosphofructokinase (PFK) and HK activities. The metabolic changes in the period of LTHA could also be seen as separate phases: in a period of 7-14 days of heat exposure there was an increase of heart Glk, Glu, G6P, HK, as well as a decrease of GPa and PFK, while in the period of 21-28 days there was more intensive rebound of Glk and G6P, increase of GPa activity and non-significant changes of Glu, HK and PFK. The results obtained have showed that acclimation to moderate hyperthermic environment has caused significant changes in examined parameters which differ depending on duration to the exposure: intensive stress-induced glycogenolytic and glycolytic processes in the period of STHA and intensive energy sparing, manifested by Glk deposition in the period of LTHA.

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“…Besides the well-known hepatic glycogenolysis in the STHA [6][7][8], we also observed intensive glycogenolysis at the level of heart Glk stores (Fig. 1).…”

Section: Short-term Heat Acclimationsupporting

confidence: 63%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heat acclimation-induced changes in heart glycogen/glucose metabolism in rats

et al. 2011

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“…Despite the fact that working muscles are the main source of endothermy (153,169) leading to fatigue and hyperthermic failure during severe heat stress, our knowledge of the impact of cross-adaptation on skeletal muscle is very limited. Young et al (245) indicated that heat acclimation lowers the aerobic metabolic rate and blood lactate accumulation during exercise in both cool and hot environments, but not at the expense of the greater glycogen reserves [noted in skeletal and cardiac muscles of adapted and cross-adapted humans and animals, (43,44,141,245)]. Lorenzo et al (126) demonstrated that active heat acclimation improves performance in temperate/cool environments and attributed this to adaptations in the vascular bed and changes in plasma volume.…”

Section: Skeletal Vs Cardiac Muscle Acclimation To Heat and Exercisementioning

confidence: 99%

Heat Acclimation, Epigenetics, and Cytoprotection Memory

Horowitz

2014

Comprehensive Physiology

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Heat acclimation is a within-life phenotypic adaptation to heat. Plasticity of the thermoregulatory system is crucial for the induction of heat acclimation. In the last two decades, it has become clear that heat causes adaptive shifts in gene expression which adjust the protein balance. These changes are part of the evolvement of the acclimated phenotype. The molecular-cellular aspects of some acclimatory mechanisms that have only been explained by physiological-effectorial mechanisms have been discovered. This review attempts to bridge the gap between the classic physiological heat acclimation profile and the molecular/cellular mechanisms underlying the evolvement of the acclimated phenotype. Heat acclimation leads to leftward and rightward shifts in temperature thresholds of heat dissipation organs and thermal injury, respectively, thereby expanding the acclimated dynamic thermoregulatory range. Interactions between ambient temperature and afferent drives from effector organs to the hypothalamic thermoregulatory center with modifications in warm/cold sensitive neuron ratio and excitability contribute to the threshold changes. The altered threshold for thermal injury is associated with progressive enhancement of inducible cytoprotective networks, including HSP70, HSF1, and HIF-1ɑ. These molecules are also important in acclimatory kinetics. Aspects of cross-adaption, cross-tolerance and interference with heat acclimation are explained using molecular-cellular physiological interactions, with the heart, skeletal muscles, and water secretory glands as models. Lastly, the roles of epigenetic mechanisms in transcriptional regulation during induction of the acclimated phenotype, its decay, and reinduction are discussed. Posttranslational histone modifications in the promoters of hsp70 and hsp90 form part of our prototype model of heat-acclimation-mediated cytoprotective memory.

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“…could be summarized in three phases: short-term heat exposure (1 to 24 h) with intensive glycogenolysis and gluconeogenesis to glucose; a period with temporary changes (24 h to 7 d) with tendency of normalization to control level, and prolonged heat acclimation (7 d to 60 d), which favours both direct and indirect glycogen synthesis [20].…”

Section: Discussionmentioning

confidence: 99%