Prior heat stress induces moderation of diabetic alterations in glycogen metabolism of rats

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

doi:10.2478/s11535-013-0260-3

Cited by 4 publications

(4 citation statements)

References 51 publications

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“…Hepatic gluconeogenesis may drive fasting plasma glucose elevation in response to heat stress. In animal models, rapid depletion of hepatic glycogen content in response to heat stress was identified as a source for peripheral glucose increase [37]. In our study, it remains unclear what occurs with liver glycogen content following exposure of an acute bout of heat stress.…”

Section: Discussionmentioning

confidence: 79%

Whole body heat exposure modulates acute glucose metabolism

Kimball

McCue

Petrie

et al. 2018

International Journal of Hyperthermia

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Aim: Exercise modulates glucose tolerance and homeostasis in both healthy and diabetic individuals. Heat stress is a fundamental element of exercise. The acute glycemic response and alterations in glucose clearance following whole body passive heat stress in the absence of muscle activity has yet to be examined in humans. Knowledge of this relationship may prove useful, particularly in populations with compromised glucoregulation from reduced activity. Purpose: To determine insulin/glucose levels before and after an acute bout of heat stress in healthy, lean individuals and examine the effects of whole body heat stress (WBHS) and exercise on acute glucose tolerance in an expanded cohort. Methods: Ten subjects (24.1 ± 0.7 years) participated in a randomized control/WBHS session (up to 30 minutes at 73 C) with fasting glucose (FG) and insulin drawn at baseline, immediately after and 30 minutes post heat stress. In the follow-up experiment, 20 anthropometrically diverse subjects (24.6 ± 2.1 years) underwent an oral glucose tolerance test (OGTT) under the conditions above. Results: FG levels rose 10% immediately following heat stress (8.6 (±5.6) mg/dl, p < .01) and returned to near baseline levels 30 minutes following WBHS. Insulin release showed its greatest increase at 30 minutes post WBHS (2.7 ± 3.5) uU/ml p < .05). WBHS resulted in a decrease in glucose uptake [AUC increased 8.2% (1430[AUC increased 8.2% ( .6 ± 1957.03) mg/dl (p ¼ .005)], particularly in nonlean individuals. Conclusion: WBHS modulates physiologic markers of metabolism. An acute bout of WBHS increases glucose and insulin levels in healthy individual and decreases glucose uptake in response to a glucose challenge, particularly those who are non-lean. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 79%

Whole body heat exposure modulates acute glucose metabolism

Kimball

McCue

Petrie

et al. 2018

International Journal of Hyperthermia

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“…In the present study, 78% of plasma AA reduction was due to the decline in gluconeogenic AA. Increased whole-body glucose utilization is a conserved response to environmental hyperthermia reported in various species: cows (Ronchi et al, 1997;Rhoads et al, 2009; al., 2011), pigs (Victoria Sanz Fernandez et al, 2015), rodents (Miova et al, 2014), goats (Okoruwa, 2014), and so on. In agreement, in this study HS cows tended to have more severe hypoglycemia compared with PFTN controls.…”

mentioning

confidence: 99%

The effects of heat stress on protein metabolism in lactating Holstein cows

Gao

Guo

Quan

et al. 2017

Journal of Dairy Science

133

123

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Heat stress (HS) decreases milk protein synthesis beyond what would be expected based on the concomitant reduction in feed intake. The aim of the present study was to evaluate the direct effects of HS on milk protein production. Four multiparous, lactating Holstein cows (101 ± 10 d in milk, 574 ± 36 kg of body weight, 38 ± 2 kg of milk/d) were individually housed in environmental chambers and randomly allocated to 1 of 2 groups in a crossover design. The study was divided into 2 periods with 2 identical experimental phases (control phase and trial phase) within each period. During phase 1 or control phase (9 d), all cows were housed in thermal neutral conditions (TN; 20°C, 55% humidity) and fed ad libitum. During phase 2 or treatment phase (9 d), group 1 was exposed to cyclical HS conditions (32 to 36°C, 40% humidity) and fed ad libitum, whereas group 2 remained in TN conditions but was pair-fed (PFTN) to their HS counterparts to eliminate the confounding effects of dissimilar feed intake. After a 30-d washout period in TN conditions, the study was repeated (period 2), inverting the environmental treatments of the groups relative to period 1: group 2 was exposed to HS and group 1 to PFTN conditions. Compared with PFTN conditions, HS decreased milk yield (17.0%), milk protein (4.1%), milk protein yield (19%), 4% fat-corrected milk (23%), and fat yield (19%). Apparent digestibility of dry matter, organic matter, neutral detergent fiber, acid detergent fiber, crude protein, and ether extract was increased (11.1-42.9%) in HS cows, as well as rumen liquor ammonia (before feeding 33.2%; after feeding 29.5%) and volatile fatty acid concentration (45.3%) before feeding. In addition, ruminal pH was reduced (9.5 and 6% before and after feeding, respectively) during HS. Heat stress decreased plasma free amino acids (AA; 17.1%) and tended to increase and increased blood, urine, and milk urea nitrogen (17.2, 243, and 24.5%, respectively). Further, HS cows had reduced plasma glucose (8%) and nonesterified fatty acid (39.8%) concentrations compared with PFTN controls. These data suggest that HS increases systemic AA utilization (e.g., decreased plasma AA and increased nitrogen excretion), a scenario that limits the AA supply to the mammary gland for milk protein synthesis. Furthermore, the increase in AA requirements during HS might represent the increased need for gluconeogenic precursors, as HS is thought to prioritize glucose utilization as a fuel at the expense of nonesterified fatty acids.

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“…Heat stress also affects metabolic regulation of glucose as evidenced in this study by the significant elevation in serum glucose level in the AWBH group without any significant changes in the SWBH group. Similarly, acute bout of whole-body heat stress elevated serum glucose level (Kimball et al, 2018) that may be attributed to the rapid depletion of hepatic glycogen content and the intensive glycogenolysis in response to HS (Miova et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Whole Body Hyperthermia-Induced Brain Injury in Rats: Forensic Biochemical, Pathological, and Immunohistochemical Investigations

El-Borai,

El-Bahrawy,

Assayed

et al. 2023

Journal of Current Veterinary Research

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Episodes of hyperthermia occur frequently from exposure to infections or adverse climatic changes. Such hyperthermia has been linked to various detrimental health effects. This study aimed to investigate the pathophysiological responses to acute versus subacute whole-body hyperthermia (WBH) in rats, particularly on the brain, with special reference to their medicolegal importance. Rats were randomly assigned to three equal groups. The normothermic group was kept at room temperature, the acute whole-body hyperthermic (AWBH) group was subjected to long-period WBH as a single bout of 4 hours at 43 °C, and the subacute whole-body hyperthermic (SWBH) group was subjected to repeated short-period WBH;2 hours daily for 7 successive days at 43 °C. A significant increase in body temperature and a significant decrease in body weight were recorded in both the acute and subacute hyperthermic groups. However, significant elevations in the serum glucose and cortisol levels and in the brain malondialdehyde and 8-hydroxy-2'-desoxyguanosine levels, with a significant reduction in brain total antioxidant capacity, were observed only in the AWBH group. Moreover, exposure to WBH induced various degrees of pathological changes, along with positive immune reactivity for heat shock protein 70 and glial fibrillary acidic protein in the cerebrum and cerebellum of rats in both hyperthermic groups. Overall, WBH induced various adverse health effects, mediated by the induction of oxidative damage, particularly following acute exposure. Hence, these findings provide evidence that acute exposure to long-term WBH may markedly exacerbate brain injury more than repeated short-term exposure, reflecting the role of the adaptive mechanisms to repeated heat exposure. Interestingly, the obtained findings may be valuable in the forensic antemortem and postmortem diagnosis of WBH and heat-related deaths.

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Prior heat stress induces moderation of diabetic alterations in glycogen metabolism of rats

Cited by 4 publications

References 51 publications

Whole body heat exposure modulates acute glucose metabolism

Whole body heat exposure modulates acute glucose metabolism

The effects of heat stress on protein metabolism in lactating Holstein cows

Whole Body Hyperthermia-Induced Brain Injury in Rats: Forensic Biochemical, Pathological, and Immunohistochemical Investigations

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