Body temperature regulation in diabetes

Kenny, Glen P.; Sigal, Ronald J.; McGinn, Ryan

doi:10.1080/23328940.2015.1131506

Cited by 204 publications

(181 citation statements)

References 186 publications

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“…46 The implications for such a deficiency are wide ranging and may increase susceptibility to metabolic disease, 46,47 impaired vascular function 48 and even contribute to the impaired thermoregulatory control evident in individuals with diabetes. 49 While there were no clear differences in the HSP70 response between either PH or EX, there were clear differences in the IL-6 response. Previous work has shown that temperature increases independently elevate IL-6.…”

Section: Discussionmentioning

confidence: 92%

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

et al. 2017

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Increasing physical activity remains the most widely publicized way of improving health and wellbeing. However, in populations that benefit most from exercise (EX), adherence is often poor and alternatives to EX are important to bring about health improvements. Recent work suggests a role for passive heating (PH) and heat shock proteins (HSP) in improving cardio-metabolic health. The aim of this study was to investigate the expression of HSP70 and interleukin-6 in response to either EX or PH and the subsequent effect on glucose control. Fourteen males volunteered and were categorized lean (BMI 23.5 § 2.2 kg¢m ¡2 ) or overweight (29.2 § 2.7 kg¢m ¡2 ) and completed 60 minutes of either moderate cycling at a fixed rate of metabolic heat production (EX) or warm water immersion in 40 C water (PH). Extracellular HSP70 increased from baseline in both conditions with no differences between PH (0.98 § 1.1 ng¢mL ¡1 ) or EX (0.84 § 1.0 ng¢mL ¡1 , p D 0.814). IL-6 increased following both conditions with a two-fold increase after PH and four-fold after EX. Energy expenditure increased by 61.0 § 14.4 kcal¢h ¡1 (79%) after PH. Peak glucose concentration after a meal immediately following PH was reduced when compared with EX (6.3 § 1.4 mmol¢L ¡1 versus 6.8 § 1.2 mmol¢L ¡1 ; p < 0.05). There was no difference in 24-hour glucose area under the curve (AUC) between conditions. These data indicate the potential for thermal therapy as an alternative treatment and management strategy for those at risk of developing metabolic disease where adherence, or ability to EX, may be compromised.

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Section: Discussionmentioning

confidence: 92%

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

et al. 2017

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“…Recently, diabetes has been linked to impairments in temperature control during exposure to thermal stress (43). Our studies reveal a direct link between temperature regulation and metabolism, indicating that a uridine-centered model of energy homeostasis may pave the way for future studies on uridine homeostasis and diabetes as well as other metabolic diseases.…”

Section: Discussionmentioning

confidence: 99%

An adipo-biliary-uridine axis that regulates energy homeostasis

Deng

Wang

Gordillo

et al. 2017

Science

117

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Uridine, a pyrimidine nucleoside present at high levels in the plasma of rodents and humans, is critical for RNA synthesis, glycogen deposition, and many other essential cellular processes. It also contributes to systemic metabolism, but the underlying mechanisms remain unclear. We found that plasma uridine levels are regulated by fasting and refeeding in mice, rats, and humans. Fasting increases plasma uridine levels, and this increase relies largely on adipocytes. In contrast, refeeding reduces plasma uridine levels through biliary clearance. Elevation of plasma uridine is required for the drop in body temperature that occurs during fasting. Further, feeding-induced clearance of plasma uridine improves glucose metabolism. We also present findings that implicate leptin signaling in uridine homeostasis and consequent metabolic control and thermoregulation. Our results indicate that plasma uridine governs energy homeostasis and thermoregulation in a mechanism involving adipocyte-dependent uridine biosynthesis and leptin signaling.

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“…Moreover, restoring purinergic receptor function might help preserve or re‐establish near‐normal levels of skin perfusion, which represents an important avenue of heat dissipation during heat stress. T2D is associated with higher rates of heat illness and death during heat stress when compared with the general population (Kenny et al., ; Kenny, Yardley, Brown, Sigal, & Jay, ).…”

Section: Discussionmentioning

confidence: 99%

Type 2 diabetes specifically attenuates purinergic skin vasodilatation without affecting muscarinic and nicotinic skin vasodilatation and sweating

Fujii

Meade

McNeely

et al. 2018

Experimental Physiology

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The present study evaluated whether type 2 diabetes (T2D) attenuates muscarinic and/or nicotinic cutaneous vasodilatation and sweating as well as purinergic cutaneous vasodilatation. Cutaneous vascular conductance and sweat rate were evaluated in 12 healthy non-diabetic older adults (Control, 60 ± 8 years) and 13 older adults with T2D (62 ± 10 years) at three intradermal forearm skin sites perfused with the following: (i) methacholine (muscarinic receptor agonist, five doses: 0.0125, 0.25, 5, 100 and 2000 mm); (ii) nicotine (nicotinic receptor agonist, five doses: 1.2, 3.6, 11, 33 and 100 mm); or (iii) ATP (purinergic receptor agonist, five doses: 0.03, 0.3, 3, 30 and 300 mm). Each agonist was administered for 25 min per dose. At the end of the protocol, 50 mm sodium nitroprusside was administered to all skin sites to elicit maximal cutaneous vasodilatation. Cutaneous vascular conductance during methacholine and nicotine administration did not differ between groups (all P > 0.05). In contrast, cutaneous vascular conductance during administration of 30 mm (42 ± 28 versus 63 ± 26% maximum, P ≤ 0.05) and 300 mm ATP (56 ± 24 versus 71 ± 20% maximum, P ≤ 0.05) was attenuated in individuals with T2D in comparison to the Control participants. Furthermore, cutaneous vascular conductance during administration of 50 mm sodium nitroprusside was lower in individuals with T2D relative to Control subjects (P = 0.04). Methacholine- and nicotine-induced sweating was similar between groups (all P > 0.05). Thus, T2D attenuates purinergic cutaneous vasodilatation without affecting muscarinic and nicotinic cutaneous vascular and sweating responses.

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Body temperature regulation in diabetes

Cited by 204 publications

References 186 publications

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

The effect of passive heating on heat shock protein 70 and interleukin-6: A possible treatment tool for metabolic diseases?

An adipo-biliary-uridine axis that regulates energy homeostasis

Type 2 diabetes specifically attenuates purinergic skin vasodilatation without affecting muscarinic and nicotinic skin vasodilatation and sweating

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