Brown adipose tissue: is it affected by intermittent hypoxia?

Martinez, Dênis; Fiori, Cíntia Zappe; Baronio, Diego; Carissimi, Alícia; Kaminski, Renata Schenkel Rivera; Kim, Lenise Jihe; Rosa, Darlan Pase da; Bós, Ângelo José Gonçalves

doi:10.1186/1476-511x-9-121

Cited by 16 publications

(10 citation statements)

References 20 publications

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“…In morbidly obese patients undergoing bariatric surgery, ARON-WISNEWSKY et al [33] found no association between intermittent hypoxia and macrophage accumulation or adipocyte size in omental or subcutaneous fat; tissue PO 2 was not measured. As BAT is concerned, a trend towards decreased body weight and BAT in rats exposed to isocapnic intermittent hypoxia for 3 weeks has been reported [34]. No study to date has examined the role of chronic intermittent hypoxia on the transition from white to brown adipocytes, a topic of great interest in the current obesity literature.…”

Section: Osa and Type 2 Diabetes: An Independent Relationship?mentioning

confidence: 99%

Sleep apnoea and metabolic dysfunction

Bonsignore¹,

Borel²,

Machan³

et al. 2013

European Respiratory Review

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Obstructive sleep apnoea (OSA) is a highly prevalent condition often associated with central obesity. In the past few years, several studies have analysed the potential independent contribution of OSA to the pathogenesis of metabolic abnormalities, including type 2 diabetes, the metabolic syndrome and nonalcoholic fatty liver disease. New perspectives in OSA patient care have been opened by the promotion of lifestyle interventions, such as diet and exercise programmes that could improve both OSA and the metabolic profile. The rich clinical literature on this subject, together with the growing amount of data on pathophysiological mechanisms provided by animal studies using the chronic intermittent hypoxia model, urged the organising Committee of the Sleep and Breathing meeting to organise a session on sleep apnoea and metabolic dysfunction, in collaboration with the European Association for the Study of Diabetes. This review summarises the state-of-the-art lectures presented in the session, more specifically the relationship between OSA and diabetes, the role of OSA in the metabolic consequences of obesity, and the effects of lifestyle interventions on nocturnal respiratory disturbances and the metabolic profile in OSA patients. @ERSpublications Treatment of obesity and metabolic diseases through diet and exercise should be part of OSA management besides CPAP

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Section: Osa and Type 2 Diabetes: An Independent Relationship?mentioning

confidence: 99%

Sleep apnoea and metabolic dysfunction

Bonsignore¹,

Borel²,

Machan³

et al. 2013

European Respiratory Review

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“…The inhibitory effects of hypoxia on the intensity of coldinduced BAT activity include a lower afferent blood flow to BAT [48], reduced sympathetic nerve activity [49], desensitized response to norepinephrine (a potent BAT activating agent [50,51]) [52], and can eventually lead to a reduction in BAT mass during prolonged exposure to hypoxia [53,54]. In addition, hypoxia results in the inhibition of shivering upon exposure to low Ta compared to normoxic controls in mice, dogs, and man [42].…”

Section: The Effect Of Hypoxia-induced Anapyrexia On Thermoregulatorymentioning

confidence: 99%

The physiology of artificial hibernation

Heger

2015

JCTRes

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Incomplete understanding of the mechanisms responsible for induction of hibernation prevent translation of natural hibernation to its artificial counterpart. To facilitate this translation, a model was developed that identifies the necessary physiological changes for induction of artificial hibernation. This model encompasses six essential components: metabolism (anabolism and catabolism), body temperature, thermoneutral zone, substrate, ambient temperature, and hibernation-inducing agents. The individual components are interrelated and collectively govern the induction and sustenance of a hypometabolic state. To illustrate the potential validity of this model, various pharmacological agents (hibernation induction trigger, delta-opioid, hydrogen sulfide, 5'-adenosine monophosphate, thyronamine, 2-deoxyglucose, magnesium) are described in terms of their influence on specific components of the model and corollary effects on metabolism. Relevance for patients: The ultimate purpose of this model is to help expand the paradigm regarding the mechanisms of hibernation from a physiological perspective and to assist in translating this natural phenomenon to the clinical setting.

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“…Mice were kept six each in cages measuring 30 x 19 x 13 cm, at an average room temperature of 22.4º ± 0.6° C and controlled humidity, on a standard 12/12 hour light-dark cycle (lights on at 0700, lights out at 1900). This method was described previously (18,19). All procedures were performed in accordance with the Guide for the Care and Use of Laboratory Animals (20) and were approved by the institutional animal care committee, Hospital de Clínicas de Porto Alegre (CEUA/HCPA #2009/09300).…”

Section: Animalsmentioning

confidence: 99%

“…The intermittent hypoxia procedure has been described previously in adult male mice (18,19), a mixture of 90% N 2 and 10% CO 2 was released into the cages over a period of 30 seconds, gradually reducing the oxy gen fraction to 7 ± 1% and increasing the CO 2 fraction to approximately 5 ± 1%; fans were then operated for 30 seconds so as to introduce room air into the cage. Overall, 480 such cycles of hypoxianormoxia occurred per day.…”

Section: Intermittent Hypoxia Systemmentioning

confidence: 99%

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Melatonin prevents hyperglycemia in a model of sleep apnea

Kaminski

Martinez

Fagundes

et al. 2015

Arch. Endocrinol. Metab.

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Objective: Obstructive sleep apnea is a common disorder associated with aging and obesity. Apneas cause repeated arousals, intermittent hypoxia, and oxidative stress. Changes in glucolipidic profile occur in apnea patients, independently of obesity. Animal models of sleep apnea induce hyperglycemia. This study aims to evaluate the effect of the antioxidants melatonin and N-acetylcysteine on glucose, triglyceride, and cholesterol levels in animals exposed to intermittent hypoxia. Materials and methods: Two groups of Balb/c mice were exposed to intermittent hypoxia (n = 36) or sham intermittent hypoxia (n = 36) for 35 days. The intermittent hypoxia group underwent a total of 480 cycles of 30 seconds reducing the inspired oxygen fraction from 21% to 7 ± 1% followed by 30 seconds of normoxia, during 8 hours daily. Melatonin or N-acetylcysteine were injected intraperitonially daily from day 21 on. Results: At day 35, glucose levels were significantly higher in the intermittent hypoxia group than in the control group. The intermittent hypoxia groups receiving N-acetylcysteine and vehicle showed higher glucose levels than the group receiving melatonin. The lipid profile was not affected by intermittent hypoxia or antioxidant administration. Conclusions:The present results suggest that melatonin prevents the well-recognized increase in glucose levels that usually follows exposure to intermittent hypoxia. Further exploration of the role of melatonin in sleep apnea is warranted. Arch Endocrinol Metab. 2015;59(1):66-70

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Brown adipose tissue: is it affected by intermittent hypoxia?

Cited by 16 publications

References 20 publications

Sleep apnoea and metabolic dysfunction

Sleep apnoea and metabolic dysfunction

The physiology of artificial hibernation

Melatonin prevents hyperglycemia in a model of sleep apnea

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