The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms

Briançon‐Marjollet, Anne; Weiszenstein, Martin; Henri, Marion; Thomas, Amandine; Godin‐Ribuot, Diane; Polàk, Jan

doi:10.1186/s13098-015-0018-3

Cited by 198 publications

(174 citation statements)

References 317 publications

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“…Sleep is of upmost importance in life, with multiple links to cognition52 and metabolism 53. In manifest HD, disturbances have been reported in all 3 of these areas, but have not been systematically studied in patients prior to motor disease onset.…”

Section: Discussionmentioning

confidence: 99%

Sleep deficits but no metabolic deficits in premanifest Huntington's disease

Lázár

Panin

Goodman

et al. 2015

Annals of Neurology

104

107

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ObjectiveHuntington disease (HD) is a fatal autosomal dominant, neurodegenerative condition characterized by progressively worsening motor and nonmotor problems including cognitive and neuropsychiatric disturbances, along with sleep abnormalities and weight loss. However, it is not known whether sleep disturbances and metabolic abnormalities underlying the weight loss are present at a premanifest stage.MethodsWe performed a comprehensive sleep and metabolic study in 38 premanifest gene carrier individuals and 36 age‐ and sex‐matched controls. The study consisted of 2 weeks of actigraphy at home, 2 nights of polysomnography and multiple sleep latency tests in the laboratory, and body composition assessment using dual energy x‐ray absorptiometry scanning with energy expenditure measured over 10 days at home by doubly labeled water and for 36 hours in the laboratory by indirect calorimetry along with detailed cognitive and clinical assessments. We performed a principal component analyses across all measures within each studied domain.ResultsCompared to controls, premanifest gene carriers had more disrupted sleep, which was best characterized by a fragmented sleep profile. These abnormalities, as well as a theta power (4–7Hz) decrease in rapid eye movement sleep, were associated with disease burden score. Objectively measured sleep problems coincided with the development of cognitive, affective, and subtle motor deficits and were not associated with any metabolic alterations.InterpretationThe results show that among the earliest abnormalities in premanifest HD is sleep disturbances. This raises questions as to where the pathology in HD begins and also whether it could drive some of the early features and even possibly the pathology. Ann Neurol 2015;78:630–648

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Section: Discussionmentioning

confidence: 99%

Sleep deficits but no metabolic deficits in premanifest Huntington's disease

Lázár

Panin

Goodman

et al. 2015

Annals of Neurology

104

107

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“…24 Van Cauter et al 25 descrevem que a presença de ondas lentas de sono, o sono mais reparador, está associada à diminuição da frequência cardíaca, pressão arterial, atividade nervosa simpática e utilização da glicose cerebral, em comparação com o estado de vigília. Durante o aparecimento dessas ondas, são liberados hormônios anabólicos, como o hormônio do crescimento (GH), enquanto outros hormônios, como o cortisol, são inibidos.…”

Section: Discussionunclassified

Efeito do estresse sobre o metabolismo glicídico de camundongos tornados obesos

Gozoli¹,

Zeca

Calzzetta

et al. 2017

Rev. Fac. Ciênc. Méd. Sorocaba

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RESUMOIntrodução: Distúrbios do sono, isoladamente ou em associação a uma dieta rica em calorias, podem determinar alterações metabólicas no sistema nervoso autônomo e no eixo hipotálamo-hipófise-adrenal, os quais podem aumentar a glicemia e produzir intolerância à glicose. O estado de intolerância à glicose geralmente precede o aparecimento de diabetes tipo 2. Objetivo: Este estudo visou avaliar os efeitos da associação da privação de sono paradoxal e dieta hipercalórica sobre o comportamento alimentar e a tolerância à glicose de camundongos. Métodos: Camundongos Swiss foram distribuídos em seis grupos: (1) controle; (2) dieta hipercalórica; (3) privação de sono paradoxal; (4) privação de sono paradoxal + dieta hipercalórica; (5) monoglutamato de sódio (MSG); e (6) privação de sono paradoxal + monoglutamato de sódio (MSG+PSP). Durante as oito semanas de acompanhamento, o consumo alimentar foi avaliado e os camundongos pesados periodicamente. A privação de sono foi realizada semanalmente. Após oito semanas executou-se o teste de tolerância oral à glicose (TTGO) e de sensibilidade à insulina (TTI). Ao final, houve pesagem do coração e da gordura epididimal. Resultados: Houve aumento significante do peso corporal nos camundongos tornados obesos, que se associou com o avanço do conteúdo de gordura visceral. Todos os animais, obesos e com privação de sono paradoxal, tiveram piora no metabolismo de glicose medido pelo TTGO e TTI. Não houve mudança no peso cardíaco. Conclusão: A administração de uma dieta hipercalórica e a privação de sono paradoxal determinam intolerância à glicose e resistência à insulina, que nesse trabalho não foi sinérgico. Palavras-chave: sono REM; obesidade; transtornos do metabolismo de glucose; camundongos. ABSTRACT Introduction: Sleep disorders, alone or in association with a high-calorie diet, may determine metabolic changes in the autonomic nervous system and in the hypothalamic-pituitary-adrenal axis, which may increase glycemia and produce glucose intolerance. The state of glucose intolerance usually precedes the onset of type 2 diabetes. Objective: This study aims to evaluate the effects of the association of paradoxical sleep deprivation and hypercaloric diet on the eating behavior and glucose tolerance of mice. Methods: Swiss mice were distributed into six groups: (1) control; (2) hypercaloric diet; (3) paradoxical sleep deprivation; (4) paradoxical sleep deprivation + hypercaloric diet; (5) monossodium glutamate (PSP); and (6) paradoxical sleep deprivation + monossodium glutamate. During the eight-week follow-up, food consumption was assessed and mice were weighed periodically. Sleep deprivation was performed weekly. After eight weeks, the oral glucose tolerance (TTGO) and insulin sensitivity test (TTI) were performed. At the end, heart and epididymal fat were weighed. Results: There was a significant increase in body weight in obese mice, which was associated with increased visceral fat content. All animals, obese and PSP, showed worsening in the parameters that measured the glucose...

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“…Yet, we cannot rule out the involvement of others toxic compounds, particularly during NAFPD progression. Indeed, some studies suggest a possible causal relationship between NAFLD/ NAFPD-related disorders with chronic intermittent hypoxia elicited by obstructive sleep apnea [165,166], bacterial endotoxin [167][168][169], glyceraldehyde [170], methylglyoxal [171][172][173], advanced glycation end products (AGE)s [174], receptor for advanced glycation end products (RAGE) [175], nitric oxide/peroxynitrite [176], and lipid peroxidation end products [177,178].…”

Section: Discussionmentioning

confidence: 99%

Nonalcoholic fatty pancreas disease as an endogenous alcoholic fatty pancreas disease

Medeiros¹,

Lima²

2016

Gastroenterol Hepatol Endosc

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Nonalcoholic fatty pancreas disease (NAFPD) is closely linked to nonalcoholic steatohepatitis (NASH), suggesting that the two conditions share a common etiopathogenetic background. In Addition, growing evidence indicates that endogenous ethanol (EE) plays a fundamental role in NASH pathogenesis. Accordingly, it is intuitively appealing to assume that EE plays also a causative role in NAFPD development. This connection is further supported by the finding that NAFPD shares with alcoholic fatty pancreas disease (AFPD) similar metabolic signaling pathways and histopathological features. However, low blood alcohol concentrations (BAC) along with the alleged inability of gut microbiota to produce toxic amounts of ethanol are the main obstacles to validate the idea of an endogenous alcoholic fatty pancreas disease (EAFPD). Here, we provide a mechanistic explanation reconciling the EAFPD hypothesis with these apparently conflicting observations. The key conclusions of our investigation are as follows. First, ethanol is a prodrug, implicating that under extensive presystemic metabolism BACs can be low and/ or absent. Second, oro-gastrointestinal microbiota may produce higher amounts of ethanol than those required to cause AFPD. Last, livers of NASH/NAFPD individuals overexpress all genes encoding alcohol-metabolizing enzymes identically to livers of patients with alcoholic hepatitis. Even more importantly, the upregulation of these genes is higher in the early steatotic stage of nonalcoholic fatty liver disease than in alcoholic hepatitis. This suggests a greater exposure of the liver, and by extension, of the pancreas, to ethanol in the former than in the latter condition. In summary, this paper provides a mechanistic framework for how NAFPD indeed may be an EAFPD.

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The impact of sleep disorders on glucose metabolism: endocrine and molecular mechanisms

Cited by 198 publications

References 317 publications

Sleep deficits but no metabolic deficits in premanifest Huntington's disease

Sleep deficits but no metabolic deficits in premanifest Huntington's disease

Efeito do estresse sobre o metabolismo glicídico de camundongos tornados obesos

Nonalcoholic fatty pancreas disease as an endogenous alcoholic fatty pancreas disease

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