Relationship Between Intermittent Hypoxia and Type 2 Diabetes in Sleep Apnea Syndrome.
Adipose Tissue
/ metabolism
Animals
Diabetes Mellitus, Type 2
/ epidemiology
Glucose
/ metabolism
Humans
Hypoxia
/ complications
Insulin
/ metabolism
Insulin Resistance
Insulin-Secreting Cells
/ metabolism
Liver
/ metabolism
Muscle, Skeletal
/ metabolism
Nerve Tissue
/ metabolism
Organ Specificity
Sleep Apnea Syndromes
/ complications
adipokines
glucose-induced insulin secretion
hepatokines
intermittent hypoxia
myokines
pancreatic β cell proliferation
sleep apnea syndrome
type 2 diabetes
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
25 Sep 2019
25 Sep 2019
Historique:
received:
26
07
2019
revised:
13
09
2019
accepted:
23
09
2019
entrez:
28
9
2019
pubmed:
29
9
2019
medline:
12
2
2020
Statut:
epublish
Résumé
Sleep apnea syndrome (SAS) is a very common disease involving intermittent hypoxia (IH), recurrent symptoms of deoxygenation during sleep, strong daytime sleepiness, and significant loss of quality of life. A number of epidemiological researches have shown that SAS is an important risk factor for insulin resistance and type 2 diabetes mellitus (DM), which is associated with SAS regardless of age, gender, or body habitus. IH, hallmark of SAS, plays an important role in the pathogenesis of SAS and experimental studies with animal and cellular models indicate that IH leads to attenuation of glucose-induced insulin secretion from pancreatic β cells and to enhancement of insulin resistance in peripheral tissues and cells, such as liver (hepatocytes), adipose tissue (adipocytes), and skeletal muscles (myocytes). In this review, we focus on IH-induced dysfunction in glucose metabolism and its underlying molecular mechanisms in several cells and tissues related to glucose homeostasis.
Identifiants
pubmed: 31557884
pii: ijms20194756
doi: 10.3390/ijms20194756
pmc: PMC6801686
pii:
doi:
Substances chimiques
Insulin
0
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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