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insulin resistance/hypoxie
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Seite 1 von 674 Ergebnisse
von Willebrand factor antagonizes nitric oxide synthase to promote insulin resistance during hypoxia.
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Hypoxic respiratory diseases or hypoxia exposures are frequently accompanied by glucose intolerance and impaired nitric oxide (NO) availability. However, the molecular mechanism responsible for impaired NO production and insulin resistance (IR) during hypoxia remains obscure. In this study, we
Effects of acute intermittent hypercapnic hypoxia on insulin sensitivity in piglets using euglycemic clamp.
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Continuous hypoxia is associated with insulin resistance, altered glucose metabolism, and increased sympathetic nervous activity. This study examined the effect of 2 successive exposures to intermittent hypercapnic hypoxia (IHH) on glucose metabolism and insulin sensitivity in neonatal piglets.
The effect of hypoxia and work intensity on insulin resistance in type 2 diabetes.
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BACKGROUND
Hypoxia and muscle contraction stimulate glucose transport in vitro. We have previously demonstrated that exercise and hypoxia have an additive effect on insulin sensitivity in type 2 diabetics.
OBJECTIVE
Our objective was to examine the effects of three different hypoxic/exercise (Hy Ex)
The severity of nocturnal hypoxia but not abdominal adiposity is associated with insulin resistance in non-obese men with sleep apnea.
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BACKGROUND
Beyond obesity, sleep apnea syndrome is frequently associated with excess abdominal adiposity that could contribute to the deteriorated cardiometabolic risk profile of apneic patients.
METHODS
The present study addressed the respective contribution of the severity of sleep apnea syndrome
Sleep fragmentation and intermittent hypoxemia are associated with decreased insulin sensitivity in obese adolescent Latino males.
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BACKGROUND
Although sleep-related breathing disorder (SRBD) has been linked to insulin resistance in adults, this has not been as well established in children. We hypothesized that the severity of SRBD in adolescents was associated with metabolic impairment.
METHODS
Polysomnography was performed on
Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans.
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Acute exposure to hypoxia decreases insulin sensitivity in healthy adult humans; the mechanism is unclear, but increased activation of the sympathetic nervous system may be involved. We have investigated the hypothesis that short-term sympathetic inhibition attenuates hypoxia induced insulin
Melatonin reduces microvascular damage and insulin resistance in hamsters due to chronic intermittent hypoxia.
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Obstructive sleep apnea (OSA) causes intermittent hypoxia (IH) associated with hypertension, insulin resistance and a systemic inflammatory response. We evaluated the effects of melatonin on vasodilation, capillary perfusion in hamster cheek pouch and insulin resistance, hypertension, and reactive
Chronic intermittent hypoxia from pedo-stage decreases glucose transporter 4 expression in adipose tissue and causes insulin resistance.
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BACKGROUND
The persistence of sleep disordered breathing (SDB) symptoms after tonsil and/or adenoid (T&A) surgery are common in children with obstructive sleep apnea (OSA). We tested the hypothesis that disturbances of glucose transporters (GLUTs) in intraabdominal adipose tissue caused by chronic
Intermittent hypoxia-induced insulin resistance is associated with alterations in white fat distribution.
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Sleep apnea syndrome is characterized by repetitive upper airway collapses during night leading to intermittent hypoxia (IH). The latter is responsible for metabolic disturbances that rely, at least in part, on abdominal white fat inflammation. Besides qualitative alterations, we hypothesized that
RAGE/NF-κB pathway mediates hypoxia-induced insulin resistance in 3T3-L1 adipocytes.
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There is growing evidence in support of an independent association between obstructive sleep apnea (OSA) and type 2 diabetes, and in which hypoxia may play an important role. Hypoxia is the hallmark feature and the most important pathophysiologic pathway of OSA. Recently, receptor for advanced
Berberine improves insulin resistance in adipocyte models by regulating the methylation of hypoxia-inducible factor-3α.
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Methylation of hypoxia-inducible factor-3α (HIF3A) was previously demonstrated to be highly associated with insulin resistance (IR) in patients with gestational diabetes mellitus (GDM). We aimed to study the therapeutic effects of Berberine (BBR) on GDM and the possible mechanisms. The expressions
Transient hypoxia reprograms differentiating adipocytes for enhanced insulin sensitivity and triglyceride accumulation.
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OBJECTIVE
To investigate the impact of transient (2-4 h) hypoxia on metabolic reprogramming of adipocytes.
METHODS
The impact of transient hypoxia on metabolic reprogramming was investigated in 3T3-L1 cells before and after differentiation. Glucose uptake, fatty acid oxidation, lipolysis and
Increased Insulin Sensitivity by High-Altitude Hypoxia in Mice with High-Fat Diet-Induced Obesity Is Associated with Activated AMPK Signaling and Subsequently Enhanced Mitochondrial Biogenesis in Skeletal Muscles
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Background: This study aimed to investigate whether and how high altitude-associated ambient hypoxia affects insulin sensitivity in mice fed a high-fat diet (HFD).
Methods:
Resveratrol attenuates intermittent hypoxia-induced macrophage migration to visceral white adipose tissue and insulin resistance in male mice.
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Chronic intermittent hypoxia during sleep (IH), as occurs in sleep apnea, promotes systemic insulin resistance. Resveratrol (Resv) has been reported to ameliorate high-fat diet-induced obesity, inflammation, and insulin resistance. To examine the effect of Resv on IH-induced metabolic dysfunction,
Disruption of hypoxia-inducible factor 1 in adipocytes improves insulin sensitivity and decreases adiposity in high-fat diet-fed mice.
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OBJECTIVE
Obesity, insulin resistance, and type 2 diabetes form a tightly correlated cluster of metabolic disorders in which adipose is one of the first affected tissues. The role of hypoxia and hypoxia-inducible factor 1 (HIF1) in the development of high-fat diet (HFD)-induced obesity and insulin
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