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Microplastic Exposure Worsens Glucose Intolerance Induced by Chronic Intermittent Hypoxia
Summary
Using four groups of adult mice exposed to combinations of chronic intermittent hypoxia and microplastics, researchers found that microplastic exposure significantly worsened glucose intolerance and insulin resistance induced by hypoxia alone. The study suggests a synergistic relationship between sleep apnea and environmental microplastic exposure in driving metabolic dysfunction.
Abstract Rationale: Obstructive sleep apnea is characterized by recurrent closure of the upper airway, causing intermittent hypoxia (IH). IH causes insulin resistance, glucose intolerance, and impaired fasting glucose in animals and humans. Microplastics (MP) are small plastic degradation byproducts; they are nearly ubiquitous in the environment, and are found in animal and human tissue. MP in animals causes similar disruptions to glucose metabolism as IH. We aimed to determine whether MP exposure would worsen dysglycemia induced by IH. Methods: 24 adult C57BL/6J mice were divided into four groups (n=6/group, half male). Group 1 was exposed to normal water and intermittent air (IA-null); group 2 was exposed to normal water and IH (IH-null); group 3 was exposed to water containing MP and intermittent air (IA-MP); and group 4 was exposed to water containing MP and IH (IH-MP). MP exposure was accomplished by adding 1 µm polystyrene microspheres (FluoSpheres, Thermo Fisher) to drinking water, 1.25 g/L. MP were given for 4 weeks in groups 3 and 4. IA or IH exposure occurred concurrently with MP exposure; in IH, FiO2 cycled between 0.21 and 0.06, once per minute, for 12 hours during the inactive phase. Intraperitoneal glucose tolerance tests were done prior to exposure and at study conclusion. Results: Mice in IH gained less weight than mice in IA (delta body weight in IA-null: 2.4 ± 0.4 g, IA-MP: 2.4 ± 0.5 g, IH-null: 1.3 ± 0.1 g, IH-MP: 1.1 ± 0.3 g, p=0.004 for 2-way ANOVA of IH vs IA effect, 0.786 for MP vs null effect). Neither MP nor IH impacted perigonadal fat weight. Fasting glucose declined over the experiment duration in all groups, without significant effects of IH or MP. Glucose tolerance test area under the curve (GTT AUC) increased over the experiment duration in each group except IA-null, with the highest magnitude of increase in the IH-MP group (delta GTT AUC in IA-null: +1316 ± 949 mg[asterisk]min/dL, IA-MP: +4561 ± 618 mg[asterisk]min/dL, IH-null: +4433 ± 574 mg[asterisk]min/dL, IH-MP: +7110 ± 1326 mg[asterisk]min/dL, p=0.006 for 2-way ANOVA of IH vs IA effect, 0.004 for MP vs null effect). Conclusions: IH and MP exposure each worsened glucose tolerance, with an additive effect in the combined stimulus group. These effects were not explained by changes in body weight or composition. No effects on fasting glucose were observed. OSA may worsen adverse metabolic effects of environmental MP.