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Acute Intermittent Hypoxia Worsens Microplastic Induced Dysglycemia
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In a mouse model, researchers investigated whether acute intermittent hypoxia (mimicking sleep apnea) compounds the metabolic disruptions caused by chronic microplastic exposure. They found that the combination worsened insulin resistance and glucose intolerance beyond what either exposure caused alone.
Abstract Rationale: Microplastics (MP) are the byproduct of disposal and breakdown of commercial plastics. MP are ubiquitous in the environment, and convincing data demonstrate that MP are present in a variety of animal and human tissue. Exogenous MP exposure in rodents results in insulin resistance and glucose intolerance. Intermittent hypoxia (IH) can be used to model obstructive sleep apnea (OSA), and has similar dysglycemic effects. It is unknown whether acute IH can worsen the maladaptive effects of chronic MP exposure on glucose homeostasis. Methods: Twenty-four C57BL/6J mice, aged 8 weeks, were evenly divided into four groups (n=6/group, half male and half female). Group designations were as follows: 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 polystyrene MP and intermittent air (IA-MP); and group 4 was exposed to water containing polystyrene microplastics and IH (IH-MP). Microplastic exposure was done by adding 1 µm fluorescently-labeled polystyrene microspheres (FluoSpheres, Thermo Fisher) to the available drinking water, 1.25 g/L, and based on typical water intake in C57BL/6J mice, resulted in each mouse drinking approximately 6-8 mg of MP per day. MP exposure was continued for 4 weeks in groups 3 and 4. Acute IA or IH exposure occurred on the final two days of the experiment (6 hours each day). IH exposure was as follows: FiO2 cycling between 0.21 and 0.06, once per minute. An intraperitoneal glucose tolerance test (GTT) was performed at the beginning and end of exposures. Results: Neither acute IH nor chronic MP exposure had any significant effect on body weight (p=0.915 for IH effect, p=858 for MP effect). Perigonadal fat mass was also similar among all groups, without effects of acute IH or chronic MP. Fasting glucose increased in IA-null (27.5 ± 5.7 mg/dL, p=0.005) and IH-null (17.7 ± 6.8 mg/dL, p=0.048) groups over the experiment duration, without significant effects in either MP exposed group. Both acute IH and chronic MP exposure worsened glucose tolerance (p<0.001 for each comparison), with an additive effect of the two exposures. Conclusions: Acute IH exposure worsens glucose intolerance induced by chronic MP ingestion. This finding is not driven solely by changes in body weight or body composition. OSA or other conditions causing acute IH (e.g., periodic breathing in acute high altitude exposure) may exacerbate deleterious metabolic effects of environmental MP.
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