Abstract Introduction Apolipoprotein A2 (ApoA2) is a subclass of lipoproteins carrying cholesterol and triglycerides through the bloodstream. In the mouse ApoA2 expression is deterministic for ventilatory instability (Gillombardo et al 2018). There are known genetic effects on lipid levels and weight identified in humans. A role in cognition and feeding is not defined, especially compared to other lipoproteins Methods Using the C57BL/B6 (B6) mouse model (WT) in which ApoA2 expression is deterministic for breathing instability awake, anesthetized, and asleep, we compared the ApoA2 knockout on a B6 background (KO) mice to the WT for sensorimotor/learning skills, and for weight gain over 20 weeks (high fat vs. low fat diet). Results ApoA2 KO mice displayed increased timidity in T-maze exploration and heightened freezing in non-contextual defensive conditions, In the fear conditioning test, twenty-four hours following the training, a higher freezing time was shown in KO mice when exposed to non-associated context (p = 0.0005) but no difference between genotype when exposed to conditioned cue as a cue-dependent fear (p = 0.61); the differences were not ascribed to learning deficit. No significant genotype differences were observed in sensory, emotional, or learning tasks, including tactile and coordinative assessments, anxiety-like behavior, locomotor activity, Y-maze alternation, novel object recognition, and fear conditioning with extinction. At ages of 20 weeks, mice fed with low-fat diet showed similar body weights, whereas WT mice fed with high-fat diet exhibited a greater body weights than KO mice fed with high-fat diet or WT mice fed with low-fat diet (p 0.0001) genotype: F(1,36) = 54.86, p 0.0001, diet: F(1,36) = 92.15, p 0.0001, and interaction: F(1,36) = 47.16, p 0.0001. Conclusion ApoA2 expression contributes to defensive behavioral expression and enhanced weight gain on high fat nutrients, highlighting its potential role in allostatic mechanisms operating to produce obstructive sleep apnea Support (if any) VA Research Service (I01BX001464), and by the NIH (R21NS0524520 and UM1TR004528).
Strohl et al. (Fri,) studied this question.