Well for me yes I'd say it does matter as being in much the same situation as you but with diabetic complications I would rather keep BS levels as low as possible.
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Thus, as indicated above, glycaemic excursions within the physiological range in healthy volunteers induce physiologically significant effects on endothelial function, oxidative stress and immune activation. Nevertheless, in normal glucose-tolerant subjects these inflammatory responses normalized within 2–3 h, while in obese impaired glucose-tolerant and type 2 diabetic subjects, glucose-induced inflammation was stronger or lasted longer, suggesting a role for hyperglycaemia in immune activation (147–150). Also in diabetic patients, after oral glucose and after meals, reactive oxygen species (ROS) and/or LDL oxidation was increased, indicating hyperglycaemia-induced activation of oxidative stress (151). Several markers have been used to assess oxidative stress and the antioxidant status in patients with diabetes, including ox-LDL and malondialdehyde (152). The short plasma half-life of these markers is one of the limiting factors for the assessment of oxidative stress in plasma samples. Thus, when available, urinary measures provide a more reliable determination of the activation of oxidative stress than plasma measurements. From several studies, both in vitro and in vivo, there is consistent evidence that hyperglycaemia is associated with an increased urinary excretion rate of the oxidative stress marker 8-iso-prostaglandin F2alpha. Ceriello (153) showed that the production of free radicals was increased in the postprandial period and that this increment was proportional to the magnitude of postprandial glucose excursions. Moreover, reductions of postmeal glucose excursions induced by a premeal bolus of a rapid insulin analogue resulted in decrements in glycaemia and nitrotyrosine, a metabolite derived from nitrosamine stress responses. Overall, numerous studies support the hypothesis of a causal relationship between hyperglycaemia and oxidative stress.
This seems consistent with findings that the metabolic syndrome may support peripheral inflammation by sensitizing leukocytes to up-regulate pro-inflammatory markers in response to glucose, which in turn increases the risk for T2DM and CVD (154)."
From here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3494382/