Poster Communications: The importance of breakfast glycemic control on systemic BDNF and dynamic cerebral autoregulation in men

It has been established that blood glucose is an important energy substrate for the human brain at rest, and accordingly, brain cognitive function after breakfast (BF) omission isn’t better than that after BF consumption with moderate-increase in blood glucose [1]. Nevertheless, although the underlying physiological mechanism remains unclear, the high-glycemic index (High GI) BF consumption with post-prandial hyperglycemia isn’t more beneficial to cognitive function than when the low-glycemic index (Low GI) BF consumption [2]. Some previous studies have shown that cognitive dysfunction may be associated with both impaired brain-derived neurotrophic factor (BDNF) metabolism [3] and dynamic cerebral autoregulation (dCA) [4], thereby we hypothesized that BF glycemic control would affect systemic BDNF and dCA as shown in cognitive response. In the present study, we examined the acute impacts of BF omission, Low, and High GI BF consumptions on plasma BDNF and dCA. Ten healthy men (age: 24 ± 1 yrs) performed three trials in a randomized crossover order; BF omission, Low, and High GI BF consumption conditions. Blood samples were collected from a cephalic vein for the assessment of blood glucose (photometry), plasma insulin and BDNF (both ELISAs) and were taken before and during the 120 min post-prandial period. Blood flow velocity in the middle cerebral artery (MCA V; Transcranial doppler ultrasonography) and mean arterial blood pressure (MAP; Finger photosplethysmography) were measured for determination of dCA via transfer function analysis. The data were analyzed using one- or two-way repeated-measures analysis of variance after normal data distribution was confirmed. Specific differences were identified with a Bonferroni post-hoc test. Blood glucose and plasma insulin were increased after both GI BF consumptions (area under the curve (AUC) of glucose; omission vs. Low GI P = 0.07 and omission vs. High GI P < 0.01, AUC of insulin; omission vs. Low P < 0.01 and omission vs. High GI P < 0.01). In addition, increased blood glucose in High GI trial was higher than that in Low GI trial (P < 0.01), but not in terms of insulin. While plasma BDNF was decreased in omission trial (Pre vs. Post P < 0.05), it was preserved during both BF trials. Transfer function phase and gain were not changed in omission trial. Meanwhile, transfer function gain and normalized gain (low-frequency) were lower during both BF trials, with lower phase (very low-frequency) observed in High GI; in other words, an inadequate dCA was observed in omission and High GI trials when compared with Low GI trial. These findings highlight that BDNF metabolism is impaired by BF omission, and dCA after BF omission and High GI BF consumption is weaker than that after Low GI BF consumption. These observations imply that BF glycemic control would be manipulation to support to prevent neurodegenerative and cerebrovascular disease in addition to metabolic dysfunction such as type 2 diabetes.