【Objective】In previous studies, it was clarified that lactic acid bacteria LAB4(Lactobacillus delbrueckii LAB4) has an inhibitory effect on blood glucose spikes, but in order to elucidate the mechanism of action, the relationship between autonomic nervous response and G/I-spike was investigated.
【Methods】In Study 1, heart rate variability(HRV) spectra were analyzed in 77 FMS(fibromyalgia syndrome) subjects with G-spikes. The control group was 60 healthy subjects. In Study 2, 22 cases of FMS were subjected to 3-hour spectral analysis of 75gOGTT and HRV in synchronization, and BS, IRI, LF / HF ratio, and HF amp were measured every 30 minutes. Max BS-Min BS≧60mg/dL after glucose loading was designated as G-spike, and Max IRI-Min IRI≧ 20μU/mL was designated as I-spike.
【Results】In Study 1, HRV was more predominantly dys-P type in the target group(63.4%). In Study 2, of the spike type(9 cases), 7 cases(77.8%) had a match between G-spike and I-spike.
【Discussion】In the early I-spike type, basal insulin secretion was insufficient, and after glucose loading, the initial additional secretion reacted excessively, resulting in postprandial hyperglycemia. In the late type of I-spike, the initial additional secretion did not occur sufficiently, and the late additional secretion reacted excessively. G-spike was 77.8% insulin dependent. Although the pancreatic parasympathetic responses of the subjects were insufficient, the pancreatic parasympathetic nerve was overreacted to the glucose load stimulus. As a result, insulin was excessively secreted to create G/I-spike. Dys-P type was seen in all cases, suggesting impaired insulin secretory function. Administration of LAB4 suppressed the sympathetic nerve activity of the pancreas, and as a result, the initial increase in blood glucose level immediately after glucose intake was suppressed(phase 1 suppression of postprandial hyperglycemia). It also reduced the peak of late additional insulin secretion and suppressed hypoglycemia(improvement of phase 2). After that, subject get to optimize the blood glucose level(Phase 3). This is probably because in the phase 2, LAB4 acted on the hepatic sympathetic nerve to promote gluconeogenesis, and further acted on the pancreatic parasympathetic nerve suppresses the excessive secretion of insulin. In this way, Lactobacillus delbrueckii LAB4 is considered to have contributed to homeostasis(optimization; phase 3) of blood glucose level. The above effects were more pronounced in the glucomannan added LAB4 group than in the LAB4 group.
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