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The arterial blood glucose concentration-dependent
cerebral uptake of glucose, as seen in the present study, suggests
that arterial blood glucose concentrations maintained
below the optimal Km of the endothelial GLUT1, that is less
than 8 mmol/l [13,44] will result in insufficient supply. This can
be overcome by maintaining arterial blood glucose levels at
about 8 mmol/l as reflected by increased metabolic stability.
This is in line with findings showing the impact of decreased
glucose supply on posttraumatic functional disturbances after
TBI in terms of induced CSD [20], increased extracellular
glutamate and elevated lactate/pyruvate ratio [19]. As pointed
out by Vespa and colleagues, cerebral oxygen consumption
was decreased in patients with higher blood glucose concentrations
(120 to 150 versus 90 to 120 mg/dl) [19]. This is also
seen in the present patients. These findings strongly suggest
that activation of glucose transporter systems influence cerebral
oxygen consumption. As shown by Abate and colleagues
[48] increased cerebral glucose consumption is associated
with elevated OER, although low cerebral glucose consumption
results in decreased OER. Thus, the present data suggest
that metabolic instability, which can also occur independently
from cerebral ischaemia [2], can be influenced substantially by
changing arterial blood glucose levels.

... This is important because the ambient glucose levels within the neuronal environment is
rather low ranging from 1 to 2 mmol/l compared with normal
blood glucose levels between 5 and 6 mmol/l. Thus, any
decrease in arterial blood glucose in conjunction with impaired
endothelial glucose transport due to reduced GLUT1 expression
will endanger neuronal function and viability.

Conclusions Maintaining arterial blood glucose levels between
6 and 8 mmol/l appears superior compared with lower and
higher blood glucose concentrations in terms of stabilised
cerebral metabolism. It appears that arterial blood glucose
values below 6 and above 8 mmol/l should be avoided.Prospective analysis is required to determine the optimal arterial
blood glucose target in patients suffering from severe TBI.

BTW I am concerned (no, not *that* one)

about your use of TLAs. Usually, these are defined the first time they are used in a paper, but you quote glibly without passing on that info, so I get totally befuddled.