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Editorial
. 2009 Aug;32(8):1357-63.
doi: 10.2337/dc09-0123.

Glucose sensing during hypoglycemia: lessons from the lab

Rory McCrimmon
Editorial

Glucose sensing during hypoglycemia: lessons from the lab

Rory McCrimmon. Diabetes Care. 2009 Aug.
No abstract available

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Figures

Figure 1
Figure 1
Neural pathways linking the VMH via sympathetic and parasympathetic neurons to the pancreas. Retrograde neuronal tracer studies using pseudorabies virus microinjected into the pancreas of the rats established the VMH as a third-order neuron reaching the parasympathetic and sympathetic innervation of the pancreas via the paraventricular hypothalamic nucleus (PVN) and interomediolateral (IML) nucleus as well as the dorsal motor nucleus of the vagus (DMV), respectively. The dorsomedial hypothalamus (DMH) and lateral hypothalamus (LHA) also feed into this pathway as well as the nucleus tractus solitarius (NTS) in the hindbrain, each of which plays a role on glucose sensing. The nucleus tractus solitarius also is the likely point of integration of inputs from peripheral sensors via vagal afferents (X). Reprinted with permission from Buijs et al. (11).
Figure 2
Figure 2
Hypothetical sensing mechanism of GE (A) and GI (B) neurons. Glucose enters the GE neuron through GLUT2 or GLUT3 and is phosphorylated by glucokinase, acting as the gatekeeper and regulating the production of cytosolic ATP in a subcellular compartment. The ATP closes KATP channels in the plasma membrane causing depolarization. In turn, this leads to Ca2+ influx through voltage-dependent calcium channels (VDCC), stimulating neurotransmitter release and/or increased action potential frequency. Lactate, produced locally by astrocytes or arriving systemically, enters the neuron via monocarboxylate transporter-2 (MCT2) and can then be metabolized to form ATP. In GI neurons, glucokinase may once again act as the gatekeeper. A falling glucose results in an increase in the AMP:ATP ratio activating AMPK and stimulates the formation of NO, which may diffuse out to adjacent glial cells or act as a neurotransmitter. In addition, AMPK may act on chloride (Cl) channels leading to neuronal depolarization and neurotransmitter release and/or increased action potential frequency.
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