Glucose Sensing During Hypoglycemia: Lessons From the Lab  

Oleh:

McCrimmon, Rory

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Diabetes Care vol. 32 no. 08 (Aug. 2009), page 1357-1363 .
Topik: Hypoglycemia

Ketersediaan

Perpustakaan FK Nomor Panggil: D05.K.2009.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Within the body a number of highly specialized regions sense alterations in glucose levels and, in the case of hypoglycemia, this leads to the generation of a glucose counterregulatory defense response. The VMH, discussed in detail in this article, reflects only one of a number of brain regions thought to be important in the detection of hypoglycemia, and together these brain regions may form an integrated neural network coordinating physiological and behavioral responses to a hypoglycemic challenge. Glucose-sensing neurons, by virtue of specific sensing systems, directly or indirectly translate the rate or quantity of glucose oxidation into a neural signal that alters neuronal firing rates. These neurons appear to use signaling mechanisms that parallel those used by pancreatic ß- and a-cells. The GE neuron, more likely to operate under conditions of euglycemia or hyperglycemia, may use glucokinase as its key regulatory step and the KATP channel to then translate that signal into altered neuronal firing rates. In contrast, the GI neuron, active under hypoglycemic conditions, may be dependent on alterations in intracellular AMPK activity that, in turn, may act via NO to alter neuronal firing rates. Potentially, the counterbalance between GI and GE neuronal activity forms the most sensitive means of regulating and maintaining blood glucose within a narrow physiological range as well as ensuring an adequate supply of glucose to the brain. Recurrent exposure to hypoglycemia disturbs this relationship in a number of ways, which may include an increased capacity of glucose-sensing regions of the brain to use glucose and/or alternate fuels, as well as changes in both the mechanisms that sense glucose and those that fine-tune the hypoglycemic stress response, the net effect being to reduce the glucose level at which counterregulation is initiated.

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