Wednesday, 7 September 2011

K(ATP) channels and fat cell multiplication

Involvement of ATP-sensitive potassium channels in proliferation and differentiation of rat preadipocytes.

These results suggest that when ATP-sensitive potassium channel expression decreases, preadipocyte proliferation is promoted, but when the expression of the channels increases, preadipocyte proliferation is inhibited.

It is to be confirmed whether the development of obesity has relation to excessive inhibition of ATP-sensitive potassium channels in preadipocytes or not.

hhhmmmm, inhibition of KATP channels, where have we seen that before? Oh yeh, here, this is what they say.....

"increased intracellular glucose, resulted from hyperglycemia, increases cytosolic ATP through glucose metabolism. This leads to closure of ATP-sensitive potassium ion channels (KATP channels) "

So how do we get increased intracellular glucose?, Yup, INSULIN.

No wonder the KATP knockout mice cannot get fat, they have no KATP channels to close in the first place! And so the downstream signalling cascade from the closure of the KATP never happens!

3 comments:

  1. you can have increased intracellular glucose with no insulin present.insulin is not required for cells to uptake insulin.

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  2. Only a few organs can uptake glucose without insulin, like the liver and brain.

    adipocytes require insulin to uptake glucose.

    ReplyDelete
  3. better check on that.even muscle can uptake glucose in the absence of insulin.

    ReplyDelete