When glucose in the blood is filtered by the kidneys, about 90% of that glucose gets reabsorbed,

and it gets reabsorbed by something called the sodium glucose transporter 2.

So if you inhibit that sodium glucose transporter 2, such as with a SGLT2 inhibitor, a sodium glucose transport 2 inhibitor, then

you are not going to reabsorb that sugar. And what you get is what is called glycosyria

or glucosuria where you are urinating out the glucose into the urine. The excretion of glucose into the urine is actually something that's been known for a very long time.

It's one of the ways it was diagnosed in the early days.

And so what would happen is physicians would actually taste the urine and it would be very sweet and that's because there

was so much sugar in the blood that you didn't reabsorb all the urine and you would have this

polyurea where you have an excessive water loss with the dehydration that occurs because of this

osmotic diuresis that the glucose is causing.

Very important medical lessons can be obtained from this historical fact.

So when the professor hands out a cup of urine to all the medical students on day one,

and he says, do as I do and he dips his finger

into the urine and then tastes it and then all the medical students do the exact same thing.

He says, now you have learned the power of observation. I dipped my ring finger into the urine that I tasted with my pinky finger.

All right.

Well, it seems that it's about the right time where I can begin to feel comfortable talking

about SGL2 inhibitors.

I'm one of those people that has the philosophy. I don't want to be

the first person using a drug and I don't want to be the last person prescribing a drug and that's how I

feel about talking about medications as well. Early on, it's very challenging to feel comfortable

providing good information since a lot will change as more is learned and indeed

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