Dr. Ben Bikman

Right.

You mentioned AKT.

That's what we would measure.

And you must have, too.

We would measure a particular protein in AKT for or an amino acid residue for phosphorylation and then look at one other downstream signal.

And then we can do some other more complicated metrics.

But that was always the absolute baseline.

In fact, I've run so many Western blots measuring phospho AKT that.

And next time I – if I ever have to run another, I'm going to, like, shove the pipette in my eyeball.

I'm so tired of it.

Oh, yeah, for sure.

Yeah.

In fact, I've already touched on a few.

Like, for example, who would have imagined that insulin regulates the enzyme that's responsible for the conversion of testosterone to estrogens, for goodness sake?

And yet it does.

Insulin has a direct inhibitory role on aromatase.

that enzyme that mediates the conversion and the synthesis of estrogens in men and women.

It also regulates nitric oxide production, regulating dilation of blood vessels, and other hormones throughout the body that affect water retention, salt signaling, neuron conducting of signals, and more.

But at the fat cell, insulin probably has its most powerful effect.

where the you cannot under now we're touching on a broader topic of why do we get fat here and i welcome that topic uh in fact of all the human tissue i've studied the most in my lab it's fat tissue that we've when we we started doing fat biopsies in my lab a few years ago and that's the tissue we study the most so i'm very comfortable talking about adipose tissue physiology