Diglyceride

Activation of a GQ subunit inhibiting adenyl cyclase, increasing cyclic AMP.

Activation of a GI subunit inhibiting adenyl cyclase, decreasing cyclic AMP or activation of the GQ subunit increasing IP3 and DAG leading to increased calcium entry.

That's certainly a bit of a humdinger.

The important things are to try and split out GS versus GQ and try and align the downstream effects to figure out which is, which is right and which is wrong.

In this case, option five is correct.

Alpha-1 adrenoreceptors are GQ subunit coupled.

GQ increases IP3 and DAG in the cell.

More random enzymes to come your way now.

No, it isn't.

Because now you've got diacylglycerol.

Diacylglycerol, remember, via allosteric activation, activates the protein kinase C-zeta.

And what does that PKC-zeta enzyme do? TCR-mediated T-cell activation.

So, those two reactions, neutrospringomyelinase and serostringomyelin synthase, will perform the activity moving through diacylglycerol activating PKC-zeta to trigger T-cell receptor activation.

In both of those studies, the fat that went up with training was triglyceride, which is the inert storage form.

The molecule triglyceride gets built from, diacylglycerol, or DAG as you might see it abbreviated, went down with training in both.

So it seems like triglyceride is the sort of inert form, which doesn't really signal anything, and then diacylglycerol is the more active, potentially more harmful form.

We're going to come back to that when we talk about the liver, but What we can conclude here is that how much fat inside your muscle doesn't necessarily tell you how well your muscle handles insulin.

But as they become progressively overfilled, they stop responding normally to insulin, which is kind of the most important hormone that's involved in this process.

And one of the molecular hallmarks of that process is the accumulation of a lipid intermediate called diacylglycerol, or DAG, or DAG, which interrupts insulin signaling.

So once that happens, the warehouse starts malfunctioning.

Instead of simply storing fat, those particular fat cells or adipocytes begin releasing fatty acids back into the bloodstream, exactly what you don't want unless you're about to use them immediately.

Now let's go before endocannabinoids.

Diacylglycerol is the precursor of 2-AG.

Diacylglycerol is actually bioactive also.

It regulates protein kinases.

So the way to think about these lipid signaling is fascinating because there's multiple...