New Available Treatment Options for Type 2 Diabetes



Davida Kruger, MSN, APN-BC, BC-ADM: Let’s talk in a little bit more detail about both the GLP-1 [glucagon-like peptide-1] receptor agonists and the SGLT2 [sodium-glucose cotransporter-2] inhibitors because if people don’t walk away with anything else from listening to this program, it’s that they need to incorporate both of these medications into their treatment plan for people with type 2 diabetes. We owe it people with type 2 diabetes to give them both of these therapies at the appropriate time.

GLP-1 receptor agonists have been around for about 18 years.

Lucia Novak, MSN, ANP-BC, BC-ADM, CDTC: Yes.

Davida Kruger, MSN, APN-BC, BC-ADM: They’re short-acting, once a day, once a week. Would you talk a little bit about how it targets the defects in the body and why we’re so enamored by GLP-1 receptor agonists?

Lucia Novak, MSN, ANP-BC, BC-ADM, CDTC: The GLP-1 receptor agonist, when we put it into perspective on what we understand, contributes to hyperglycemia in patients with type 2 diabetes. There’s a lot of shame and blame, so we typically blame right away what the patients are eating, what they’re drinking, and whether they are exercising. What I love about the ominous octet, and what I share with my patients, is this: there are 8 pathological problems within the body that are contributing to hyperglycemia regardless of the type of diet a patient has and regardless of the physical activity they’re engaged in. It’s not that those are not important because they are critical to all diseases. It’s a buy 1, get 3 free situation that we see with diabetes: the hypertension, the dyslipidemia, all of it.

Again, we have these 8 pathological issues going on with certain glands, certain organs, and certain systems within the body. The GLP-1 native hormone that we secrete upon eating—and probably upon smelling food when we get those triggers going—actually innervate. There are GLP-1 receptors on almost all of the ominous octet, but we see GLP-1 really active on helping with first phase insulin secretion, which is lost in people with type 2 diabetes or blunted in people with prediabetes. I say that you either have diabetes or you don’t. It’s like how you’re either pregnant or you’re not. It also works to suppress the glucagon that we see with the alpha cells that is also dysregulated in people with type 2 diabetes.

We see it acting on the liver as far as glycogenolysis and gluconeogenesis at an inappropriate time such as when you are eating. There is also innervation along the central nervous system, so it impacts satiety. Your brain should be telling you when you’re going to stop eating even before you start. It also innervates the esophagus and gastric emptying. Upon eating, those mechanisms should slow down, which is what regulates the postprandial elevations. That this also not functioning in someone with type 2 diabetes. We also see it maybe in the GLUT4 [glucose transporter-4], so it’s helping with some insulin resistance in that mechanism as well.

We see it acting on so many different areas. The only area where we’re not seeing a strong response is in the kidneys on the SGLT2 receptor. That’s where the SGLT2 inhibitors come in. When you can combine those 2 classes of medications, you’re very much acting in a synergistic fashion and addressing the pathology that’s behind the disease, which is why, if we can use these medications earlier in the process, we might be able to delay the need for insulin for a much longer time in patients with type 2 diabetes.

Davida Kruger, MSN, APN-BC, BC-ADM: Thank you. We’ll talk a little bit later about how the mechanism of action actually works. I want to say a couple of things about SGLT2 inhibitors. You did say that that’s the only thing that GLP-1 receptor agonists don’t cover. The nice simple explanation about SGLT2 inhibitors is that, rather than all this glucose going back into circulation, it allows the patient to be peeing off the glucose and lowering glucose systemically. If we use a GLP-1 receptor agonist, we’re targeting 7 of those problems, and if we add an SGLT2 inhibitor, we get the 8th. Thank you very much.

Lucia Novak, MSN, ANP-BC, BC-ADM, CDTC: Without low sugar.

Davida Kruger, MSN, APN-BC, BC-ADM: And without hypoglycemia, right. The big difference between that and basal insulin is that it has a cardiovascular benefit. It targets all the defects in the body, and it doesn’t cause hypoglycemia weight gain. Again, we’ll talk a little bit more about that as we move on.

I want to thank the audience for watching this HCPLive® Peers & Perspectives®. If you enjoyed the content, please subscribe to our e-newsletter to receive upcoming Peers & Perspectives® and other great content right in your inbox. Thank you all for joining us today.

Transcript Edited for Clarity

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