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Bring GLP-1 Activity into the conversation for a different perspective on an old problem

GLP-1 Activity is an element of type 2 diabetes and should be included when talking with your patients in order to help them understand what is happening in their body to cause high blood sugar.1-3



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Why does GLP-1 matter?

GLP-1 hormone

Glucagon-like peptide-1 (GLP-1) is a natural hormone that plays a role in maintaining normal blood glucose levels.4

See how native GLP-1 works


Healthy people
Patients with T2D
In healthy individuals, the natural hormone GLP-1 plays a role in stimulating the pancreas to secrete insulin when blood glucose rises.4,5
Patients with type 2 diabetes have inadequate GLP-1 response when blood glucose rises, which contributes, along with other things, to insufficient insulin secretion.1-3,6
primary_msg

Native GLP-1 is associated with multiple systems in the body6-8

Select an icon to see the effects of GLP-1.


Pancreas
 
Stimulates insulin secretion and inhibits glucagon production.4,5
Liver
(indirect action)a
Inhibits pancreatic glucagon secretion, causing reduced hepatic glucose production.
GI tract
 
Delays gastric emptying.
Brain
 
Suppresses appetite resulting in decreased energy intake and subsequent weight loss. Improved insulin sensitivity via weight loss leads to improved peripheral glucose uptake.9

a“Indirect action” means that the expression of a GLP-1 receptor in that tissue has not been definitively identified or that its biologic role is not fully recognized.

secondary_msg

How is GLP-1 Activity different in my patients with type 2 diabetes?

Because native GLP-1 is associated with various tissues and organ systems, it is directly or indirectly linked to metabolic defects in type 2 diabetes.6,10,11 Patients with type 2 diabetes have insufficient GLP-1 Activity in the pancreas.6

Insulin resistance starts developing in the early stages of type 2 diabetes12

Beta cells try to keep up but eventually can’t compensate for insulin resistance, leading to elevated blood glucose12

At the same time, incretin response (including GLP-1 Activity) declines, which contributes to beta cells' growing inability to secrete insulin3,6,10

In addition to other things, insufficient GLP-1 Activity leads to reduced insulin secretion and impaired suppression of glucagon6

GLP-1 Activity

Beta-cell response to GLP-1 Activity, along with many other stimuli, declines in patients with type 2 diabetes13,14

Type 2 diabetes progression chart
Natural History of Type 2 Diabetes ©2010, International Diabetes Center at Park Nicollet, Minneapolis, MN. Used with permission.
IFG=impaired fasting glucose.
IGT=impaired glucose tolerance.

Beta-cell function declines over time

At prediabetes onset:

40%

loss in
beta-cell mass12

At T2D diagnosis:

60%

loss in
beta-cell mass12

80%

decrease in
beta-cell function10

tertiary_msg

Talk with patients about GLP-1 Activity and how it may factor into their type 2 diabetes

You cover a number of topics in your conversations with patients with type 2 diabetes. Make sure GLP-1 Activity is one of them.

Talk with patients about GLP-1 Activity and how it may factor into their type 2 diabetes

You cover a number of topics in your conversations with patients with type 2 diabetes. Make sure GLP-1 Activity is one of them.

Join the conversation about GLP-1 Activity

Sign up to learn more about GLP-1 Activity.


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References:

  1. Højberg PV, Vilsbøll T, Rabøl R, et al. Four weeks of near-normalisation of blood glucose improves the insulin response to glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes. Diabetologia. 2009;52(2):199-207.
  2. Kjems LL, Holst JJ, Vølund A, Madsbad S. The influence of GLP-1 on glucose-stimulated insulin secretion: effects on beta-cell sensitivity in type 2 and nondiabetic subjects. Diabetes. 2003;52(2):380-386.
  3. Calanna S, Christensen M, Holst JJ, et al. Secretion of glucagon-like peptide-1 in patients with type 2 diabetes mellitus: systematic review and meta-analyses of clinical studies. Diabetologia. 2013;56(5):965-972.
  4. Aronoff SL, Berkowitz K, Shreiner B, Want L. Glucose metabolism and regulation: beyond insulin and glucagon. Diabetes Spectrum. 2004;17(3):183-190.
  5. Drucker DJ. Mechanisms of action and therapeutic application of glucagon-like peptide-1. Cell Metab. 2018;27(4):740-756.
  6. Campbell JE, Drucker DJ. Pharmacology, physiology, and mechanisms of incretin hormone action. Cell Metab. 2013;17(6):819-837.
  7. Korner M, Stöckli M, Waser B, Reubi JC. GLP-1 receptor expression in human tumors and human normal tissues: potential for in vivo targeting. J Nucl Med. 2007;48(5):736-743.
  8. Muscogiuri G, DeFronzo RA, Gastaldelli A, Holst JJ. Glucagon-like peptide-1 and the central/peripheral nervous system: crosstalk in diabetes. Trends Endocrinol Metab. 2017;28(2):88-103.
  9. Nauck MA, Meier JJ. Incretin hormones: their role in health and disease. Diabetes Obes Metab. 2018;20:5-21. https://doi.org/10.1111/dom.13129.
  10. DeFronzo RA. From the triumvirate to the ominous octet: a new paradigm for the treatment of type 2 diabetes mellitus. Diabetes. 2009;58(4):773-795.
  11. Holst JJ, Knop FK, Vilsbøll T, Krarup T, Madsbad S. Loss of incretin effect is a specific, important, and early characteristic of type 2 diabetes. Diabetes Care. 2011;34(suppl 2):S251-S257.
  12. Leahy JL. Pathogenesis of type 2 diabetes. Arch Med Res. 2005;36(3):197-209.
  13. Herzberg-Schäfer S, Heni M, Stefan N, Häring H-U, Fritsche A. Impairment of GLP1-induced insulin secretion: role of genetic background, insulin resistance and hyperglycaemia. Diabetes Obes Metab. 2012;14(suppl 3):85-90.
  14. Nauck MA, Meier JJ. GIP and GLP-1: stepsiblings rather than monozygotic twins within the incretin family. Diabetes. 2019;68(5):897-900.
  15. Simonson G, Cuddihy R, Reader D, Bergenstal R. International diabetes center treatment of type 2 diabetes glucose algorithm. Diabetes Manage. 2011:1(2):175-189.