A Common but Complex Condition
In the United States, nearly one in 10 people have type 2 diabetes¹ and each year, 1.5 million more Americans are diagnosed.² While a healthy diet and exercise are often the first steps to managing type 2 diabetes, some people may need medication to help manage the condition.³ Diabetes is also complex and progressive, which is why it’s often seen as a journey – at different points, many people either need to advance their treatment or switch to other therapies to meet their goals. Researchers at Lilly have a deep understanding of type 2 diabetes and are harnessing this knowledge into creating a new chapter of treatment.
An Era of Innovation
The last 100 years have represented an era of significant advancement in diabetes care. Since the first person treated with insulin in 1922, treatments have continued to evolve. In the mid-20th century, insulin syringes were developed to be used as a universal tool for diabetes management.4 Additional tools, such as insulin pens, insulin pumps and other diabetes technologies, were also introduced to help people better manage their diabetes.4
Later, oral medicines were introduced to help control blood glucose in people whose bodies still produce insulin, such as people with type 2 diabetes. But, as we now know, treating type 2 diabetes goes beyond insulin – not only is the pancreas unable to produce enough insulin, the cells in the body also become resistant to the hormone.
The Next Chapter
Despite the significant leaps forward in the last 100 years, there is still work to be done. Through better understanding of type 2 diabetes, Lilly is able to develop new molecules addressing what’s happening in the body as a result of the disease.
Lilly has led the charge in the research of GLP-1 receptor agonists – an important class of medicines which have helped millions of people with this condition to date. But the quest for treatments rooted in science hasn’t stopped there.
To bring this to life, Lilly is studying the gastric inhibitory polypeptide (GIP), a naturally occurring incretin hormone that, in healthy humans, is responsible for nearly two-thirds of the incretin effect.5 Additionally, preclinical research to date has shown endogenous GIP receptors found within the brain may act on appetite control centers impacting weight-related mechanisms, such as food intake and appetite.6,7 Endogenous GIP may play a bigger role in blood glucose and weight regulation than previously thought.6,7,8
Lilly is always striving for a deeper understanding of the science behind type 2 diabetes – and how we can use it to develop next-generation therapies. We look forward to writing the next chapter with you.
PP-TR-US-0018 10/2021 ©Lilly USA, LLC 2021. All rights reserved.
References: Type 2 diabetes. Centers for Disease Control and Prevention. http://www.cdc.gov/diabetes/basics/type2.html. Published August 10, 2021. Accessed October 7, 2021.  Statistics about diabetes. Statistics About Diabetes | ADA. http://www.diabetes.org/resources/statistics/statistics-about-diabetes. Accessed October 7, 2021.  ADA Diabetes Overview. Diabetes Symptoms, Causes, Treatment. The path to understanding diabetes starts here. | ADA. http://www.diabetes.org/diabetes. Accessed October 7, 2021.  Kesavadev J, Saboo B, Krishna MB, Krishnan G. Evolution of Insulin Delivery Devices: From Syringes, Pens, and Pumps to DIY Artificial Pancreas. Diabetes Ther. 2020;11(6):1251-1269. doi: 10.1007/s13300-020-00831-z.  Nauck MA, Meier JJ. GIP and GLP-1: Stepsiblings rather than monozygotic twins within the incretin family. Diabetes. 2019;68(5):897-900. doi: 10.2337/dbi19-0005.  Samms RJ, Coghlan MP, Sloop KW. How may GIP enhance the therapeutic efficacy of GLP-1? Trends Endocrinol Metab. 2020;31(6):410-421. doi: 10.1016/j.tem.2020.02.006.  Finan B, Müller TD, Clemmensen C, Perez-Tilve D, DiMarchi RD, Tschöp MH. Reappraisal of GIP pharmacology for metabolic diseases. Trends Mol Med. 2016;22(5):359-376. doi: 10.1016/j.molmed.2016.03.005. Mroz PA, Finan B, Gelfanov V, et al. Optimized GIP analogs promote body weight lowering in mice through GIPR agonism not antagonism. Mol Metab. 2019;20:51-62. doi: 10.1016/j.molmet.2018.12.001.