Epidemiology and Pathophysiology


Diabetes is a major public health problem that is approaching epidemic proportions globally. Approximately 34.2 million Americans, or 10.5% of the US population, have diabetes, including 7.3 million Americans who have not been diagnosed yet.1

Source: CDC. Diabetes Info Cards. https://www.cdc.gov/diabetes/library/socialmedia/infocards.html.

Diabetes affects people of all races and ethnicities, but disparities exist.3

  • American Indians/Alaskan Natives comprise the largest age-adjusted racial/ethnic group of people with diagnosed diabetes.
  • The proportion of African American, Hispanic, and Asian American populations who have diabetes is higher than in the non-Hispanic white population.

Source: CDC. Addressing Health Disparities in Diabetes. https://www.cdc.gov/diabetes/disparities.html.

Approximately 1.5 million new cases of diabetes were diagnosed in adults in the United States in 2018. An estimated 452,000 new cases of diabetes occurred in patients age 18-44 years, 706,000 new cases in patients age 45-64 years, and 326,000 new cases in patients 65 years or older.1

Figure 3: Estimated incidence of diagnosed diabetes among US adults (2017-2018)1

In 2014 and 2015, approximately 5,700 people less than 20 years of age were diagnosed with type 2 diabetes each year.1

  • The proportion of newly diagnosed cases in people under 20 years of age was higher among US minority populations than in non-Hispanic whites.1
  • Between 2001 and 2009, the adjusted overall prevalence of type 2 diabetes among children and adolescents increased by 30.5%.4

Figure 4: Trends in type 2 diabetes prevalence among children and adolescents, 2001-2009, by sex and age and race/ethnicity4

In 2018, 88 million Americans age 20 and older had prediabetes.1

  • From 2013-2016, based on fasting glucose or A1c levels, 34.5% of US adults aged 18 years or older had prediabetes.1
  • On the basis of fasting glucose or A1c levels, and after adjusting for population age differences, the percentage of US adults aged 20 years or older with prediabetes between 2013−2016 was similar for non-Hispanic whites (33.9%), non-Hispanic blacks (36.9%), non-Hispanic Asians (32.8%), and Hispanics (35.4%).1

Diabetes was the seventh leading cause of death in the United States in 2018.5

  • The death rate from diabetes may be underreported.6
  • Studies have reported that only about 35% to 40% of people with diabetes who died had diabetes listed anywhere on the death certificate.6
  • Approximately 10% to 15% of death certificates had diabetes listed as the underlying cause of death.6


Diabetes is characterized by the dysfunction of insulin-producing pancreatic beta cells, insulin hormone resistance in cells of the body, or a combination of both.8,9

Figure 5: Pathophysiology of type 2 diabetes9

Five to ten years before most patients are diagnosed with diabetes, resistance develops to the effects of insulin in muscle and liver. Early on, in this state of “pre-diabetes,” pancreatic beta cells offset this resistance by increasing insulin secretion.10 Over time, insulin resistance in muscle worsens and pancreatic β-cells begin to fail, initially increasing post-prandial glucose levels. As insulin secretion declines further and the liver overproduces glucose at night, fasting plasma glucose levels subsequently rise.10,11 Progressive loss of β-cell mass and function continues as glucotoxicity worsens.10 Once insulin over-production no longer keeps pace with insulin resistance, plasma glucose levels remain persistently elevated.10 On average, patients have lost 50% to 80% of their β-cell function at diagnosis.11,12

Insulin resistance in muscle and liver and progressive pancreatic β-cell dysfunction represent only three of at least eight core defects implicated in the pathogenesis of type 2 diabetes.11

  • Insulin resistance in fat cells increases the release of free fatty acids from triglycerides and further contributes to pancreatic β-cell death.11
  • In response to food, the gut releases two incretin hormones, GLP-1 and GIP. Incretin hormones bind to pancreatic cells, increasing insulin production from β-cells and decreasing glucagon release from α-cells. In type 2 diabetes, incretin production is significantly reduced and β-cells become resistant to incretin effects, reducing insulin secretion.13,14
  • Hepatic glucose production is further exacerbated by the overproduction of glucagon from pancreatic α-cells in both fasting and post-prandial states.11 As plasma glucose levels rise, excess plasma glucose is reabsorbed by the kidneys, instead of being excreted, contributing to hyperglycemia.11,15
  • CNS resistance to the effects of insulin contributes to decreased satiety, weight gain, and peripheral insulin resistance in muscle and liver.11


  1. Centers for Disease Control and Prevention (CDC). National Diabetes Statistics Report, 2020. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2020. https://www.cdc.gov/diabetes/data/statistics/statistics-report.html.
  2. CDC. Diabetes Info Cards. https://www.cdc.gov/diabetes/library/socialmedia/infocards.html.
  3. CDC. Addressing Health Disparities in Diabetes. https://www.cdc.gov/diabetes/disparities.html.
  4. Dabelea D, et al. SEARCH for Diabetes in Youth Study. Prevalence of type 1 and type 2 diabetes among children and adolescents from 2001 to 2009. JAMA. 2014;311:1778-1786.
  5. Xu JQ, Murphy SL, Kochanek KD, Arias E. Mortality in the United States, 2018. NCHS Data Brief, 355. Hyattsville, MD: National Center for Health Statistics. 2020. https://www.cdc.gov/nchs/products/databriefs/db355.htm#section_2.
  6. American Diabetes Association. Statistics about diabetes. https://www.diabetes.org/resources/statistics/statistics-about-diabetes?loc=db-slabnav.
  7. Levin PA. Practical combination therapy based on pathophysiology of type 2 diabetes. Diabetes Metab Syndr Obes. 2016;9:355-369.
  8. Kahn SE, et al. Pathophysiology and treatment of type 2 diabetes: perspectives on the past, present, and future. Lancet. 2014;383:1068-1083.
  9. DeFronzo RA, et al. Pathogenesis of NIDDM. A balanced overview. Diabetes Care. 1992;15:318-368.
  1. Weir GC, Bonner-Weir S. Islet β cell mass in diabetes and how it relates to function, birth, and death. Ann N Y Acad Sci. 2013;1281:92-105.
  2. DeFronzo RA, Eldor R, Abdul-Ghani M. Pathophysiologic approach to therapy in patients with newly diagnosed type 2 diabetes. Diabetes Care. 2013;36(suppl 2):S127-S138.
  3. Butler AE, Janson J, Bonner-Weir S, et al. β-cell deficit and increased β-cell apoptosis in humans with type 2 diabetes. Diabetes. 2003;52:102-110.
  4. Drucker DJ. Enhancing incretin action for the treatment of type 2 diabetes. Diabetes Care. 2003;26:2929-2940.
  5. Meloni AR, DeYoung MB, Lowe C, et al. GLP-1 receptor activated insulin secretion from pancreatic β-cells: Mechanism and glucose dependence. Diabetes Obes Metab. 2013;15:15-27.
  6. Gerich JE. Role of the kidney in normal glucose homeostasis and in the hyperglycaemia of diabetes mellitus: Therapeutic implications. Diabet Med. 2010;27(2):136-142.
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