Type 2 Diabetes

Type 2 Diabetes is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • T2DM results from defective insulin secretion followed by loss of β-cell mass in response to increased demand as a result of insulin resistance.1
  • T2DM is usually diagnosed in adults, with both incidence and prevalence increasing with age. However, type 2 diabetes prevalence has increased substantially since 2001 in youth aged 10–19, comprising about 20% of cases of diabetes in that age group in 2017.2
  • T2DM is associated with obesity, family history of diabetes, history of GDM or prediabetes, hypertension, physical inactivity, race/ethnicity, and other social determinants of health (socioeconomic status, food insecurity). African Americans, Latinos, Asian Indians, Native Americans, Pacific Islanders, and some groups of Asians have a greater risk of developing T2DM than Caucasians.
  • T2DM may be asymptomatic and, therefore, can remain undiagnosed for months to years.
  • The loss of pancreatic β cells is progressive. Insulin secretion is usually sufficient to prevent ketosis, but DKA or HHS can develop during severe stress. T2DM in patients who present with or later develop ketosis or DKA, but who do not require insulin between episodes, is termed ketosis-prone T2DM.
  • The mechanisms underlying the β-cell loss and defective insulin secretory dysfunction in T2DM are not clear, but cell death, transdifferentiation, and de-differentiation in response to oxidative stress and endoplasmic reticulum stress in the setting of environmental exposure and genetic predisposition have been proposed. Glycemic state may also affect the beta cell over prolonged periods of time.3

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General Principles

  • T2DM results from defective insulin secretion followed by loss of β-cell mass in response to increased demand as a result of insulin resistance.1
  • T2DM is usually diagnosed in adults, with both incidence and prevalence increasing with age. However, type 2 diabetes prevalence has increased substantially since 2001 in youth aged 10–19, comprising about 20% of cases of diabetes in that age group in 2017.2
  • T2DM is associated with obesity, family history of diabetes, history of GDM or prediabetes, hypertension, physical inactivity, race/ethnicity, and other social determinants of health (socioeconomic status, food insecurity). African Americans, Latinos, Asian Indians, Native Americans, Pacific Islanders, and some groups of Asians have a greater risk of developing T2DM than Caucasians.
  • T2DM may be asymptomatic and, therefore, can remain undiagnosed for months to years.
  • The loss of pancreatic β cells is progressive. Insulin secretion is usually sufficient to prevent ketosis, but DKA or HHS can develop during severe stress. T2DM in patients who present with or later develop ketosis or DKA, but who do not require insulin between episodes, is termed ketosis-prone T2DM.
  • The mechanisms underlying the β-cell loss and defective insulin secretory dysfunction in T2DM are not clear, but cell death, transdifferentiation, and de-differentiation in response to oxidative stress and endoplasmic reticulum stress in the setting of environmental exposure and genetic predisposition have been proposed. Glycemic state may also affect the beta cell over prolonged periods of time.3

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