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Type 2 diabetes, characterized by insulin resistance, arises when the insulin receptors on cells lose responsiveness to insulin, diminishing the cell's capacity to take up glucose, resulting in elevated blood glucose levels. To receive a diagnosis of Type 2 diabetes, a series of blood glucose tests are necessary to assess whether the blood glucose falls within normal parameters. If the result is out of the normal range, a patient may be diagnosed as prediabetic or diabetic, depending on the...
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The therapy for diabetes aims to alleviate hyperglycemia-related symptoms, prevent acute metabolic decompensation, and reduce chronic end-organ complications. Glycemic control is evaluated through short-term (self-monitoring, continuous glucose monitoring) and long-term (A1c, fructosamine) metrics, enabling near real-time tracking of blood glucose levels and reflecting glycemic control over specific time frames.
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Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
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For most patients, experiencing several weeks of polyuria, polydipsia, fatigue, and significant weight loss may indicate the presence of diabetes. Furthermore, adults displaying the phenotypic appearance of type 2 diabetes (particularly those who are obese and not initially insulin-requiring), may have islet cell autoantibodies, suggesting autoimmune-mediated β cell destruction and a diagnosis of latent autoimmune diabetes of adults (LADA). The categorization of glucose homeostasis is...
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Carbohydrates consumed through foods are converted into glucose, a crucial energy source for the body. In the prandial state, high blood glucose levels stimulate the secretion of insulin from the pancreas. Insulin inhibits hepatic glucose production and stimulates glucose uptake and metabolism by muscle and adipose tissue. The excess glucose is converted into glycogen and stored in the liver and muscles.
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Diabetes mellitus is a chronic metabolic disorder characterized by high blood glucose levels due to inadequate insulin production, insulin resistance, or both. The condition affects millions worldwide and can significantly impact their health and quality of life.
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Beyond Glucose-Rethinking Prediabetes for Precision Prevention.

Robert Wagner1,2,3, Elizabeth Selvin4, Ratika Sehgal5

  • 1Department of Endocrinology and Diabetology, Medical Faculty, and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.

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Prediabetes is biologically diverse, with six identified subtypes. Three high-risk subtypes show different paths to diabetes and complications, enabling precision prevention strategies.

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Area of Science:

  • Endocrinology and Metabolism
  • Precision Medicine
  • Public Health

Background:

  • Prediabetes affects over a third of U.S. adults but is poorly defined by current glycemic measures.
  • Existing categories (impaired fasting glucose, impaired glucose tolerance, elevated HbA1c) fail to capture the full biological heterogeneity.

Purpose of the Study:

  • To identify distinct prediabetes subtypes using comprehensive phenotyping.
  • To understand the differential risks and trajectories of these subtypes toward type 2 diabetes and its complications.
  • To inform precision prevention and treatment strategies for prediabetes.

Main Methods:

  • Unsupervised clustering analysis was applied to comprehensively phenotyped cohorts.
  • Integration of data included insulin sensitivity, insulin secretion, visceral and hepatic fat, and genetic risk.
  • Subtypes were analyzed for their distinct progression patterns toward diabetes and complication development.

Main Results:

  • Six reproducible prediabetes subtypes were identified.
  • Three high-risk subtypes were characterized: progressing prediabetes with fatty liver, progressing prediabetes with β-cell failure, and slow progressors with hyperinsulinemic insulin resistance.
  • These subtypes exhibit unique trajectories toward diabetes and distinct complication patterns, with some complications like albuminuria and excess mortality observed even before a diabetes diagnosis in slow progressors.

Conclusions:

  • Recognizing prediabetes subtypes allows for improved risk stratification and precision prevention.
  • Tailored interventions, including lifestyle modification, bariatric surgery, and pharmacologic therapies (e.g., GLP-1-based), show potential for subtype-specific benefits.
  • Future trials should focus on subtype-guided interventions and evaluate early complication outcomes, not just diabetes incidence, to reduce the public health burden.