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Related Concept Videos

Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Diabetic Retinopathy01:27

Diabetic Retinopathy

DefinitionDiabetic retinopathy is a microvascular complication of diabetes affecting the retinal blood vessels.Risk FactorsDiabetic retinopathy is present in almost all individuals with type 1 diabetes and more than 60% of those with type 2 diabetes after two decades of disease.The risk increases with poor glycemic control, hypertension, dyslipidemia, smoking, pregnancy, and puberty.Although cataracts and glaucoma are also more frequent in people with diabetes, retinopathy remains the leading...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis01:25

Type II Diabetes Mellitus III: Clinical Manifestations and Diagnosis

Type 2 diabetes mellitus develops gradually and is often asymptomatic in early stages.Clinical ManifestationsWhen symptoms appear, they include fatigue, blurred vision, pruritus, delayed wound healing, and recurrent infections, particularly candidal infections. Peripheral neuropathy may present as numbness or tingling in the extremities. Classic hyperglycemia symptoms—polyuria, polydipsia, and polyphagia—are less common. Most patients are overweight and frequently have associated hypertension...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.

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Related Experiment Video

Updated: Jul 11, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
05:49

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Published on: May 5, 2021

Oral infection, hyperglycemia, and endothelial dysfunction.

Sok-Ja Janket1, Judith A Jones, Jukka H Meurman

  • 1Department of General Dentistry, Boston University School of Dental Medicine, Boston, MA 02118, USA. skjanket@bu.edu

Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics
|October 2, 2007
PubMed
Summary

Metabolic syndrome and type 2 diabetes (T2DM) increase cardiovascular disease (CVD) risk. This review explores how hyperglycemia and periodontitis share inflammatory pathways (IL-6, TNF-alpha, CRP) contributing to CVD.

Related Experiment Videos

Last Updated: Jul 11, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
05:49

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish

Published on: May 5, 2021

Area of Science:

  • Cardiovascular Medicine
  • Endocrinology
  • Periodontology

Background:

  • Metabolic syndrome and type 2 diabetes (T2DM) are linked to cardiovascular disease (CVD), but mechanisms remain unclear.
  • Sustained hyperglycemia promotes advanced glycation end products (AGEs), stimulating inflammatory mediators like IL-6, TNF-alpha, and CRP.

Purpose of the Study:

  • To review evidence linking hyperglycemia-induced inflammation and periodontitis-associated inflammation.
  • To explore their shared role in cardiopathogenesis and CVD risk.

Main Methods:

  • Literature review of published studies.
  • Analysis of inflammatory pathways (IL-6, TNF-alpha, CRP) in T2DM and periodontitis.
  • Synthesis of evidence for a consensus on CVD contribution.

Main Results:

  • Hyperglycemia and periodontitis share common inflammatory mediators (IL-6, TNF-alpha, CRP).
  • These mediators are implicated in both T2DM and periodontal disease, contributing to CVD pathogenesis.
  • The link between periodontitis and CVD is under-recognized in the medical community.

Conclusions:

  • Shared inflammatory pathways provide a potential mechanism for T2DM and periodontitis to increase CVD risk.
  • Further research and interdisciplinary understanding are needed to address this link.
  • Targeting these inflammatory mediators may offer novel therapeutic strategies for CVD prevention in diabetic patients.