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Related Concept Videos

Diabetes Mellitus: Type 2 and Gestational01:22

Diabetes Mellitus: Type 2 and Gestational

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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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Type I Diabetes III: Clinical Manifestations01:19

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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...
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Diabetic Nephropathy01:28

Diabetic Nephropathy

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Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration...
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Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

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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...
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Diabetic Neuropathy01:22

Diabetic Neuropathy

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DefinitionDiabetic neuropathy is nerve damage caused by long-standing diabetes mellitus. It results directly from prolonged high blood sugar levels.PathophysiologyThe pathophysiology of diabetic neuropathy involves both metabolic and vascular disturbances triggered by chronic hyperglycemia.Metabolic injury: Elevated glucose levels activate the polyol pathway within nerve cells, leading to the accumulation of sorbitol and fructose. This increases oxidative stress, disrupts normal nerve...
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Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

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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: Apr 28, 2026

Alternate Immersion in Glucose to Produce Prolonged Hyperglycemia in Zebrafish
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Galectin-3 in diabetic patients.

Giuseppe Pugliese, Carla Iacobini, Carlo Ricci

    Clinical Chemistry and Laboratory Medicine
    |June 19, 2014
    PubMed
    Summary

    Galectin-3 is a heart failure marker and mediator. Its role in diabetes complications requires further study, with conflicting results in animal models influencing potential therapeutic strategies.

    Area of Science:

    • Biochemistry
    • Cardiology
    • Immunology

    Background:

    • Galectin-3 is a molecule with diverse roles in disease.
    • It's a prognostic marker for heart failure and mortality.
    • Plasma galectin-3 levels correlate with diabetes and metabolic conditions.

    Purpose of the Study:

    • Investigate galectin-3's role in heart failure, particularly in diabetic patients.
    • Clarify galectin-3's function as both a marker and mediator of heart failure.
    • Determine the impact of galectin-3 on organ damage and fibrosis.

    Main Methods:

    • Review of existing studies on galectin-3 in pathophysiological processes.
    • Analysis of studies in galectin-3 deficient mice.
    • Consideration of experimental settings involving advanced glycation endproducts (AGEs) and advanced lipoxidation endproducts (ALEs).

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    Main Results:

    • Galectin-3 acts as a prognostic marker for heart failure.
    • Its role as a disease mediator is complex, with conflicting results in animal models.
    • Galectin-3's function is influenced by AGEs/ALEs levels, affecting tissue outcomes.
    • Deficiency in galectin-3 has shown both protective and detrimental effects on organ fibrosis and inflammation.

    Conclusions:

    • Further prospective studies in diabetic patients are needed to link galectin-3 levels with complications.
    • Additional animal research is required to fully elucidate galectin-3's role in organ damage.
    • The therapeutic potential of galectin-3 blockade needs to be established before clinical application.