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Related Concept Videos

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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Type II Diabetes I: Introduction01:26

Type II Diabetes I: Introduction

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Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance, in which target tissues such as the liver, muscle, and adipose tissue respond poorly to insulin. It is also associated with inadequate compensatory insulin secretion, where pancreatic β-cells fail to produce sufficient insulin. Together, these abnormalities lead to persistent hyperglycemia.EtiologyT2DM develops through a complex interaction of genetic predisposition and environmental or...
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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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Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

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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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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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Oral Hypoglycemic Agents: Biguanides and Glitazones01:26

Oral Hypoglycemic Agents: Biguanides and Glitazones

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Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
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Related Experiment Video

Updated: Apr 30, 2026

Osmotic Minipump Implantation for Increasing Glucose Concentration in Mouse Cerebrospinal Fluid
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[Insulin resistance and cognitive function].

Toshiyasu Sasaoka, Tsutomu Wada, Hiroshi Tsuneki

    Nihon Rinsho. Japanese Journal of Clinical Medicine
    |May 7, 2014
    PubMed
    Summary

    Diabetes increases Alzheimer disease risk by impairing brain insulin signaling. Understanding these links may lead to new Alzheimer

    Area of Science:

    • Neuroscience
    • Endocrinology
    • Pathology

    Context:

    • Alzheimer disease (AD) risk is elevated in diabetic patients.
    • Insulin resistance is a key factor in cognitive dysfunction.
    • Brain insulin signaling defects are implicated in AD pathogenesis.

    Purpose:

    • To elucidate the molecular mechanisms linking insulin resistance to Alzheimer disease.
    • To explore therapeutic strategies targeting insulin signaling in AD.

    Summary:

    • Amyloid beta oligomers disrupt insulin signaling via TNF-alpha and JNK, affecting IRS-1.
    • PI-3 kinase pathway attenuation contributes to Tau hyper-phosphorylation.
    • Impaired orexin function and synapse loss result from defective brain insulin signaling.

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    Impact:

    • Novel therapeutic targets for Alzheimer disease can be identified.
    • Treatments like nasal insulin, thiazolidinediones, and GLP-1 agonists show neuroprotective effects.
    • Further research can advance treatments for mild cognitive dysfunction and AD.