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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 II: Pathophysiology01:24

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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 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...
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Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but this inhibition is released...
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Studying the Hypothalamic Insulin Signal to Peripheral Glucose Intolerance with a Continuous Drug Infusion System into the Mouse Brain
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Periapical lesions decrease insulin signal and cause insulin resistance.

Rafael Dias Astolphi1, Mariane Machado Curbete, Natalia Helena Colombo

  • 1Basic Sciences, Araçatuba Dental School, UNESP-Universidade Estadual Paulista, Araçatuba, Sao Paulo, Brazil.

Journal of Endodontics
|April 25, 2013
PubMed
Summary

Periapical lesions (PLs) in rats increase tumor necrosis factor-alpha (TNF-α), impairing insulin signaling and insulin sensitivity. Preventing oral inflammation is crucial for avoiding insulin resistance.

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Area of Science:

  • Endocrinology
  • Oral Pathology
  • Metabolic Syndrome

Background:

  • Inflammatory cytokines negatively impact insulin signal transduction.
  • Local oral inflammation, like periodontal disease, correlates with insulin resistance and type 2 diabetes.
  • Periapical lesions (PLs) represent a source of local oral inflammation.

Purpose of the Study:

  • To investigate the effect of periapical lesions (PLs) on insulin signaling and sensitivity in a rat model.
  • To test the hypothesis that PLs elevate plasmatic tumor necrosis factor-alpha (TNF-α), thereby altering systemic insulin signaling and sensitivity.

Main Methods:

  • Wistar rats developed PLs by pulpal exposure.
  • Insulin sensitivity assessed via insulin tolerance tests.
  • Plasmatic TNF-α measured by ELISA; insulin signaling evaluated by Western blotting in adipose tissue.

Main Results:

  • Rats with PLs exhibited elevated plasmatic TNF-α.
  • A decreased rate of glucose disappearance was observed in the PL group.
  • Reduced tyrosine phosphorylation of insulin receptor substrate (IRS) was noted, but serine phosphorylation remained unchanged.

Conclusions:

  • Periapical lesions can disrupt insulin signaling and reduce insulin sensitivity, likely mediated by increased TNF-α.
  • These findings highlight the importance of preventing local inflammatory conditions, such as PLs, to mitigate insulin resistance.