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The thyroid gland is a small, butterfly-shaped gland located in the neck and covers the anterior surface of the trachea. The gland has two lateral lobes connected by a thin tissue mass called the isthmus. Internally, each lobe comprises many small spherical structures known as thyroid follicles, surrounded by a network of blood vessels.
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The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Hyperlipidemia induces meibomian gland dysfunction.

Jinghua Bu1, Yang Wu1, Xiaoxin Cai1

  • 1Department of Ophthalmology, Xiang'an Hospital of Xiamen University; Fujian Provincial Key Laboratory of Ophthalmology and Visual Science; Eye Institute of Xiamen University; School of Medicine, Xiamen University, China.

The Ocular Surface
|June 16, 2019
PubMed
Summary
This summary is machine-generated.

Apolipoprotein E knockout mice exhibit meibomian gland dysfunction (MGD) and ocular surface changes linked to hyperlipidemia. Rosiglitazone treatment improved these conditions, suggesting a therapeutic target for MGD.

Keywords:
Apolipoprotein EHyperlipidemiaInflammationMeibomian gland dysfunctionPPAR-γ

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Area of Science:

  • Ophthalmology
  • Genetics
  • Biochemistry

Background:

  • Hyperlipidemia is a systemic condition with potential ocular manifestations.
  • Meibomian gland dysfunction (MGD) is a common cause of dry eye disease.
  • The link between hyperlipidemia and MGD requires further investigation in animal models.

Purpose of the Study:

  • To investigate pathological changes in the meibomian gland (MG) and ocular surface of Apolipoprotein E knockout (ApoE-/-) mice.
  • To explore the association between MGD and hyperlipidemia in this model.

Main Methods:

  • ApoE-/- and wild-type mice were analyzed for plasma cholesterol and ocular surface changes.
  • Meibomian gland tissues underwent histological examination, including H&E, Oil Red O, TUNEL, and immunostaining.
  • Gene expression and protein levels were assessed using RT-PCR and Western blot.

Main Results:

  • ApoE-/- mice displayed eyelid abnormalities, MG dropout, altered acinar morphology, duct dilation, and orifice plugging.
  • Exaggerated lipid accumulation, increased keratinization, reduced proliferation, and increased apoptosis were observed in MG acini.
  • Inflammation, activated NF-κB signaling, and oxidative stress were evident; PPAR-γ was downregulated.
  • Rosiglitazone treatment ameliorated eyelid and corneal pathology and MG inflammation.

Conclusions:

  • Apolipoprotein E deficiency in mice leads to MGD and ocular surface pathology associated with hyperlipidemia.
  • This mouse model provides a valuable tool for studying MGD pathophysiology related to dyslipidemia.
  • PPAR-γ activation shows therapeutic potential for MGD in the context of hyperlipidemia.