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Quantification of Atherosclerosis in Mice
06:59

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Loss of small heterodimer partner protects against atherosclerosis in apolipoprotein E-deficient mice

Min Joo Kim1, Kwan Jae Lee, Ji-Yeon Hwang

  • 1Department of Internal Medicine, Seoul National University College of Medicine, Seoul 110-744, Republic of Korea.

Endocrine Journal
|August 6, 2013
PubMed

Insights

Small heterodimer partner (SHP) deficiency reduces atherosclerosis by improving resistance to diet-induced obesity. Loss of SHP in ApoE-/- mice decreased body weight, improved glucose intolerance, and lowered atherosclerotic lesions.

Area of Science:

  • Metabolic disease research
  • Cardiovascular research
  • Molecular biology

Background:

  • Small heterodimer partner (SHP) regulates bile, lipid, and glucose metabolism.
  • Atherosclerosis is a complex disease influenced by metabolic factors.

Purpose of the Study:

  • To investigate the role of SHP in the development of atherosclerosis.
  • To determine if SHP deficiency impacts diet-induced obesity and related metabolic changes.

Main Methods:

  • Generation of double knockout mice (Apolipoprotein E knockout and SHP knockout).
  • Feeding ApoE-/- and ApoE-/-SHP-/- mice a western diet for 20 weeks.
  • Assessment of body weight, adipocyte size, liver lipid accumulation, glucose tolerance, and atherosclerotic lesion size.

Main Results:

  • ApoE-/-SHP-/- mice exhibited significantly lower body weight compared to ApoE-/- mice.
  • Loss of SHP reduced adipocyte size, liver lipid accumulation, and improved glucose intolerance.
  • Atherosclerotic lesion proportion in the aorta was significantly reduced in ApoE-/-SHP-/- mice.

Conclusions:

  • SHP deficiency prevents atherosclerosis development in ApoE-/- mice.
  • Resistance to diet-induced obesity is the primary mechanism behind SHP's protective effect against atherosclerosis.

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