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Exercise Increases Bone in SEIPIN Deficient Lipodystrophy, Despite Low Marrow Adiposity.

Cody McGrath1, Sarah E Little-Letsinger1, Jeyantt Srinivas Sankaran1

  • 1Department of Medicine, Division of Endocrinology & Metabolism, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States.

Frontiers in Endocrinology
|February 11, 2022
PubMed
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This summary is machine-generated.

Exercise benefits skeletal health, even in lipodystrophy models lacking SEIPIN. Running improved bone density in both normal and lipodystrophic mice, suggesting metabolic flexibility.

Area of Science:

  • Endocrinology
  • Bone Biology
  • Metabolic Disorders

Background:

  • Lipodystrophy is characterized by a lack of white adipose tissue, often leading to diabetes and steatosis.
  • The role of exercise in lipodystrophy, particularly concerning skeletal health, remains uninvestigated.
  • SEIBold (SEIPIN) is crucial for lipid droplet formation and adipose tissue development.

Purpose of the Study:

  • To investigate the effects of exercise on skeletal health in a mouse model of lipodystrophy with SEIPIN deficiency.
  • To examine bone marrow adipose tissue (BMAT) quantity and distribution in SEIPIN-deficient mice.
  • To assess exercise's impact on bone parameters and metabolic adaptations in this model.

Main Methods:

  • Utilized a global SEIPIN knockout (KO) mouse model and wild-type (WT) littermates.
Keywords:
BSCL2SEIPINanabolismbonebone marrow adipose tissue (BMAT)congenital lipodystrophyendocrinology and metabolismexercise

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  • Assigned mice to six weeks of voluntary running exercise (E) or no exercise (N).
  • Assessed body weight, adipose tissue, liver steatosis (Plin1 expression), bone marrow adiposity (9.4T MRI), and bone structure (μCT).
  • Main Results:

    • SEIPIN KO mice exhibited reduced body weight, absence of epididymal adipose tissue, and significant liver steatosis.
    • BMAT was present but lower in KO mice, with notable regional differences in the femur.
    • Exercise reduced weight in WT but not KO mice; however, exercise increased trabecular bone volume fraction (BV/TV) in both KO and WT mice.

    Conclusions:

    • SEIPIN deficiency leads to lipodystrophy, altered BMAT distribution, and preserved bone structure.
    • Exercise can induce skeletal benefits (increased trabecular bone) in SEIPIN-deficient mice, despite metabolic differences.
    • These findings suggest potential metabolic flexibility during exercise-induced bone anabolism, even in lipodystrophy.