Original Article | Published:

Clinical Studies and Practice

Visceral obesity is associated with white matter hyperintensity and lacunar infarct

International Journal of Obesity volume 41, pages 683688 (2017) | Download Citation

Abstract

Background:

The presence of white matter hyperintensity (WMH) and lacunar infarct are recognized as risk factors of dementia, stroke and mortality. It is undetermined whether visceral adipose tissue (VAT) area is associated with an increased risk of cerebral small vessel disease. We explored whether VAT area was responsible for cerebral small vessel disease through the identification of WMH and lacunar infarct.

Subjects:

A total of 2046 subjects free of cerebrovascular disease who underwent brain magnetic resonance imaging and abdominal fat computed tomography during a general health check-up were enrolled.

Results:

The prevalence of cerebral WMH was 37.7%. Subjects with WMH had greater VAT area and higher BMI and waist circumference than those without WMH, although significant differences in subcutaneous adipose tissue (SAT) area were not shown. Subjects with lacunar infarct also had significantly greater VAT area and higher waist circumference and BMI than those without lacunar infarct. Multivariate analyses adjusted for age, sex, diabetes, hypertension, smoking and alcohol, showed VAT area was an independent risk factor of cerebral WMH (odds ratio (OR): 1.13, 95% confidence interval (CI): 1.02–1.24, P=0.016), whereas waist circumference and SAT area were not significantly associated with the risk of WMH. Likewise, VAT area was also independently associated with lacunar infarct (OR: 1.38, 95% CI: 1.06–1.81, P=0.018), whereas the other anthropometric measures were not related with lacunar infarct.

Conclusions:

VAT has a significant association with cerebral small vessel disease, which was defined as WMH or lacunar infarct. Visceral obesity can be a potential therapeutic target for the prevention of cerebral small vessel disease.

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Acknowledgements

This study was supported by a grant (04-2009-0670) from the Seoul National University Hospital Research Fund.

Author information

Author notes

    • K W Kim
    •  & H Seo

    These authors contributed equally to this work.

Affiliations

  1. Department of Internal Medicine, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea

    • K W Kim
    • , M-S Kwak
    •  & D Kim
  2. Department of Internal Medicine, Seoul National University College of Medicine, Seoul National University Hospital, Seoul, Korea

    • K W Kim
  3. Department of Diagnostic Radiology, Seoul National University Hospital Healthcare System Gangnam Center, Seoul, Korea

    • H Seo
  4. Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA, USA

    • D Kim

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Competing interests

The authors declare no conflict of interest.

Corresponding author

Correspondence to D Kim.

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DOI

https://doi.org/10.1038/ijo.2017.13