Obesity Surgery

, Volume 19, Issue 7, pp 894–904

Increased Expression and Activity of Hepatic Lipase in the Liver of Morbidly Obese Adult Patients in Relation to Lipid Content

  • Eva Pardina
  • Juan A. Baena-Fustegueras
  • Roberto Catalán
  • Rosa Galard
  • Albert Lecube
  • Jose M. Fort
  • Helena Allende
  • Víctor Vargas
  • Julia Peinado-Onsurbe
Research Article

DOI: 10.1007/s11695-008-9739-9

Cite this article as:
Pardina, E., Baena-Fustegueras, J.A., Catalán, R. et al. OBES SURG (2009) 19: 894. doi:10.1007/s11695-008-9739-9

Abstract

Background

The types and sources of lipid deposition in the liver of most patients with morbid obesity, as well as the effects of bariatric surgery, are discussed.

Methods

In 26 patients with morbid obesity who underwent bariatric surgery, we analyzed different kinds of lipids and hepatic lipase (HL) from both plasma and liver biopsies performed 12–18 months after surgery.

Results

The HL activity and HL-mRNA in morbidly obese (MO) livers were high (258 ± 17 mU/g, and 4.5-fold, respectively); after surgery, the activity decreased (137 ± 15 mU/g, p < 0.001) but not the levels of HL-mRNA (4.3-fold). Plasma HL activity was also high (4.31 ± 0.94 mU/mL plasma), and it decreased during weight loss (2.01 ± 0.29 mU/mL, p < 0.01); moreover, it correlated (r = 0.3694, p < 0.05) with decreased liver HL activity. Adrenocorticotropic hormone in MO was higher (27 ± 3 pg/mL) than after surgery (13 ± 1 pg/mL, p < 0.001). All hepatic and plasma lipids were significantly increased in MO patients, but, after bariatric surgery, most of those parameters recovered or normalized. Liver HL activity correlated with total and esterified cholesterol (r = 0.4399, p < 0.001 and r = 0.4395, p < 0.01, respectively).

Conclusion

High HL in MO patients could allow for liver intake of cholesterol that could be re-exported to steroidogenic organs to synthesize steroidal hormones. A decrease of plasma HL during weight loss could be a good index for improvement of liver disease.

Keywords

Metabolic syndrome Hepatic steatosis NAFLD HL LIPC ACTH 

Abbreviations

NAFLD

nonalcoholic fatty liver disease

HL

hepatic lipase

ALT

alanine aminotransferase

AST

aspartate aminotransferase

HOMA-IR

homeostasis model assessment of insulin resistance

Copyright information

© Springer Science + Business Media, LLC 2008

Authors and Affiliations

  • Eva Pardina
    • 1
  • Juan A. Baena-Fustegueras
    • 2
  • Roberto Catalán
    • 3
  • Rosa Galard
    • 3
  • Albert Lecube
    • 4
  • Jose M. Fort
    • 2
  • Helena Allende
    • 5
  • Víctor Vargas
    • 6
  • Julia Peinado-Onsurbe
    • 1
  1. 1.Department of Biochemistry and Molecular Biology, Faculty of BiologyUniversity of BarcelonaBarcelonaSpain
  2. 2.Endocrinology Surgery Unit, Hospital Universitari Vall D’hebron, Institut De Recerca Vall D’hebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  3. 3.Biochemistry Department, Hospital Universitari Vall D’hebron, Institut De Recerca Vall D’hebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  4. 4.CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III (ISCIII), Diabetes Research Unit, Institut de Recerca Vall D’HebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  5. 5.Pathology Division, Hospital Universitari Vall D’hebron, Institut De Recerca Vall D’hebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  6. 6.Liver Unit, Hospital Universitari Vall D’hebron, Institut De Recerca Vall D’hebronUniversitat Autònoma De BarcelonaBarcelonaSpain

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