Obesity Surgery

, Volume 19, Issue 8, pp 1150–1158 | Cite as

Lipoprotein Lipase but Not Hormone-Sensitive Lipase Activities Achieve Normality After Surgically Induced Weight Loss in Morbidly Obese Patients

  • E. Pardina
  • A. Lecube
  • R. Llamas
  • R. Catalán
  • R. Galard
  • J. M. Fort
  • H. Allende
  • V. Vargas
  • J. A. Baena-Fustegueras
  • J. Peinado-OnsurbeEmail author
Clinical Research



Although bariatric surgery is currently the most common practice for inducing weight loss in morbidly obese patients (BMI > 40 kg/m2), its effect on the lipid content of adipose tissue and its lipases (lipoprotein lipase [LPL] and hormone-sensitive lipase [HSL]) are controversial.


We analyzed LPL and HSL activities and lipid content from plasma as well as subcutaneous (SAT) and visceral (VAT) adipose tissue of 34 morbidly obese patients (MO) before and after (6 and 12 months) Roux-en-Y gastric bypass surgery and compare the values with those of normal weight (control) patients.


LPL activity was significantly higher in MO (SAT = 32.9 ± 1.0 vs VAT = 36.4 ± 3.3 mU/g tissue; p < 0.001) than in control subjects (SAT = 8.2 ± 1.4 vs VAT = 6.8 ± 1.0 mU/g tissue) in both adipose depots. HSL activity had similar values in both types of tissue (SAT = 32.8 ± 1.6 and VAT = 32.9 ± 1.6 mU/g) of MO. In the control group, we found similar results but with lower values (SAT = 11.9 ± 1.4 vs VAT = 12.1 ± 1.4 mU/g tissue). Twelve months after surgery, SAT LPL activity diminished (9.8 ± 1.4 mU/g tissue, p < 0.001 vs morbidly obese), while HSL (46.6 ± 3.7 mU/g tissue) remained high. All lipids in tissue and plasma diminished after bariatric surgery except plasma nonesterified fatty acids, which maintained higher levels than controls (16 ± 3 vs 9 ± 0 mg/dL; p < 0.001, respectively).


When obese patients lose weight, they lose not only part of the lipid content of the cells but also the capacity to store triacylglycerides in SAT depots.


Adipocyte size Obesity Weight loss NEFA LPL HSL 



Homeostasis model assessment of insulin resistance


Nonesterified fatty acid


Lipoprotein lipase


Hormone-sensitive lipase.



This research was funded by the Fondo de Investigación Sanitaria del Instituto de Salud Carlos III of the Spanish Ministry for Health and Consumer Affairs (PI030042, PI030024, and PI070079). Both R. Llamas and E. Pardina were awarded grants by the same institution. We express thanks to Professor M. Llobera for his inestimable help.

Conflict of interest

The authors have declared that no conflict of interest exists. The authors who have taken part in this study do not have a relationship, past or present, with the manufacturers of the drugs involved and did not receive funding from the manufacturers to carry out their research.

Writing assistance

English grammar and language have been corrected by American Journal Experts (


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Copyright information

© Springer Science + Business Media, LLC 2009

Authors and Affiliations

  • E. Pardina
    • 1
  • A. Lecube
    • 2
  • R. Llamas
    • 1
  • R. Catalán
    • 3
  • R. Galard
    • 3
  • J. M. Fort
    • 4
  • H. Allende
    • 5
    • 7
  • V. Vargas
    • 6
    • 7
  • J. A. Baena-Fustegueras
    • 4
  • J. Peinado-Onsurbe
    • 1
    Email author
  1. 1.Biochemistry and Molecular Biology Department, Biology FacultyUniversitat de BarcelonaBarcelonaSpain
  2. 2.Diabetes Research Unit, Institut De Recerca Vall D’Hebron, CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM)Instituto de Salud Carlos III (ISCIII)BarcelonaSpain
  3. 3.Biochemistry DepartmentInstitut De Recerca Vall D’HebronBarcelonaSpain
  4. 4.Endocrinology Surgery Unit, Institut De Recerca Vall D’HebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  5. 5.Pathology Division, Institut De Recerca Vall D’HebronUniversitat Autònoma De BarcelonaBarcelonaSpain
  6. 6.Liver UnitInstitut De Recerca Vall D’Hebron Universitat Autònoma De BarcelonaBarcelonaSpain
  7. 7.CIBER de Enfermedades Hepáticas y Digestivas (CIBEREHD)Instituto de Salud Carlos III (ISCIII)BarcelonaSpain

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