Original Article

Obesity (2007) 15, 117–125; doi:10.1038/oby.2007.508

Desaturation of Skeletal Muscle Structural and Depot Lipids in Obese Individuals during a Very-Low-Calorie Diet Intervention*

Steen B. Haugaard*,, Allan Vaag, Carl-Erik Høy§ and Sten Madsbad*

  1. *Department of Endocrinology and Internal Medicine, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark
  2. Clinical Research Unit, Hvidovre Hospital, University of Copenhagen, Hvidovre, Denmark
  3. Steno Diabetes Centre, University of Copenhagen, Gentofte, Denmark
  4. §BioCentrum, Technical University of Denmark, Lyngby, Denmark

Correspondence: Steen B. Haugaard Clinical Research Unit 136, Hvidovre University Hospital, DK-2650 Hvidovre, Copenhagen, Denmark. E-mail: sbhau@dadlnet.dk

*The costs of publication of this article were defrayed, in part, by the payment of page charges. This article must, therefore, be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Carl-Erik Høy is deceased.

Received 22 June 2006; Revised  0000; Accepted 28 August 2006.

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Abstract

Objective:

 

This study investigated whether a very-lowcalorie dietary intervention (VLCD) may influence composition of skeletal muscle cell membrane phospholipid and composition and concentration of intramyocellular triglyceride (IMTG) in obese subjects. The working hypothesis proposed that a VLCD would decrease saturated fatty acids (FAs) and increase long-chain polyunsaturated FAs (LCPUFAs) in muscular structural lipids, as such changes have been associated with improved insulin sensitivity.

Research Methods and Procedures:

 

Skeletal muscle biopsies (vastus lateralis) were obtained from 13 obese subjects (nine women) before and after 8 weeks on VLCD (approx600 to 800 kcal/d). FA composition in muscle cell membrane phospholipid and concentration and FA composition of IMTG were determined by gas-liquid chromatography.

Results:

 

Baseline BMI was 36.0 plusminus 3.4 kg/m2. Weight loss was 9.3 plusminus 1.1 kg (8.8 plusminus 1.1%; p < 0.0001); loss of adipose tissue was 5.9 plusminus 0.9 kg (p < 0.0001). Insulin resistance (by homeostasis model assessment) decreased (-44 plusminus 7%; p < 0.001). Muscle cell membrane phospholipid saturated FAs decreased (-3.2 plusminus 1.3%; p < 0.05), whereas monounsaturated FAs (4.3 plusminus 1.7%; p < 0.05), LCPUFAs (11 plusminus 6%; p < 0.05), and the ratio of LCPUFAs to saturated FAs (12 plusminus 5%; p < 0.05) increased. IMTG decreased, but not significantly (-5%). IMTG-saturated FAs decreased (-3.3 plusminus 1.5%; p < 0.05), whereas LCPUFAn-3 (29 plusminus 9%; p < 0.01), LCPUFAn-6 (33 plusminus 9%; p < 0.01), and the ratio of LCPUFAs to saturated FAs (34 plusminus 8%; p < 0.001) increased. Plasma total cholesterol (-15 plusminus 6%; p < 0.05), low-density lipoprotein-cholesterol (-16 plusminus 5%; p < 0.01), high-density lipoprotein-cholesterol (-8 plusminus 2%; p < 0.01), and plasma triglyceride (-19 plusminus 12%; p = 0.10) all decreased during the VLCD.

Discussion:

 

Desaturation of both muscle cell membrane phospholipid and IMTG was significant but modest during a VLCD in obese subjects. Further research must delineate whether such changes in skeletal muscle structural and depot lipid composition themselves are enough to promote the observed improvements in insulin action.

Keywords:

dietary intervention, membrane phospholipids, intramyocellular triglyceride, insulin sensitivity, weight loss

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