International Congress on Abnominal Obesity
Am J Clin Nutr 90: 1002-1010, 2009. First published August 26, 2009; doi:10.3945/ajcn.2008.27296
 American Journal of Clinical Nutrition, doi:10.3945/ajcn.2008.27296
Vol. 90, No. 4, 1002-1010, October 2009
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© 2009 American Society for Clinical Nutrition

ORIGINAL RESEARCH COMMUNICATION

High protein intake reduces intrahepatocellular lipid deposition in humans1,2,3

Murielle Bortolotti, Roland Kreis, Cyrille Debard, Bertrand Cariou, David Faeh, Maud Chetiveaux, Michael Ith, Peter Vermathen, Nathalie Stefanoni, Kim-Anne Lê, Philippe Schneiter, Michel Krempf, Hubert Vidal, Chris Boesch and Luc Tappy

1 From the Department of Physiology, University of Lausanne, Lausanne, Switzerland (MB, DF, NS, K-AL, PS, and LT); the Department of Clinical Research, University of Bern, Bern, Switzerland (RK, MI, PV, and CB); INSERM U870 and INRA U1235, Oullins, France/Université Lyon 1, Faculté de Médecine, Hospices Civils de Lyon, Lyon, France (CD and HV); INSERM U915, Nantes, France/Université de Nantes, Faculté de Médecine, Institut du Thorax, Nantes, France (BC, MC, and MK); and the Department of Endocrinology, Diabetes, and Metabolism, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland (LT).

2 Supported by the Swiss National Science Foundation (grant 310000-109737 to LT and CB).

3 Address correspondence to L Tappy, Faculty of Biology and Medicine, Department of Physiology, Rue du Bugnon 7, CH-1005 Lausanne, Switzerland. E-mail: luc.tappy{at}unil.ch.

Background: High sugar and fat intakes are known to increase intrahepatocellular lipids (IHCLs) and to cause insulin resistance. High protein intake may facilitate weight loss and improve glucose homeostasis in insulin-resistant patients, but its effects on IHCLs remain unknown.

Objective: The aim was to assess the effect of high protein intake on high-fat diet–induced IHCL accumulation and insulin sensitivity in healthy young men.

Design: Ten volunteers were studied in a crossover design after 4 d of either a hypercaloric high-fat (HF) diet; a hypercaloric high-fat, high-protein (HFHP) diet; or a control, isocaloric (control) diet. IHCLs were measured by 1H-magnetic resonance spectroscopy, fasting metabolism was measured by indirect calorimetry, insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp, and plasma concentrations were measured by enzyme-linked immunosorbent assay and gas chromatography–mass spectrometry; expression of key lipogenic genes was assessed in subcutaneous adipose tissue biopsy specimens.

Results: The HF diet increased IHCLs by 90 ± 26% and plasma tissue-type plasminogen activator inhibitor-1 (tPAI-1) by 54 ± 11% (P < 0.02 for both) and inhibited plasma free fatty acids by 26 ± 11% and β-hydroxybutyrate by 61 ± 27% (P < 0.05 for both). The HFHP diet blunted the increase in IHCLs and normalized plasma β-hydroxybutyrate and tPAI-1 concentrations. Insulin sensitivity was not altered, whereas the expression of sterol regulatory element-binding protein-1c and key lipogenic genes increased with the HF and HFHP diets (P < 0.02). Bile acid concentrations remained unchanged after the HF diet but increased by 50 ± 24% after the HFHP diet (P = 0.14).

Conclusions: Protein intake significantly blunts the effects of an HF diet on IHCLs and tPAI-1 through effects presumably exerted at the level of the liver. Protein-induced increases in bile acid concentrations may be involved. This trial was registered at www.clinicaltrials.gov as NCT00523562.