title: Body fat loss induced by calcium in co-supplementation with conjugated linoleic acid is associated with increased expression of bone formation genes in adult mice.
abstract: The potential of conjugated linoleic acids (CLA) and calcium in weight management in animal models and human studies has been outlined, as well as their use to prevent bone loss at critical stages. In addition, it has been suggested that bone remodeling and energy metabolism are regulated by shared pathways and involve common hormones such as leptin. We have previously shown that supplementation with CLA and calcium in adult obese mice decreases body weight and body fat. The aim of the present study was to assess the effects of these two compounds on bone and energy metabolism markers on bone. Mice (C57BL/6J) were divided into five groups according to diet and treatment (up to 56 days): control (C), high-fat diet (HF), HF+CLA (CLA), HF+calcium (Ca) and HF with both compounds (CLA+Ca). At the end of treatment, bone formation markers were determined in plasma and expression of selected bone and energy markers was determined in tibia by quantitative polymerase chain reaction. Results show that CLA was associated with decreased tibia weight and minor impact on bone markers, whereas calcium, either alone or co-supplemented with CLA, maintained bone weight and promoted the expression of bone formation genes such as bone gamma-carboxyglutamate protein 2 (Bglap2) and collagen Iα1 (Col1a1). Furthermore, it had a significant effect on key players in energy metabolism, in particular leptin and adiponectin tibia receptors. Overall, in addition to the weight loss promoting properties of calcium, on its own or co-supplemented with CLA, our results support beneficial effects on bone metabolism in mice.
authors.affiliation: Laboratory of Molecular Biology, Nutrition and Biotechnology, University of the Balearic Islands and Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Palma de Mallorca, Spain.
authors.forename: Alice
authors.initials: A
authors.lastname: Chaplin
authors.affiliation: Laboratory of Molecular Biology, Nutrition and Biotechnology, University of the Balearic Islands and Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Palma de Mallorca, Spain. Electronic address: andreu.palou@uib.es.
authors.forename: Andreu
authors.initials: A
authors.lastname: Palou
authors.affiliation: Laboratory of Molecular Biology, Nutrition and Biotechnology, University of the Balearic Islands and Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Palma de Mallorca, Spain.
authors.forename: Francisca
authors.initials: F
authors.lastname: Serra
mesh_terms: D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D001842:Bone and Bones / Q000378:metabolism; D002118:Calcium / Q000737:chemistry*; D024042:Collagen Type I / Q000378:metabolism*; D000090602:Collagen Type I, alpha 1 Chain; D059305:Diet, High-Fat; D019587:Dietary Supplements; D005786:Gene Expression Regulation; D020738:Leptin / Q000097:blood; D044243:Linoleic Acids, Conjugated / Q000737:chemistry*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism; D015675:Osteocalcin / Q000378:metabolism; D010012:Osteogenesis / Q000187:drug effects / Q000235:genetics*; D054419:Receptors, Adiponectin / Q000378:metabolism; D054411:Receptors, Leptin / Q000378:metabolism; D013977:Tibia / Q000378:metabolism
chemical_list: D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D024042:Collagen Type I; D000090602:Collagen Type I, alpha 1 Chain; D020738:Leptin; D044243:Linoleic Acids, Conjugated; D054419:Receptors, Adiponectin; D054411:Receptors, Leptin; D015675:Osteocalcin; D002118:Calcium
keywords: Bone; CLA; Calcium; Obesity; Osteocalcin