title: Supplementary dietary calcium stimulates faecal fat and bile acid excretion, but does not protect against obesity and insulin resistance in C57BL/6J mice.
abstract: There is increased interest in the potential protective role of dietary Ca in the development of metabolic disorders related to the metabolic syndrome. Ca-induced intestinal precipitation of fatty acids and bile acids as well as systemic metabolic effects of Ca on adipose tissue is proposed to play a causal role. In this experiment, we have studied all these aspects to validate the suggested protective effect of Ca supplementation, independent of other dietary changes, on the development of diet-induced obesity and insulin resistance. In our diet intervention study, C57BL/6J mice were fed high-fat diets differing in Ca concentrations (50 v. 150 mmol/kg). Faecal excretion analyses showed an elevated precipitation of intestinal fatty acids (2·3-fold; P < 0·01) and bile acids (2-fold; P < 0·01) on the high-Ca diet. However, this only led to a slight reduction in fat absorption (from 98 to 95 %; P < 0·01), mainly in the distal small intestine as indicated by gene expression changes. We found no effect on body-weight gain. Lipolysis and lipogenesis-related parameters in adipose tissue also showed no significant changes on the high-Ca diet, indicating no systemic effects of dietary Ca on adiposity. Furthermore, early gene expression changes of intestinal signalling molecules predicted no protective effect of dietary Ca on the development of insulin resistance, which was confirmed by equal values for insulin sensitivity on both diets. Taken together, our data do not support the proposed protective effect of dietary Ca on the development of obesity and/or insulin resistance, despite a significant increase in faecal excretion of fatty acids and bile acids.
authors.affiliation: Nutrigenomics Consortium, TI Food and Nutrition, Wageningen, The Netherlands.
authors.forename: Nicole J W
authors.initials: NJ
authors.lastname: de Wit
authors.forename: Hanneke
authors.initials: H
authors.lastname: Bosch-Vermeulen
authors.forename: Els
authors.initials: E
authors.lastname: Oosterink
authors.forename: Michael
authors.initials: M
authors.lastname: Müller
authors.forename: Roelof
authors.initials: R
authors.lastname: van der Meer
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism; D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism*; D002136:Calcium, Dietary / Q000494:pharmacology*; D004041:Dietary Fats / Q000009:adverse effects / Q000378:metabolism*; D019587:Dietary Supplements; D005227:Fatty Acids / Q000378:metabolism*; D005243:Feces / Q000737:chemistry; D015870:Gene Expression / Q000187:drug effects; D007333:Insulin Resistance; D007408:Intestinal Absorption; D007421:Intestine, Small / Q000187:drug effects* / Q000378:metabolism; D050155:Lipogenesis / Q000187:drug effects; D008066:Lipolysis / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000139:chemically induced / Q000378:metabolism*; D014131:Trace Elements / Q000494:pharmacology
chemical_list: D001647:Bile Acids and Salts; D002136:Calcium, Dietary; D004041:Dietary Fats; D005227:Fatty Acids; D014131:Trace Elements