Dairy product consumption and the metabolic syndrome

L.E.C. van Meijl, R. Vrolix, R.P. Mensink

    Research output: Contribution to journalArticleAcademicpeer-review

    68 Citations (Scopus)

    Abstract

    The metabolic syndrome is an important risk factor for type 2 diabetes mellitus and CVD. Epidemiological studies have now suggested protective effects of dairy product consumption on the development of this syndrome. Here we review the physiological effects and possible mechanisms involved of three main dairy constituents (Ca, protein, fat) on important components of the metabolic syndrome. Ca supplements improve the serum lipoprotein profile, particularly by decreasing serum total and LDL-cholesterol concentrations. They also lower systolic and diastolic blood pressure. Insufficient evidence exists for a significant role of Ca supplements or dairy in body-weight management. Effects of Ca may be related to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones. Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake. They have also been reported to improve the serum lipoprotein profile as compared with carbohydrates. Dairy proteins are precursors of angiotensin-I-converting enzyme-inhibitory peptides, which may lower blood pressure. Such effects, however, have inconsistently been reported in human studies. Finally, conjugated linoleic acid, which effectively lowers body weight in animals, has no such effect in humans in the quantities provided by dairy products. To reduce the intake of SFA, the consumption of low-fat instead of high-fat dairy products is recommended. In conclusion, more research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the prevention and treatment of the metabolic syndrome.
    Original languageEnglish
    Pages (from-to)148-57
    JournalNutrition Research Reviews
    Volume21
    Issue number2
    DOIs
    Publication statusPublished - 1 Jan 2008

    Cite this