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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.

Although increased concentrations of plasma inflammatory markers are not one of the criteria to diagnose the metabolic syndrome, low-grade systemic inflammation is receiving large attention as a metabolic syndrome component and cardiovascular risk factor. As several epidemiological studies have suggested a negative relationship between low-fat dairy consumption and the metabolic syndrome, we decided to investigate the effects of low-fat dairy consumption on inflammatory markers and adhesion molecules in overweight and obese subjects in an intervention study. Thirty-five healthy subjects (BMI . 27 kg/m 2 ) consumed, in a random order, low-fat dairy products (500 ml low-fat milk and 150 g low-fat yogurt) or carbohydrate-rich control products (600 ml fruit juice and three fruit biscuits) daily for 8 weeks. Plasma concentrations of TNF-a were decreased by 0·16 (SD 0·50) pg/ml (P¼0·070), and soluble TNF-a receptor-1 (s-TNFR-1) was increased by 110·0 (SD 338·4) pg/ml (P¼ 0·062) after the low-fat dairy period than after the control period. s-TNFR-2 was increased by 227·0 (SD 449·0) pg/ml (P¼ 0·020) by the dairy intervention. As a result, the TNF-a index, defined as the TNF-a:s-TNFR-2 ratio, was decreased by 0·000053 (SD 0·00 012) (P¼0·015) after the dairy diet consumption. Low-fat dairy consumption had no effect on IL-6, monocyte chemoattractant protein-1, intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 concentrations. The present results indicate that in overweight and obese subjects, low-fat dairy consumption for 8 weeks may increase concentrations of s-TNFR compared with carbohydrate-rich product consumption, but that it has no effects on other markers of chronic inflammation and endothelial function. Low-fat dairy consumption: Inflammatory markers: Adhesion moleculesThe metabolic syndrome is a metabolic disorder that strongly enhances the risk of developing CVD and type 2 diabetes mellitus. Abdominal obesity, atherogenic dyslipidaemia, hypertension, insulin resistance, a pro-thrombotic state and a low-grade pro-inflammatory state have now been identified as components of the metabolic syndrome that are related to CVD risk. Although inflammatory markers are currently not included in the ATP III or WHO diagnostic criteria for the metabolic syndrome (1) , low-grade systemic inflammation is receiving large attention as a metabolic syndrome component and cardiovascular risk factor. Inflammatory markers such as C-reactive protein (2) , IL-6 (3) , TNF-a (4) and fibrinogen (5) , among others, have been linked to the metabolic syndrome.The consumption of dairy products has been inversely associated with the prevalence or incidence of the metabolic syndrome in a number of epidemiological studies (6 -12) . In the Coronary Artery Risk Development in Young Adults Study (11) , for example, the intake of dairy products was negatively correlated with the development of obesity, dyslipidaemia, glucose intolerance and hypertension over the next 10 years in overweight subjects. However, the relationship betwe...

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Hepatic insulin resistance and inflammatory cytokine production contribute to the manifestation of the metabolic syndrome. As amino acids have been implicated in modulating insulin signaling and inflammation, we have investigated the effects of glutamine, leucine and proline on markers of inflammation and insulin sensitivity in HepG2 liver cells. Cells were incubated with IL-1β (5 ng/mL) to stimulate IL-8 production. After 24 h, glutamine inhibited IL-8 production significantly (p<0.05) at 2, 5 and 10 mM (to 82, 73 and 72% of control), whereas leucine reduced IL-8 production significantly only at 10 mM (66%) and proline at 5 and 10 mM (71 and 52%). Glutamine, leucine and proline all reduced NF-κB activity after 3 h of IL-1β stimulation at 2, 5 and 10 mM (p<0.001). Insulin-induced (1 nM) Akt phosphorylation was reduced in cells treated with tumour necrosis factor-α (10 ng/mL) for 24 h, but was partly restored by simultaneous incubation with glutamine, leucine and proline (25 mM). Phosphorylation of glycogen synthase kinase-3β was unaffected by insulin stimulation and amino acid treatment. Our results indicate that glutamine, leucine and proline attenuate IL-8 production, probably through inhibition of NF-κB, and that they increase Akt phosphorylation in HepG2 cells.