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Objectives: A 6-week cross-over study design was used to determine the effect of increased dairy consumption in typically low-dairy consumers (n = 37) with metabolic syndrome (MetS) on systemic inflammation and hepatic enzymes., Methods: This was a randomized study in which participants consumed low-fat dairy (LFD) (10 oz 1% milk, 6 oz nonfat yogurt, 4 oz 2% cheese) or a carbohydrate-based control (CNT) (1.5 oz granola bar and 12 oz 100% juice) for 6 weeks. After a 4-week washout, they were allocated to the alternate dietary treatment. Inflammatory status was assessed by fasting plasma concentrations of C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant -1 (MCP-1). In addition, gene expression of interleukin (IL)-1, IL-6, and TNF-α was evaluated in peripheral blood mononuclear cells isolated from a subset of 17 subjects (13 women, 3 men) at the end of each dietary period. Liver enzymes were also assessed to evaluate whether dairy components would affect hepatic function., Results: Participants had lower concentrations of both hepatic alanine aminotransferase (p < 0.05) and aspartate aminotransferase (p < 0.005) after the LFD period. No significant changes in any of the plasma inflammatory compounds were found when all data were analyzed together. In contrast, expression of IL-1b and IL-6 were reduced by 46% and 63%, respectively, compared to the control period. When stratified by gender, women had lower TNF-α, (p = 0.028) and MCP-1 (p = 0.001) following LFD consumption compared to CNT. In addition, hepatic steatosis index scores were significantly lower (p < 0.001) during the LFD period., Conclusions: We conclude that three dairy servings per day improved both liver function and systemic inflammation in subjects with MetS.

Background: The consequences of increased body mass index (BMI) on the metabolic disorders associated with metabolic syndrome (MetS) have not been thoroughly examined., Methods: We analyzed data from 262 individuals, 97 men and 165 women (aged 18-70 years), classified with MetS to investigate whether variations in BMI could be associated with parameters of dyslipidemia, insulin resistance, or low-grade inflammation. We hypothesized that increases in BMI would positively correlate with the major dysregulations in metabolism that define MetS. For this purpose, individuals were separated into four subgroups based on their BMI: normal weight (<25 kg/m(2)), overweight (≥25 to <30 kg/m(2)), obese (≥30 to <40 kg/m(2)), and morbidly obese (≥40 kg/m(2))., Results: As expected, body weight and waist circumference increased significantly as BMI increased (P < 0.0001). Both systolic and diastolic blood pressure were lower in the normal BMI group compared with the other three BMI groups (P = 0.001). Markers of HDL metabolism were adversely impacted in elevated BMI groups, as both high-density lipoprotein cholesterol (HDL-C) and large HDL decreased as BMI increased (P = 0.01). BMI was negatively correlated with HDL-C (r = -0.193, P = 0.002), HDL size (r = (-)0.227, P = 0.002), and large HDL (r = -0.147, P = 0.037). In addition, plasma insulin was highest in subjects classified as morbidly obese (P < 0.0001). There was also a strong positive correlation between BMI and plasma insulin (r = 0.413, P < 0.0001), whereas adiponectin, a marker of insulin sensitivity, was negatively correlated with BMI (r = -0.288, P = 0.001). Finally, BMI was positively correlated with proinflammatory C-reactive protein (r = 0.312, P = 0.0001) and interleukin-6 (r = 0.238, P = 0.001)., Conclusions: The data from this study suggest that the physiological factors associated with increased BMI exacerbate the metabolic abnormalities characteristic of MetS.