Dairy Consumption Lowers Systemic Inflammation and Liver Enzymes in Typically Low-Dairy Consumers with Clinical Characteristics of Metabolic Syndrome.

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.

A Larger Body Mass Index is Associated with Increased Atherogenic Dyslipidemia, Insulin Resistance, and Low-Grade Inflammation in Individuals with Metabolic Syndrome.

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.

Effects of dairy on metabolic syndrome parameters: a review.

Metabolic syndrome (MetS), characterized by central obesity, dyslipidemias, hypertension, and hyperglycemia, impacts 34 percent of the U.S. adult population. MetS has been demonstrated to be affected by dietary components. Data from epidemiological studies and clinical interventions suggest that one or more dairy components might directly affect MetS parameters. For example, calcium has been postulated to reduce body weight by modulating vitamin D concentrations in plasma and therefore attenuating intracellular calcium effects in activating genes involved in fatty acid synthesis and reducing those involved in lipolysis. Peptides present in milk have been associated with the inhibition of angiotensin converting enzyme and, therefore, with blood pressure reductions. Branched chain amino acids may increase post-prandial insulin secretion and regulate plasma glucose levels, and leucine, an abundant amino acid in milk, may be responsible for decreased plasma glucose through modulation of mTOR. Through different proposed mechanisms, dairy nutrients may target all components of MetS.

Increased dairy consumption differentially improves metabolic syndrome markers in male and female adults.

BACKGROUND: Effects of dairy consumption on metabolic health and adiposity are inconsistent. Most clinical trials have investigated dairy intake, frequently during caloric restriction, in overweight or obese populations but not in a metabolic syndrome population. We investigated the effect of increased dairy intake without caloric restriction on anthropometrics, plasma lipids, and glucose in typically low-dairy consumers who met the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) metabolic syndrome criteria. METHODS: Male (n=14) and female (n=23) adults (54.1 ± 9.7 years) with metabolic syndrome were randomized to consume low-fat dairy (LFD) (10 oz of 1% milk, 6 oz of nonfat yogurt, 4 oz of 2% cheese) or carbohydrate control (CNT) (1.5-oz granola bar and 12 oz of 100% juice) foods for 6 weeks in a crossover study design. Anthropometrics, metabolic syndrome parameters, insulin resistance, and parathyroid hormone were measured. Body composition was analyzed by a dual-energy X-ray absorptiometry scan for a subset of subjects (n=22). RESULTS: LFD modulated metabolic syndrome parameters differently according to gender. Following LFD, men had lower glucose (95.4 ± 9.1 vs. 98.9 ± 10.6 mg/dL, P=0.048), whereas women had lower body weight (BW), waist circumference, and body mass index (P<0.01) compared to CNT. Women also had lower energy intake following LFD compared to CNT. Increases in phosphorus (a dairy nutrient) were negatively correlated with decreases in BW (r=-0.537; P<0.01) and body fat in women (r=-0.593, P<0.025), whereas the decreases in energy intake had no correlation with anthropometrics. CONCLUSIONS: Three dairy servings/day promoted small but significant improvements differentially by gender in a metabolic syndrome population.

Green tea extract protects leptin-deficient, spontaneously obese mice from hepatic steatosis and injury.

The incidence of nonalcoholic fatty liver disease (NAFLD) has risen along with the ongoing obesity epidemic. Green tea extract (GTE) inhibits intestinal lipid absorption and may regulate hepatic lipid accumulation. The objective of this study was to determine whether GTE protects against hepatic lipid accumulation during the development of NAFLD in an obese mouse model. Five-wk-old ob/ob (obese) mice and their lean littermates (8 mice x genotype(-1) x dietary treatment(-1)) were fed GTE at 0, 1, or 2% (wt:wt) for 6 wk. The body weights of obese mice and lean littermates fed diets containing GTE were 23-25% and 11-20% lower (P < 0.05) than their respective controls fed no GTE. Histologic evaluation showed a significant reduction in hepatic steatosis in GTE-fed obese mice only and histologic scores were correlated with hepatic lipid concentration (r = 0.84; P < 0.05), which was reduced dose dependently by GTE. GTE protected against hepatic injury as suggested by 30-41% and 22-33% lower serum alanine aminotransferase and aspartate aminotransferase activities, respectively. Hepatic alpha-tocopherol was 36% higher in obese mice than lean mice. GTE tended (P = 0.06) to lower hepatic alpha-tocopherol, which was not fully explained by the GTE-mediated reduction in hepatic lipid. Hepatic ascorbic acid was lower in obese mice than in lean mice (P < 0.05) and was unaltered by GTE. Obese mice had lower serum adiponectin than lean mice and this was not affected by GTE. The results suggest that GTE protects against NAFLD by limiting hepatic lipid accumulation and injury without affecting hepatic antioxidant status and adiponectin-mediated lipid metabolism. Further study is underway to define the events by which GTE protects against obesity-triggered NAFLD.