Effects of glycemic load on metabolic risk markers in subjects at increased risk of developing metabolic syndrome.

BACKGROUND: Epidemiologic studies suggest that diets with a low glycemic index (GI) or glycemic load (GL) are associated with a decreased risk of developing metabolic syndrome. Intervention studies are inconsistent, however, possibly due to differences in macronutrient and fiber compositions of the experimental diets. OBJECTIVE: We tested side-by-side test foods with similar macronutrient and fiber compositions but with different sucrose-flour ratios or carbohydrate source to determine the effects of different GIs and GLs on metabolic risk markers in overweight subjects. DESIGN: Overweight men (n = 9) and women (n = 6) received in random order for 11 wk 4 test foods with an increased GI or a decreased GI (69 compared with 40, 86 compared with 48, 63 compared with 37, and 51 compared with 20, respectively). There was a GL difference of 32 units between the 2 interventions. RESULTS: At the end of the 11-wk intervention periods, the decreased GL test foods did not change fasting plasma glucose (mean +/- SD: 5.83 +/- 0.6 compared with 5.94 +/- 0.6 mmol/L) or insulin (8.3 +/- 2.8 compared with 9.8 +/- 5.1 mU/L) concentrations compared with increased GL test foods. Serum total cholesterol (5.56 +/- 0.90 compared with 5.76 +/- 1.04 mmol/L), LDL-cholesterol (3.57 +/- 0.72 compared with 3.68 +/- 0.80 mmol/L), HDL-cholesterol (1.21 +/- 0.38 compared with 1.24 +/- 0.37 mmol/L), and triacylglycerol (1.61 +/- 0.77 compared with 1.78 +/- 1.04 mmol/L) concentrations were also not significantly different for decreased and increased GL test foods, respectively. Finally, proinflammatory (high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-alpha, monocyte chemoattractant protein 1) and prothrombotic (plasminogen activator inhibitor 1) markers were not affected. Glucose and lipids were also analyzed after 1 and 5 wk of intervention and were not affected by the intervention. CONCLUSION: When incorporated into a habitual diet, consumption of test foods with a decreased GL does not ameliorate metabolic risk markers in overweight subjects.

Variability of the glycemic response to single food products in healthy subjects.

BACKGROUND: Many studies on the health effects of the glycemic index (GI) are confounded by differences in the intakes of other macronutrients and fibre. Little data exist about the within- and between-subject variability of the GI. OBJECTIVE: Our objectives were therefore (i) to calculate the GI of eight commonly used food products with similar macronutrient and fibre composition, but with different sources of carbohydrates, (ii) to examine the inter- and intra-individual variability of the incremental area under the curve (iAUC) after consuming the reference solution, and (iii) to compare the effect of three different methods on 2-h postprandial blood glucose responses. DESIGN: Four groups of 10 healthy subjects consumed in random order the increased (iGI) and decreased GI (dGI) variants and twice a glucose solution. All products consisted of 25g available carbohydrates (CHO). For the fruit drink, glucose values were simultaneously analyzed using venous and capillary blood samples, and by using a continuous glucose monitoring system (CGMS). RESULTS: The GIs for increased and decreased variants were (mean+/-standard error of the mean (SEM)) 69+/-15 and 40+/-4 for bread, 86+/-14 and 48+/-8 for a fruit drink, 51+/-12 and 20+/-4 for cake, and 63+/-17 and 37+/-10 for a cookie. The inter- and intra-individual coefficient of variation (CV) of the iAUCs of the reference solution was large and varied respectively between 13 and 38%, and between 33 and 80%. CONCLUSIONS: These data suggest that the GI is difficult to use at the individual level.

Dairy product consumption and the metabolic syndrome.

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.

Induction of cancer cell apoptosis by flavonoids is associated with their ability to inhibit fatty acid synthase activity.

The consumption of food products containing high amounts of flavonoids has been reported to lower the risk of various cancers. The mechanisms underlying the cancer-protective effects of these naturally occurring polyphenolic compounds, however, remain elusive. Based on our previous finding that the cytotoxic effect of the flavanol epigallocatechin-3-gallate on prostate cancer cells correlates with its ability to inhibit fatty acid synthase (FAS, a key lipogenic enzyme overexpressed in many human cancers), we examined the anti-lipogenic effects of a panel of 18 naturally occurring polyphenolic compounds. In addition to epigallocatechin-3-gallate, five other flavonoids, more particularly luteolin, quercetin, kaempferol, apigenin, and taxifolin, also markedly inhibited cancer cell lipogenesis. Interestingly, in both prostate and breast cancer cells, a remarkable dose-response parallelism was observed between flavonoid-induced inhibition of fatty acid synthesis, inhibition of cell growth, and induction of apoptosis. In support for a role of fatty acid synthesis in these effects, the addition of exogenous palmitate, the end product of FAS, markedly suppressed the cytotoxic effects of flavonoids. Taken together, these findings indicate that the potential of flavonoids to induce apoptosis in cancer cells is strongly associated with their FAS inhibitory properties, thereby providing a new mechanism by which polyphenolic compounds may exert their cancer-preventive and antineoplastic effects.