Effect of olive oil consumption on serum resistin concentrations in healthy men.

Resistin has been linked to atherosclerosis and inflammatory processes in humans. Some polyphenols have been shown to downregulate resistin expression in adipocytes. The effects of olive oil phenolics on resistin are not known; therefore, we investigated the impact of olive oil consumption on serum resistin as a function of the olive oils' phenolic content. In a randomized, controlled, cross-over study 38 healthy German men aged 38+/-2 years replaced their usual consumption of raw fat during 3 periods of 3 weeks each by 25 ml of virgin, common and refined olive oil varying in phenolic content. Serum resistin, blood lipids and urine biomarkers of subjects' compliance were analysed at baseline and at the end of each intervention period. The integration of olive oil in the subjects' habitual diet led to a decrease in total cholesterol (p=0.025) and triglycerides (p=0.013) independent of the content of phenolic compounds in the oil. Serum resistin concentrations were not affected by the olive oils' phenolic content. After low phenolic olive oil consumption, a decrease in serum resistin level was observed compared to medium and high phenolic olive oil (-0.4+/-0.1 ng/ml; p=0.040). Our results suggest that olive oil consumption has only marginal beneficial effects on serum resistin levels.

Serum resistin increases in a postprandial state during liquid meal challenge test in healthy human subjects.

The role of resistin in humans is controversial although resistin has been linked to atherosclerotic and inflammatory processes. In rodents, resistin expression is suppressed after food restriction while central administration of resistin promotes short-term satiety. However, the nature of postprandial responses in circulating resistin in humans is unknown. Therefore, we investigated postprandial resistin concentrations in a pilot study in 19 healthy subjects and 19 controls matched for age and body mass index (BMI). Serum resistin, insulin and non-esterified fatty acids (NEFA) concentrations as well as plasma glucose and triglycerides were repeatedly assessed before and after ingestion of an isocaloric standardized liquid meal during a 300 min period.After consumption of liquid meal, serum resistin levels increased compared to fasting control (p=0.037). Postprandial plasma glucose and serum insulin increased (p<0.001) with lower glucose responses in females (p=0.001) and lower insulin responses in males (p=0.012). Plasma triglycerides increased and serum NEFA decreased with similar gender responses (p=0.025 and p<0.001, respectively). Serum resistin was not correlated to glucose, insulin, triglyceride, and NEFA responses to liquid meal challenge tests. The present data suggest that serum resistin increases postprandially in healthy humans. Additional studies are needed to elucidate normal 24-h daytime profiles in humans and differential response of serum resistin to macronutrient composition of meals.

Increase in serum resistin during weight loss in overweight subjects is related to lipid metabolism.

OBJECTIVE: Human resistin has been stated to influence preadipocyte cell numbers and to stimulate adipocyte triglyceride lipolysis in vivo and in vitro. However, its role in human obesity remains unclear. DESIGN: Cross-sectional study for comparisons of lean and obese subjects, and subsequent longitudinal 4-month weight loss intervention study in obese subjects. SUBJECTS: Healthy subjects, lean (n=20, BMI<25) and overweight (n=43, BMI>or=25). MEASUREMENTS: Serum resistin, body weight, body fat, waist-to-hip ratio, as well as markers of insulin resistance and lipid metabolism at baseline and after 4 months of intervention. RESULTS: Serum resistin was positively correlated to HOMA-IR (partial r=0.288; P=0.055), serum fructosamines (partial r=0.280; P=0.062), serum NEFA (partial r=0.276; P=0.066) and negatively to age (partial r=-0.349; P=0.019) and serum apolipoprotein A-1 (partial r=-0.363; P=0.014). During the intervention, serum resistin increased significantly (P<0.001). The increase was inversely related to changes in waist-to-hip ratio (P=0.025) and positively to serum apolipoprotein B (P=0.011). In males only, the increase in resistin during weight loss was predicted by total serum cholesterol at baseline (r=0.703, P=0.007). No relation was observed between changes in resistin and changes in HOMA-IR. CONCLUSION: The present study indicates an association between serum resistin and markers of abdominal fat distribution as well as the regulation of lipid metabolism. However, human resistin is unlikely to play an independent role in the regulation of glucose metabolism.

Double-blind, randomized feedback control fails to improve the hypocholesterolemic effect of a plant-based low-fat diet in patients with moderately elevated total cholesterol levels.

OBJECTIVE: To determine whether the cholesterol-lowering effect of a plant-based low-fat diet can be improved by a flexible control design that controls the extent of fat reduction based on the individual response of blood cholesterol. DESIGN: Randomized, double-blind intervention study. SETTING: A hotel in Prerow, Germany. SUBJECTS: A total of 32 participants (21 female and 11 male participants) with total cholesterol level > 5.7 mmol/l. INTERVENTION: The control group consumed a plant-based low-fat diet with constantly 20% of energy as fat; the intervention group received a diet with either 20 or 15% of energy as fat, depending on the serum cholesterol response of the preceding week. A flexible control design based on the individual cholesterol response during a run-in period of 1 week was used within a low-fat intervention. RESULTS: During the run-in period, the consumption of a plant-based low-fat diet led to a reduction in total cholesterol by 18+/-6 mmol/l (P < 0.001), in LDL cholesterol by 19+/-9 mmol/l (P < 0.001) and triglycerides by 13+/-3 mmol/l (P < 0.001). During the feedback control period, an additional reduction in total cholesterol by 13+/-8 (P < 0.001) and in LDL cholesterol by 17+/-11 (P < 0.001) was observed compared to 15+/-15 and 7+/-18 in the control group. The effect of an additional feedback control was only marginal and not statistically significant compared to the effect of the low-fat diet alone. CONCLUSIONS: On a level of fat intake already reduced to 20% of energy, the use of a feedback control to adapt the fat content of the diet depending on the individual serum cholesterol response was not more effective in reducing blood cholesterol levels than a plant-based low-fat diet alone.