Premeal Low-Fat Yogurt Consumption Reduces Postprandial Inflammation and Markers of Endotoxin Exposure in Healthy Premenopausal Women in a Randomized Controlled Trial

Abstract

Background: Metabolic endotoxemia is associated with obesity and contributes to postprandial inflammation.

Objective: We aimed to determine if low-fat yogurt consumption prevents postprandial inflammation and dysmetabolism in healthy women by inhibiting biomarkers of metabolic endotoxemia.

Methods: Premenopausal women defined as obese and nonobese [body mass index (BMI, in kg/m2) 30-40 and 18.5-27, respectively, n = 120] were randomly assigned to consume 339 g of low-fat yogurt (YN, yogurt nonobese; YO, yogurt obese) or 324 g of soy pudding (CN, control nonobese; CO, control obese) for 9 wk (n = 30/group). The intervention foods each supplied 330 kcal with 3 g fat, 66 g carbohydrate, and 4-6 g protein. At weeks 0 and 9, participants ingested 226 g of yogurt or 216 g of soy pudding before a meal providing 56-60 g fat, 82 g carbohydrate, and 28-30 g protein. Plasma soluble CD14 (sCD14), lipopolysaccharide-binding protein (LBP), LPS activity, interleukin-6 (IL-6), glucose, triglyceride, and insulin were measured hourly for 4 h to assess differences in postprandial responses between groups by 2-factor ANOVA.

Results: Premeal yogurt consumption prevented the postprandial decrease in sCD14 net incremental area under the curve (net iAUC) by 72% in obese individuals at week 0 (P = 0.0323). YN and YO had ≥40% lower net iAUC of LBP-to-sCD14 ratio and plasma IL-6 concentration than CN and CO, respectively (P < 0.05). CO had postprandial hyperglycemia which was not evident in YO; in contrast YN had 57% less postprandial hypoglycemia than did CN (P-interaction = 0.0013). After 9 wk of yogurt consumption, ΔAUC of LBP-to-sCD14 ratios of YO and YN were less than half of those of the control groups (P = 0.0093).

Conclusion: Yogurt consumption improved postprandial metabolism and biomarkers of metabolic endotoxemia in healthy premenopausal women. Premeal yogurt consumption is a feasible strategy to inhibit postprandial dysmetabolism and thus may reduce cardiometabolic risk. This trial was registered at clinicaltrials.gov as NCT01686204.

Figures

FIGURE 1

Incremental postprandial changes in plasma sCD14 (A), LBP:sCD14 ratio (B), IL-6 (C), and glucose (D) at week 0 of the intervention and in plasma sCD14 (E), LBP:sCD14 ratio (F), IL-6 (G), and glucose (H) at week 9 of the intervention in healthy obese and nonobese premenopausal women who consumed low-fat yogurt or the control food followed by the challenge meal. Data are means ± SEMs, n = 30. The effects of obesity status (obese compared with nonobese), dietary treatment (low-fat yogurt compared with control food), and the obesity × treatment interaction on net iAUC were determined by 2-factor ANOVA (PROC GLM). A post hoc F test (sliceby) was applied when P-interaction was <0.05. *YO different from CO, P < 0.05. #YN different from CN, P < 0.05. CN, control nonobese; CO, control obese; iAUC, incremental AUC; LBP, LPS-binding protein; sCD14, soluble CD14; YN, yogurt nonobese; YO, yogurt obese; Δ, difference.

FIGURE 2

Incremental changes in postprandial plasma insulin in healthy obese and nonobese premenopausal women after consuming either low-fat yogurt or control food followed by a challenge meal at week 9 of the intervention. Data are means ± SEMs, n = 30. The effects of obesity status (obese compared with nonobese), dietary treatment (low-fat yogurt compared with control food), and the obesity × treatment interaction on net iAUC were determined by 2-factor ANOVA (PROC GLM). CN, control nonobese; CO, control obese; iAUC, incremental AUC; YN, yogurt nonobese; YO, yogurt obese; Δ, difference.