Date of Completion

9-10-2015

Embargo Period

9-9-2017

Keywords

Obesity; Low-fat yogurt; Inflammation; Intestinal Barrier Function

Major Advisor

Bradley Bolling, Ph.D.

Associate Advisor

Maria Luz Fernandez, Ph.D.

Associate Advisor

Hedley Freake, Ph.D.

Associate Advisor

Richard Bruno, Ph.D., R.D.

Associate Advisor

Jeff Volek, Ph.D., R.D.

Field of Study

Nutritional Science

Degree

Doctor of Philosophy

Open Access

Open Access

Abstract

The objective of this study was to conduct an intervention study to test how low-fat yogurt consumption affects postprandial metabolism, chronic inflammation, and intestinal barrier function. Apparently healthy premenopausal women with body mass index (BMI) of 18.5 to 27 (lean) or 30 to 40 kg/m2 (obese) participated in a 9-week controlled intervention study. Participants in each BMI range were randomly assigned to either a low-fat yogurt-supplemented group (Y, yogurt lean; YO, yogurt obese) or a soy pudding-supplemented control group (C, control lean; CO, control obese), with n = 30/group. Participants consumed 12 oz. of yogurt or the control food daily for 9 weeks while maintaining usual caloric intake. At wk 0, 3, 6 and 9, participants provided fasting blood samples for determination of inflammation and endotoxemia, and for weight and blood pressure measurement. At wk 0 and 9, participants consumed 8 oz. of yogurt or the control food, followed by a high-fat, high-carbohydrate challenge meal. Blood samples were taken at baseline, 1, 2, 3, and 4 h after the meal to assess postprandial metabolism. At baseline, obese participants had increased plasma glucose, triglyceride, insulin, interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP), tumor necrosis factor alpha (TNF-α), lipopolysaccharide-binding protein (LBP), LBP/soluble CD14 (sCD14) ratio, but less immunoglobulin M endotoxin-core antibody (IgM EndoCAb) than lean participants. The challenge meal induced postprandial increases in IL-6, glucose, and LBP/sCD14 ratio in CO. However these postprandial responses were suppressed in YO. Yogurt consumption also reduced postprandial hypoglycemia in Y, possibly by preventing insulin over-secretion. Both challenge meals had similar responses, except 15% decreased IL-6 area under the curve in the second test. After 9 weeks, YO had decreased fasting plasma IL-6, hsCRP, TNF-α, TNF-α/soluble tumor necrosis factor receptor II (sTNF-RII) ratio, but increased IgM EndoCAb. These improvements occurred despite ~ 0.9 kg weight gain in YO and CO. YO diastolic blood pressure decreased at wk 3, but was not maintained at wk 6 and 9. In conclusion, consuming low-fat yogurt improved postprandial metabolism and reduced biomarkers of chronic inflammation in healthy obese premenopausal women, in part because of improved intestinal barrier function.

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