A Pilot Study Comparing the Effects of Consuming 100% Orange Juice or Sucrose-Sweetened Beverage on Risk Factors for Cardiometabolic Disease in Women

Abstract

Overconsumption of sugar-sweetened beverages increases risk factors associated with cardiometabolic disease, in part due to hepatic fructose overload. However, it is not clear whether consumption of beverages containing fructose as naturally occurring sugar produces equivalent metabolic dysregulation as beverages containing added sugars. We compared the effects of consuming naturally-sweetened orange juice (OJ) or sucrose-sweetened beverages (sucrose-SB) for two weeks on risk factors for cardiometabolic disease. Healthy, overweight women (n = 20) were assigned to consume either 3 servings of 100% orange juice or sucrose-SB/day. We conducted 16-hour serial blood collections and 3-h oral glucose tolerance tests during a 30-h inpatient visit at baseline and after the 2-week diet intervention. The 16-h area under the curve (AUC) for uric acid increased in subjects consuming sucrose-SB compared with subjects consuming OJ. Unlike sucrose-SB, OJ did not significantly increase fasting or postprandial lipoproteins. Consumption of both beverages resulted in reductions in the Matsuda insulin sensitivity index (OJ: -0.40 ± 0.18, p = 0.04 within group; sucrose-SB: -1.0 ± 0.38, p = 0.006 within group; p = 0.53 between groups). Findings from this pilot study suggest that consumption of OJ at levels above the current dietary guidelines for sugar intake does not increase plasma uric acid concentrations compared with sucrose-SB, but appears to lead to comparable decreases of insulin sensitivity.

Keywords: fruit juice; insulin sensitivity; lipids; sugar-sweetened beverage; uric acid.

Figure 1

Schematic of 2-day inpatient visits. Oral glucose tolerance test (OGTT).

Figure 2

Uric acid concentrations: Sixteen-hour circulating uric acid concentrations before (black line) and after (orange line, orange juice (OJ); blue line, sucrose-sweetened beverage (sucrose-SB) consumption of either (A) OJ or (B) sucrose-SB for two weeks. Change of 16-h area under the curve (AUC) for (C) uric acid and (D) fasting uric acid in women consuming either naturally-sweetened OJ (orange bars) or sucrose-SB (blue bars) for two weeks. ++ p < 0.01, effect of group. * p < 0.05, LS mean of change different from zero.

Figure 3

Changes of fasting and late-night postprandial low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C) and apolipoprotein B (ApoB) in women consuming either naturally-sweetened OJ (orange bars) or sucrose-SB (blue bars) for two weeks. * p < 0.05, ** p < 0.01, LS mean of change different from zero, primary ANCOVA.

Figure 4

Sixteen-hour circulating triglyceride (TG) concentrations before (black line) and after (blue line) consumption of either (A) OJ or (B) sucrose-SB for two weeks. Changes in fasting and postprandial (C) triglyceride and (D) ApoCIII after two weeks of OJ or sucrose-SB consumption. * p < 0.05, LS mean of change different from zero. Apolipoprotein CIII (ApoCIII).

Figure 5

Metrics of insulin sensitivity measured by oral glucose tolerance test (OGTT) and the metabolite, 2-hydroxybutyrate. Glucose curves during the OGTT before (black line) and after (blue line) consumption of either (A) OJ or (B) sucrose-SB for two weeks; Insulin curves during the OGTT before (black line) and after (blue line) consumption of either (C) OJ or (D) sucrose-SB for two weeks; (E) Changes in Matsuda Index; (F) 2-hydroxybutyrate concentrations measured after a 4-h fast. * p < 0.05, ** p < 0.01, *** p < 0.001 LS mean of change different from zero.

Figure 5

Metrics of insulin sensitivity measured by oral glucose tolerance test (OGTT) and the metabolite, 2-hydroxybutyrate. Glucose curves during the OGTT before (black line) and after (blue line) consumption of either (A) OJ or (B) sucrose-SB for two weeks; Insulin curves during the OGTT before (black line) and after (blue line) consumption of either (C) OJ or (D) sucrose-SB for two weeks; (E) Changes in Matsuda Index; (F) 2-hydroxybutyrate concentrations measured after a 4-h fast. * p < 0.05, ** p < 0.01, *** p < 0.001 LS mean of change different from zero.

Figure 6

The 16-hour circulating glucose and insulin concentrations before (black line) and after (blue line) consumption of either (A,C) OJ or (B,D) sucrose-SB beverage for two weeks. Plasma was collected during consumption of energy-balanced meals at breakfast, lunch and dinner containing 55% Ereq as complex carbohydrate at baseline and during consumption of energy-balanced baseline diets containing 30% Ereq as complex carbohydrate and 25% as OJ or sucrose-SB at 2 weeks.

Figure 7

Baseline (week 0) and intervention (week 2) plasma ethyl-β-D-glucuronide before (18:00-h) and after (19:00-h and 20:00-h) consumption of an energy-balanced dinner. At baseline, dinner contained 55% Ereq as complex carbohydrate; at intervention, dinner contained 30% Ereq as complex carbohydrate and 25% as OJ or sucrose-SB.