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. 2013 Dec;21(12):2471-80.
doi: 10.1002/oby.20437. Epub 2013 Jun 13.

Effects of sugar-sweetened beverages on plasma acylation stimulating protein, leptin and adiponectin: relationships with metabolic outcomes

Reza Rezvani  1 , Katherine Cianflone, John P McGahan, Lars Berglund, Andrew A Bremer, Nancy L Keim, Steven C Griffen, Peter J Havel, Kimber L Stanhope
Affiliations

Effects of sugar-sweetened beverages on plasma acylation stimulating protein, leptin and adiponectin: relationships with metabolic outcomes

Reza Rezvani et al. Obesity (Silver Spring). 2013 Dec.

Abstract

Objective: The effects of fructose and glucose consumption on plasma acylation stimulating protein (ASP), adiponectin, and leptin concentrations relative to energy intake, body weight, adiposity, circulating triglycerides, and insulin sensitivity were determined.

Design and methods: Thirty two overweight/obese adults consumed glucose- or fructose-sweetened beverages (25% energy requirement) with their ad libitum diets for 8 weeks, followed by sweetened beverage consumption for 2 weeks with a standardized, energy-balanced diet. Plasma variables were measured at baseline, 2, 8, and 10 weeks, and body adiposity and insulin sensitivity at baseline and 10 weeks.

Results: Fasting and postprandial ASP concentrations increased at 2 and/or 8 weeks. ASP increases correlated with changes in late-evening triglyceride concentrations. At 10 weeks, fasting adiponectin levels decreased in both groups, and decreases were inversely associated with baseline intra-abdominal fat volume. Sugar consumption increased fasting leptin concentrations; increases were associated with body weight changes. The 24-h leptin profiles increased during glucose consumption and decreased during fructose consumption. These changes correlated with changes of 24-h insulin levels.

Conclusions: The consumption of fructose and glucose beverages induced changes in plasma concentrations of ASP, adiponectin, and leptin. Further study is required to determine if these changes contribute to the metabolic dysfunction observed during fructose consumption.

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Figures

Figure 1
Figure 1. Effects of glucose or fructose consumption on fasting and postprandial plasma ASP concentrations
Changes (Δ) at 2wk, 8wk and 10wk compared to baseline (0wk) in the fasting (A) and postprandial (B) ASP levels of subjects who consumed 25% of energy requirement as either glucose (n=15) or fructose-sweetened beverages (n=17). Effect of: Time** p<0.01 in PROC MIXED 4-factor (sugar, time, gender, MSRF) repeated measures (RM) model with outcome at 0wk (OutcomeB) as continuous covariable. *P<0.05, **P<0.01, ***P<0.001, Least squares mean of the change different from zero. Results are presented as mean ± SEM. (C) Correlation between change (Δ) in fasting ASP and change (Δ) in late-evening (postprandial) triglyceride (TG) at 2wk, 8wk and 10wk .
Figure 2
Figure 2. Effects of metabolic syndrome risk factors (MSRF) and gender on the changes in postprandial plasma ASP concentrations in subjects consuming glucose or fructose
Changes at 2wk, 8wk and 10wk compared to baseline (0wk) in postprandial ASP levels of subjects grouped by number of MSRF during consumption of glucose (A) (n=15) or fructose-sweetened beverages (B) (n=17). Changes at 2wk, 8wk and 10wk compared to baseline (0wk) in postprandial ASP levels of subjects grouped by gender during consumption of glucose (C) (n=15) or fructose-sweetened beverages (D) (n=17). Effect of: Time*** p<0.001, MSRF* p<0.05, MSRF × time*** p<0.001, gender* p<0.05, gender × time*** p<0.001 in sugar-specific PROC MIXED 3-factor (time, gender, MSRF) RM model with outcome at 0wk as continuous covariable. **P<0.01, ***P<0.001, ****P<0.0001, Least squares mean of the change different from zero.
Figure 3
Figure 3. Effects of glucose or fructose consumption on fasting plasma adiponectin concentrations in overweight and obese subjects
Changes (Δ) at 2wk, 8wk and 10wk compared to baseline (0wk) in the fasting (A) adiponectin levels of subjects who consumed 25% of energy requirement as either glucose (n=15) or fructose-sweetened beverages (n=17). Effect of: Time**** P<0.0001 in PROC MIXED 4-factor (sugar, time, gender, MSRF) RM model with outcome at 0wk as continuous covariable. *P<0.05, **P<0.01, Least squares mean of the change different from zero. Changes at 2wk, 8wk and 10wk compared to baseline (0wk) in fasting adiponectin levels of women (B) and men (C) during consumption of glucose (n=15) or fructose-sweetened beverages (B). Effect of: Time** P<0.05, Time**** P<0.0001, Sugar × time*** P<0.001 in gender-specific PROC MIXED 3-factor (time, sugar, MSRF) RM model with outcome at 0wk as continuous covariable. *P<0.05, Least squares mean of the change different from zero. Results are presented as mean ± SEM. (D) Correlation between the 10wk changes (Δ) in fasting adiponectin and baseline intra-abdominal fat volume.
Figure 4
Figure 4. Effects of glucose or fructose consumption on fasting leptin concentrations
Changes (Δ) at 2wk, 8wk and 10wk compared to baseline (0wk) in the fasting leptin levels of subjects who consumed 25% of energy requirement as either glucose (n=15) or fructose-sweetened beverages (n=17). PROC MIXED 4-factor (sugar, time, gender, MSRF) RM model with outcome at 0wk as continuous covariable. *P<0.05, Least squares mean of the change different from zero.
Figure 5
Figure 5. Effects of glucose or fructose consumption on 24-h leptin profiles
24-h circulating TG concentrations in subjects before and after 2, 8, and 10 weeks of consuming glucose-sweetened beverages (A) (n=14) or fructose-sweetened beverages (B) (n=17). (C) Changes (Δ) at 2wk, 8wk and 10wk compared to baseline (0wk) in the 24-h leptin AUCs of the subjects who consumed glucose or fructose-sweetened beverages. Effect of: Sugar* P < 0.05 in PROC MIXED 4-factor (sugar, time, gender, MSRF) RM model. Mean ± SEM. (D) Correlation between changes (Δ) in 24-h leptin AUC and 24-h insulin AUC at 2wk, 8wk and 10wk.
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