Effects of sugar-sweetened soda on plasma saturated and monounsaturated fatty acids in individuals with obesity: A randomized study.

BACKGROUND

High carbohydrate, i.e., sugars, intake potentially drives the liver into a lipogenic state leading to elevated plasma fatty acids. Excessive intake of saturated fat and sugar-sweetened soda induces liver fat accumulation, but studying the effect of high intake from sugar-sweetened soda on the lipogenesis (DNL) fatty acids in long-term randomized trials is lacking.

OBJECTIVE

To study the effect of consuming 1 L/day of sugar-sweetened soda, semi-skimmed milk (milk), aspartame-sweetened soda or water over 24 weeks on DNL-derived fatty acids (i.e., palmitate (primary outcome) and other saturated and monounsaturated fatty acids), and markers of stearoyl-CoA desaturase activity (SCD1) in plasma phospholipids (PL), cholesteryl esters (CE), and triglycerides (TG).

DESIGN AND METHODS

A randomized parallel study was conducted simultaneously at Aarhus University Hospital and Copenhagen University, Denmark, including ( = 41) individuals aged 20-50 years, with BMI of 26-40 kg/m, and without diabetes. The groups consisted of 9 individuals in the sugar-sweetened soda, 10 in the milk, 11 in the aspartame-sweetened soda, and 11 in the water. The change at 24 weeks was assessed and compared across the groups using ANCOVA and mixed-effects models. Correlations of fatty acid changes with liver fat accumulation (magnetic resonance imaging) were explored.

RESULTS

After 24 weeks, the groups differed in palmitate proportions in PL, oleate in CE and PL, and palmitoleate and SCD1 in all fractions ( < 0.05). Compared with water, the relative proportion of palmitate in PL increased by approximately 1% during both sugar-sweetened soda ( = 0.011) and milk ( = 0.006), whereas oleate and palmitoleate increased only during sugar-sweetened soda (CE 2.77%, < 0.001; PL 1.51%, = 0.002 and CE 1.46%, PL 0.24%, TG 1.31%, all < 0.001, respectively). Liver fat accumulation correlated consistently with changes in palmitoleate, whereas correlations with palmitate and oleate were inconsistent across lipid fractions.

CONCLUSIONS

Although both sugar-sweetened soda and milk increased palmitate in PL, only excess intake of sugar-sweetened soda increased palmitoleate in all lipid fractions and correlated with liver fat. In contrast, isocaloric milk intake did not increase plasma monounsaturated fatty acids.

CLINICAL TRIAL REGISTRATION

[https://clinicaltrials.gov/ct2/show/NCT00777647], identifier [NCT00777647].