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

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DOI

  • Mohammed Fahad Bajahzer, Uppsala Univ Hosp, Uppsala University, Uppsala University Hospital, Dept Oncol
  • ,
  • Jens Meldgaard Bruun
  • Fredrik Rosqvist, Uppsala Univ Hosp, Uppsala University, Uppsala University Hospital, Dept Oncol
  • ,
  • Matti Marklund, Uppsala Univ Hosp, Uppsala University, Uppsala University Hospital, Dept Oncol
  • ,
  • Bjørn Richelsen
  • Ulf Risérus, Uppsala Univ Hosp, Uppsala University, Uppsala University Hospital, Dept Oncol

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 de novo 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 (n = 41) individuals aged 20-50 years, with BMI of 26-40 kg/m2, 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 (p < 0.05). Compared with water, the relative proportion of palmitate in PL increased by approximately 1% during both sugar-sweetened soda (p = 0.011) and milk (p = 0.006), whereas oleate and palmitoleate increased only during sugar-sweetened soda (CE 2.77%, p < 0.001; PL 1.51%, p = 0.002 and CE 1.46%, PL 0.24%, TG 1.31%, all p < 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].

OriginalsprogEngelsk
Artikelnummer936828
TidsskriftFrontiers in Nutrition
Vol/bind9
Sider (fra-til)1-11
Antal sider11
DOI
StatusUdgivet - aug. 2022

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