Effects of step-wise increases in dietary carbohydrate on circulating saturated Fatty acids and palmitoleic Acid in adults with metabolic syndrome

Abstract

Recent meta-analyses have found no association between heart disease and dietary saturated fat; however, higher proportions of plasma saturated fatty acids (SFA) predict greater risk for developing type-2 diabetes and heart disease. These observations suggest a disconnect between dietary saturated fat and plasma SFA, but few controlled feeding studies have specifically examined how varying saturated fat intake across a broad range affects circulating SFA levels. Sixteen adults with metabolic syndrome (age 44.9±9.9 yr, BMI 37.9±6.3 kg/m2) were fed six 3-wk diets that progressively increased carbohydrate (from 47 to 346 g/day) with concomitant decreases in total and saturated fat. Despite a distinct increase in saturated fat intake from baseline to the low-carbohydrate diet (46 to 84 g/day), and then a gradual decrease in saturated fat to 32 g/day at the highest carbohydrate phase, there were no significant changes in the proportion of total SFA in any plasma lipid fractions. Whereas plasma saturated fat remained relatively stable, the proportion of palmitoleic acid in plasma triglyceride and cholesteryl ester was significantly and uniformly reduced as carbohydrate intake decreased, and then gradually increased as dietary carbohydrate was re-introduced. The results show that dietary and plasma saturated fat are not related, and that increasing dietary carbohydrate across a range of intakes promotes incremental increases in plasma palmitoleic acid, a biomarker consistently associated with adverse health outcomes.

Conflict of interest statement

Competing Interests: Professional associations (Dairy Research Institute, The Beef Checkoff and the Egg Nutrition Center) were sponsors of this research. This does not alter the authors' adherence to PLOS ONE policies on sharing data and materials.

Figures

Figure 1. Experimental approach.

CHO = carbohydrate, SFA  =  saturated fat.

Figure 2. Cumulative change from baseline in (A) body mass and fat mass from dual-energy x-ray absorptiometry, (B) fasting lipoproteins, (C) insulin resistance determined from homeostatic model assessment (HOMA), and (D) blood pressure in 16 subjects who switched to a very low carbohydrate diet and then incrementally increased carbohydrate every 3 wk over six sequential phases (C1→C2→C3→C4→C5→C6).

BL  =  baseline, FL  =  free-living low-carbohydrate diet). Significant differences from Baseline vs C1 were determined by dependent t-test and indicated by an asterisk. Differences from C1 to C6 were determined by repeated measures ANOVA and Fisher's LSD post hoc. Different letters at a time point indicate statistical significance.

Figure 3

(A) Change from baseline in plasma palmitoleic acid (16∶1) in triglyceride (TG) and cholesteryl ester (CE) in subjects who consumed a very low carbohydrate diet (C1) and then gradually transitioned to a high carbohydrate diet over six sequential phases (C1→C2→C3→C4→C5→C6). (B) Individual responses in plasma TG 16∶1 from C1 to C4 to C6 corresponding to 47, 179, and 344 g carbohydrate/day. Open circles are subjects who went from low- to high-carbohydrate, and shaded triangles are subjects who went from high- to low-carbohydrate intake.