Limited Effect of Dietary Saturated Fat on Plasma Saturated Fat in the Context of a Low Carbohydrate Diet

Abstract

We recently showed that a hypocaloric carbohydrate restricted diet (CRD) had two striking effects: (1) a reduction in plasma saturated fatty acids (SFA) despite higher intake than a low fat diet, and (2) a decrease in inflammation despite a significant increase in arachidonic acid (ARA). Here we extend these findings in 8 weight stable men who were fed two 6-week CRD (12%en carbohydrate) varying in quality of fat. One CRD emphasized SFA (CRD-SFA, 86 g/d SFA) and the other, unsaturated fat (CRD-UFA, 47 g SFA/d). All foods were provided to subjects. Both CRD decreased serum triacylglycerol (TAG) and insulin, and increased LDL-C particle size. The CRD-UFA significantly decreased plasma TAG SFA (27.48 ± 2.89 mol%) compared to baseline (31.06 ± 4.26 mol%). Plasma TAG SFA, however, remained unchanged in the CRD-SFA (33.14 ± 3.49 mol%) despite a doubling in SFA intake. Both CRD significantly reduced plasma palmitoleic acid (16:1n-7) indicating decreased de novo lipogenesis. CRD-SFA significantly increased plasma phospholipid ARA content, while CRD-UFA significantly increased EPA and DHA. Urine 8-iso PGF2α, a free radical-catalyzed product of ARA, was significantly lower than baseline following CRD-UFA (−32%). There was a significant inverse correlation between changes in urine 8-iso PGF2α and PL ARA on both CRD (r = −0.82 CRD-SFA; r = −0.62 CRD-UFA). These findings are consistent with the concept that dietary saturated fat is efficiently metabolized in the presence of low carbohydrate, and that a CRD results in better preservation of plasma ARA.

Dietary carbohydrate restriction improves insulin sensitivity, blood pressure, microvascular function, and cellular adhesion markers in individuals taking statins

“…The significant increase in phospholipid arachidonic acid and other essential fatty acid end-products on a CRD may be due to greater synthesis in the body, but all the levels of metabolic intermediates and enzyme activities point in the opposite direction, indicating that production goes down. We have also observed an inverse correlation between changes in plasma phospholipid arachidonic acid and urinary F 2 -isoprostane [9]. The most likely explanation is that a well-controlled CRD results in better preservation of arachidonic acid, a response likely mediated by less free radical-induced peroxidation of highly unsaturated fatty acids.…”

“…The beneficial effects of a verylow carbohydrate diet on inflammation may be mediated, in part, by increases in circulating ketones which in addition to their role as providing fuel also suppress oxidative stress through epigenetic mechanisms [7]. As inflammation-induced oxidative stress potentially mediates endothelial dysfunction in middle-aged and older adults [8], a very lowcarbohydrate diet may lead to improvements in VEF by reducing oxidative stress [9] and inflammation [5].…”

The Role of the Novel Lipokine Palmitoleic Acid in Health and Disease

“…It is known that carbohydrate intake increases SCD1 expression (36) and, therefore, a direct relation between dietary carbohydrate and palmitoleate concentrations was expected. Various other studies in humans also have exposed a direct association between carbohydrate intake and plasma palmitoleate, indicating upregulation of de novo lipogenesis (37)(38)(39). Because cis-palmitoleate is synthesized endogenously, diet components modifying SCD1 activity as carbohydrate necessarily change serum cis-palmitoleate concentrations, which range approximately from 0.19% to 0.5% of FAs (40).…”

Palmitoleic acid is elevated in fatty liver disease and reflects hepatic lipogenesis

“…Stearoyl-CoA desaturase 1 (SCD1) desaturates stearate (18:0) and 16:0 into oleate (18:1n-9) and palmitoleate (16:1n-7), respectively (14). The plasma FA composition has been used to provide insight into cellular metabolic pathways; specifically, the ratios (molar percentage:molar percentage) of 18:1n-9 to 18:0 [SCD1 (18) ] and 16:1n-7 to 16:0 [SCD1 (16) ] are used to estimate SCD1 activity (15)(16)(17)(18)(19)(20). The SCD1 (16) index has also been proposed as an indirect biomarker of DNL.…”