Following the two 12-wk dietary interventions, there were significant differences in the change in the iAUC summary measure for total FA response between the modified and
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control test meals (Table 4.5). The iAUC response for total SFA significantly decreased after consumption of the modified test meals, and compared to control (P = 0.0001). In particular, the iAUC of 15:0 and 18:0 were significantly lower following the modified test meals and compared to control test meals (P = 0.0001 and P = 0.01, respectively).
Change in iAUC response of total cis-MUFA was not significantly different between the two diets. However, the iAUC change in total trans-MUFA and total trans FA response was significantly lower following the modified test meals (P = 0.009 and P = 0.008
respectively), compared to control.
For total PUFA, change in iAUC was significantly lower following the modified test meals, compared to the control (P = 0.001). Similarly, change iAUC response for both n-3 and n-6 PUFA reflected the iAUC change in total PUFA (P = 0.002 and P = 0.001,
respectively). For all other FAs presented in Table 5.4, postprandial iAUC summary response measures were not influenced by the intervention test meals.
4.5 Discussion
Using an acute-within-chronic design, the aim of this novel study was to compare the effect of long-term consumption of FA-modified dairy products and conventional
counterparts on postprandial changes in endothelial function, lipaemia and inflammation in adults at moderate CVD risk. We observed a lower response in the iAUC for apoB response following a sequential two-meal challenge of the FA-modified dairy products. Additionally, our total lipid FA results reflected the current dietary intervention and test meals fat
composition.
ApoB is considered a marker of the number of circulating TRLs (243). Several studies have investigated the long-term consumption of diets with a differential FA composition and the subsequent impact on the postprandial state following ingestion of test meals
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on an enrichment of dietary interventions with PUFA, while sources of MUFA have mainly originated from plant oils, particularly olive oil, which is in contrast to our study design (232, 233). In an 8-wk cross-over study, Roche et al. (232) investigated the long-term effect of two dietary interventions (41%TE total fat) rich in either SFA (51% SFA; 38% MUFA) or MUFA (39% SFA; 56% MUFA) in the form of spreads and oils, which was followed by a
postprandial investigation in healthy men. The MUFA-rich diet led to a significant beneficial impact in fasting LDL-C and an attenuation in the postprandial activation of factor VII (232). An additional study used spreads and cooking oils to implement a chronic substitution of a dietary SFA (16% SFA; 12% MUFA) with either a moderate (13% SFA; 15% MUFA) or high (10% SFA; 18% MUFA) MUFA diet for 8-wk in 51 healthy adults (244). A sub-cohort of the main study’s population completed a postprandial intervention which included a standard test meal and resulted in a 30-40% reduction in the postprandial number of circulating intestinally derived lipoproteins following the moderate and high MUFA diets respectively (244). It is worth noting, that in addition to the implementation of MUFA-rich test meals sourced from plant oils, the aforementioned studies also present a degree of heterogeneity in study populations which precludes from making definite comparisons with our study. However, the evidence from these studies suggests an impact in the kinetics of postprandial responses following MUFA-rich diets, influencing the number and size of TRLs and increasing the rate of clearance in the circulation (107). The decrease in postprandial iAUC of apoB may therefore be related to the observed fasting LDL-C attenuation we observed following intake of the SFA-reduced, MUFA-enriched dairy products in the 12-wk dietary intervention, compared to conventional dairy products (239). Furthermore, the findings from a previously published in vitro study investigating the consumption of a single SFA-rich meal, suggested greater competition for LDL-C uptake between circulating TRLs in HepG2 liver cells, compared to circulating TRLs following MUFA-rich meals(245). This may
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in turn suggest a potential mechanism to explain higher circulating LDL-C observed following ingestion of SFA-rich diets (245).
Postprandial studies which have investigated the impact of FA-modified dairy products following modifications of the dairy cow diet, have primarily focused on
implementing a dietary intervention using modified butter fat. Tholstrup et al. (223) compared the effects of 4-wk consumption of Danish butter (40%TE from fat; 37% palmitic acid; 15% oleic acid) and a FA-modified butter (21% palmitic acid; 25% oleic acid) in 18 healthy men in a cross-over design. The postprandial investigation following each standard meal resulted in no significant changes in postprandial lipid markers, which the authors suggest may be
attributed to a 5-fold increase in trans 18:1 in the modified butter compared to the control diet (223). However, in contrast to our study design, Tholstrup et al. (223) used only butter fat in the chronic intervention and a standard test meal not representative of the dietary intervention in a small number of participants, which may explain null findings.
The FA composition of study meals have specific characteristics, which may influence digestion rate and absorption (108). In the current study, we observed significant changes in postprandial iAUC responses in the plasma concentration of total lipid FA classes, which appear reflective of the FA composition of the test meals. In particular, there was a marked difference in the postprandial iAUC response of total trans FA (TFA) and trans MUFA following the modified diet, reflecting the observed increase in ruminant TFA (rTFA) of the dairy products following supplementation of the dairy cow feed (201, 203). Although there is less evidence for a detrimental effect of rTFA compared to their industrial counterparts (220), the recommended TFA intake from all sources should not exceed 2% total food energy (10). The FA modified study meals had a higher (2.9 g/d) rTFA content compared to the control study meals, which do not appear to have detrimental effects postprandially. Similarly, differences in the iAUC postprandial response of total and specific classes of SFA is in line with the observed partial replacement of SFA in the modified dairy products (201, 203).
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Inflammation and endothelial function in the postprandial state have also been attributed to a progressive detrimental effect on CVD risk, in particular following high SFA intake (98). In our previous publication, we observed a significant increase in fasted nitrite concentrations following 12-wk consumption of the modified diet, and compared to control diet (239). Postprandial TAG and NEFA following, high-fat meals, have been shown to reduce concentrations of NO, impacting on postprandial NO-dependent FMD of the brachial artery (246, 247). In the current study, we observed a tendency for a non-significant decrease in the postprandial iAUC for the plasma nitrite response following the modified test meals, compared to control. Interestingly, this response supports the change in fasted nitrite
concentrations, which significantly increased following 12-wk consumption of the modified diet , relative to baseline, when compared with the control (238).
The two dairy test meals did not significantly impact on the postprandial summary response measures of the cellular adhesion molecules. This is in agreement with a study which compared the postprandial effects of 3 iso-caloric high fat milkshakes (95 g total fat), either high in SFA (54%TE), MUFA (83%TE) or n3 PUFA (40%TE) in lean and obese middle aged men (248). Previous studies have demonstrated a triggering of postprandial, pro- inflammatory cytokine production following high-fat meal intake with a moderate to high SFA content (249-251). It is therefore possible that the moderate reduction in total SFA and parallel increase of MUFA in the modified dairy products, compared to the control (201, 238), did not elicit a differential impact on adhesion molecules or LPS-stimulated cytokines.
Additionally, the evidence to date on inflammatory postprandial biomarker response to meal FA composition remains inconclusive (252). This may allude to variations in measurements observed in both healthy and at risk individuals, linked to additional participant characteristics which may affect the concentration of inflammatory markers (including age, overall diet and genetics) (98).
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A strength of the current study is the double-blinded, crossover, randomized and long- term design. Additionally, the sequential two-meal challenge and 480 min postprandial investigation more closely reflected Western dietary patterns. Furthermore, the breakfast and lunch test meals of the postprandial intervention contained representative quantities of the dairy study products which were used in the chronic dietary intervention. Our study population was at moderate CVD risk and evidence supports that compared with healthy subjects, individuals at risk may be more sensitive to meal challenges (108). However, as the eligibility of participants was based on an overall scoring ≥2 CVD risk markers, baseline fasting characteristics of all participants were not homogenous with respect to CVD risk factors. This may potentially have led to the lack of an impact on the change in postprandial responses of specific markers of postprandial lipaemia, such as TAG and NEFA. Lastly, as described in our previous publication (238), there were modest differences in the SFA and cis- MUFA content between the FA-modified and control dairy products and test meals which may also explain a lack of differential postprandial responses in some of our secondary outcome measures.
In conclusion, the present study indicates that 12-wk consumption of SFA-reduced, MUFA-enriched dairy products, led to a reduction in the postprandial iAUC response of apoB, following sequential test meals representative of the dietary intervention, suggesting an effect on TRL metabolism. The results of the postprandial FMD response, particularly in light of the postprandial nitrite response, may further add to a better understanding of the impact of FA-modified dairy consumption
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