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Dietary palmitic and oleic acid exert similar effects on serum cholesterol and lipoprotein profiles in normo­cholesterolemic men and women

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To compare the effects of dietary palmitic acid (16:0) vs oleic acid (18:1) on serum lipids, lipoproteins, and plasma eicosanoids, 33 normocholesterolemic subjects (20 males, 13 females; ages 22-41 years) were challenged with a coconut oil-rich diet for 4 weeks. Subsequently they were assigned to either a palm olein-rich or olive oil-rich diet followed by a dietary crossover during two consecutive 6-week periods. Each test oil served as the sole cooking oil and contributed 23% of dietary energy or two-thirds of the total daily fat intake. Dietary myristic acid (14:0) and lauric acid (12:0) from coconut oil significantly raised all the serum lipid and lipoprotein parameters measured. Subsequent one-to-one exchange of 7% energy between 16:0 (palm olein diet) and 18:1 (olive oil diet) resulted in identical serum total cholesterol (192, 193 mg/dl), low-density lipoprotein cholesterol (LDL-C) (130, 131 mg/dl), high-density lipoprotein cholesterol (HDL-C) (41, 42 mg/dl), and triglyceride (TG) (108, 106 mg/dl) concentrations. Effects attributed to gender included higher HDL in females and higher TG in males associated with the tendency for higher LDL and LDL/HDL ratios in men. However, both sexes were equally responsive to changes in dietary fat saturation. The results indicate that in healthy, normocholesterolemic humans, dietary 16:0 can be exchanged for 18:1 within the range of these fatty acids normally present in typical diets without affecting the serum lipoprotein cholesterol concentration or distribution. In addition, replacement of 12:0 + 14:0 by 16:0 + 18:1, but especially 16:0 or some component of palm olein, appeared to have a beneficial impact on an important index of thrombogenesis, i.e., the thromboxane/prostacyclin ratio in plasma.
... Nwagha et al., 2010). The signi cance of dyslipidemia is based on the triad of an increase in LDL and triglycerides (Ng et al., 1992) particles and a decrease in HDL levels (Rached et al., 2014). Lowering LDL-C levels is well established as an intervention for reducing CVDs (Rached et al., 2014). ...
... According to the ndings of (Haber et al., 2019), honey bees had an increased amount of palmitic and oleic acid, which was the dominant fatty acid determined in the larvae. Therefore, diets richer in palmitic and oleic acid like diet 3 increase the HDL-C levels and decrease LDL-C or lower the ratio of LDL-C to HDL-C (CRI-II) (Cook et al., 1997;Ng et al., 1992;Tinahones et al., 2004). Also, this Monounsaturated Fatty Acids (MUFA) omega-9 fatty acid is important in the human diet; it has been proven effective to reduce LDL and TC levels (Mattson & Grundy, 1985). ...
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Background- Cardiovascular disease is the cause of one-third of deaths worldwide and this status is likely to progress because of increasing CVD's risk factors like intake of cholesterol and saturated fat. There is no clear evidence that a poor diet in childhood is associated with CVD risk factor development and adverse vascular health in adulthood. Hence, it is important to look at the effects of complementary foods. Therefore, this study assessed the cardioprotective effects of insect bee larvae (Apis Melifera) based complementary foods in young white albino mice Methods- The experiment was conducted using a randomized control design. Data were analyzed using IBM SPSS version 23. A total of Seventy-five male white Albino mice were randomly assigned to five diets in triplicate. The diets were Diet 1= Casein diet; Diet 2= (57% Maize, 29% Teff, 14% Soybean); Diet 3= (58% Maize, 29% Teff, 13% Bee larvae); Diet 4=Commercial wean mix; and Diet 5= Basal diet alone. The study was conducted for 28 days with seven days of acclimatization. Diet and water were given ad libitum. The mice blood sample was collected from a cardiac puncture. Lipid profiles of TC, TG, HDL-C and LDL-C evaluations were analyzed using automated pentra C400 made in France. Results- The results showed a statistically significant difference (P<0.001) of lipid profiles between treatments. Biochemical (mg/dl) parameters showed Diet 3 were recorded high TG (167.79) and HDL-C (67.18) and low in LDL-C (71.73). Atherogenic indices of Diet 3 were low in CRI-I (1.84), CRI-II (1.07), and AC (0.84). LDL-C levels were positively correlated with all atherogenic indices, while HDL-C levels were negatively correlated. Atherogenicity indices showed significant positive associations (P<0.001) with one another; CRI-I vs CRI-II (r=0.919), CRI-I vs AC (r=1), CRI-II vs AC (r= 0.919). Nevertheless, AIP was positively correlated with CRI-I, CRI-II, and AC, however, this was not statistically significant (P>0.05). Conclusions- Intake of insect bee larvae-based diet could have the potential to protect from atherosclerotic cardiovascular disease in infants and young children. However, further studies on the adverse effects of the developed complementary foods on clinical and histopathological trials should be conducted.
... While SFA has been shown to increase the level of total and LDL-C, MUFAs are considered to be low-risk for CVDs (DiNicolantonio and O'Keefe 2018). Ng et al. (1992) analyzed the effect of palm olein, olive oil, and coconut oil on serum cholesterol and lipoprotein profiles by organizing the diet of 33 normocholesterolemic participants according to different oil types. It was reported that palm olein and olive oil had a similar effect after 6 weeks (Ng et al. 1992). ...
... Ng et al. (1992) analyzed the effect of palm olein, olive oil, and coconut oil on serum cholesterol and lipoprotein profiles by organizing the diet of 33 normocholesterolemic participants according to different oil types. It was reported that palm olein and olive oil had a similar effect after 6 weeks (Ng et al. 1992). In another study conducted with 21 normocholesterolemic individuals, their diets were adjusted to contain 50% of fat as palm olein or olive oil, and after 30 days, no difference could be found between the 2 oil types on the blood lipid and lipoprotein profiles (Choudhury, Tan, and Truswell 1995). ...
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... One randomized controlled trial found that a palm oil-enriched diet did not lead to negative effects on the lipid profile compared to a coconut oil-enriched diet [11]. Furthermore, two clinical trials conducted in Malaysia [12,13] demonstrated that there was a significant increase of LDLcholesterol by coconut oil compared to palm oil. However, subsequent study from the same country [14] indicated that coconut oil decreased LDL-cholesterol over palm oil. ...
... Some studies that compared olive oil (SFA:MUFA:PUFA ratio ∼15:75:10) with palm oil (SFA:MUFA:PUFA ∼50: 40:10) found no difference in serum cholesterol concentrations of young, healthy human volunteers. Palm oil diets had much more SFAs than olive oil diets; however, because the diets contained the same amount of PUFAs, serum cholesterol did not change with these changes in dietary SFA (55,56). It is estimated that ≤6-8 g/d PUFAs (8-10% of total fatty acids; 2-3% of energy) in the diet would be sufficient to satisfy normal requirements for production of bioactive products without causing adverse health effects. ...
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PUFAs are known to regulate cholesterol synthesis and cellular uptake by multiple mechanisms that do not involve SFAs. Polymorphisms in any of the numerous proteins involved in cholesterol homeostasis, as a result of genetic variation, could lead to higher or lower serum cholesterol. PUFAs are susceptible to lipid peroxidation, which can lead to oxidative stress, inflammation, atherosclerosis, cancer, and disorders associated with inflammation, such as insulin resistance, arthritis, and numerous inflammatory syndromes. Eicosanoids from arachidonic acid are among the most powerful mediators that initiate an immune response, and a wide range of PUFA metabolites regulate numerous physiological processes. There is a misconception that dietary SFAs can cause inflammation, although endogenous palmitic acid is converted to ceramides and other cell constituents involved in an inflammatory response after it is initiated by lipid mediators derived from PUFAs. This article will discuss the many misconceptions regarding how dietary lipids regulate serum cholesterol, the fact that all-cause death rate is higher in humans with low compared with normal or moderately elevated serum total cholesterol, the numerous adverse effects of increasing dietary PUFAs or carbohydrate relative to SFAs, as well as metabolic conversion of PUFAs to SFAs and MUFAs as a protective mechanism. Consequently, dietary saturated fats seem to be less harmful than the proposed alternatives.
... Palmitic acid and stearic acid can reduce the content of cholesterol in serum. Therefore, it has been suggested that replacing dietary lauric acid and myristic acid with palmitic acid and oleic acid may be beneficial for the treatment of thrombosis [22]. In addition, some studies have shown that pentadecanoic acid can improve hyperinsulinemia, protect islet cells and improve the inflammatory state of diabetic mice [23]. ...
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Chapter
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