A macadamia nut-rich diet reduces total and LDL-cholesterol in mildly hypercholesterolemic men and women. J Nutr

Department of Nutritional Sciences, Pennsylvania State University, University Park, PA, 16802, USA.
Journal of Nutrition (Impact Factor: 3.88). 04/2008; 138(4):761-7.
Source: PubMed


Epidemiologic studies and clinical trials have demonstrated that the unique fatty acid profile of nuts beneficially affects serum lipids/lipoproteins, reducing cardiovascular disease (CVD) risk. Nuts are low in SFA and high in PUFA and monounsaturated fatty acids (MUFA). Macadamia nuts are a rich source of MUFA. A randomized, crossover, controlled feeding study (5-wk diet periods) compared a Macadamia nut-rich diet [42.5 g (1.5 ounces)/8.79 MJ (2100 kcal)] [MAC; 33% total fat (7% SFA, 18% MUFA, 5% PUFA)] vs. an average American diet [AAD; 33% total fat (13% SFA, 11% MUFA, 5% PUFA)] on the lipid/lipoprotein profile of mildly hypercholesterolemic (n = 25; 15 female, 10 male) subjects. Serum concentrations of total cholesterol (TC) and LDL cholesterol (LDL-C) following the MAC (4.94 +/- 0.17 mmol/L, 3.14 +/- 0.14 mmol/L) were lower than the AAD (5.45 +/- 0.17 mmol/L, 3.44 +/- 0.14 mmol/L; P < 0.05). The serum non-HDL cholesterol (HDL-C) concentration and the ratios of TC:HDL-C and LDL-C:HDL-C were reduced following consumption of the MAC diet (3.83 +/- 0.17, 4.60 +/- 0.24, and 2.91 +/- 0.17, respectively) compared with the AAD (4.26 +/- 0.17, 4.89 +/- 0.24, and 3.09 +/- 0.18, respectively; P < 0.05). There was no change in serum triglyceride concentration. Thus, macadamia nuts can be included in a heart-healthy dietary pattern that reduces lipid/lipoprotein CVD risk factors. Nuts as an isocaloric substitute for high SFA foods increase the proportion of unsaturated fatty acids and decrease SFA, thereby lowering CVD risk.

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    • "Palmitoleic acid is also found in animal products such as fish oils (Ozogul, Ozogul, Cicek, Polat, & Kuley, 2008). Experiments in cell culture (Morgan & Dhayal, 2010; Morgan, Dhayal, Diakogiannaki, & Welters, 2008), animal models (Cao et al., 2008; Matthan, Dillard, Lecker, Ip, & Lichtenstein, 2009; Yang, Miyahara, & Hatanaka, 2011), and humans (Garg, Blake, & Wills, 2003; Griel et al., 2008) have shown that palmitoleic acid (or a diet rich in palmitoleic acid) may favorably influence glucose and lipid metabolism. Furthermore, palmitoleic acid increases the release of CCK from STC-1 cells (Tanaka et al., 2008). "
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    ABSTRACT: We have analyzed the effect of palmitoleic acid on short-term food intake in male rats. Administration of omega-7 palmitoleic acid by oral gavage significantly decreased food intake compared to palmitic acid, omega-9 oleic acid, or a vehicle control. Palmitoleic acid exhibited a dose-dependent effect in this context and did not cause general malaise. A triglyceride form of palmitoleate also decreased food intake, whereas olive oil, which is rich in oleic acid, did not. Palmitoleic acid accumulated within the small intestine in a dose-dependent fashion and elevated levels of the satiety hormone cholecystokinin (CCK). Both protein and mRNA levels of CCK were affected in this context. The suppression of food intake by palmitoleic acid was attenuated by intravenous injection of devazepide, a selective peripheral CCK receptor antagonist. Palmitoleic acid did not alter the expression of peroxisome proliferator-activated receptor alpha (PPARα) target genes, and a PPARα antagonist did not affect palmitoleic acid-induced satiety. This suggests that the PPARα pathway might not be involved in suppressing food intake in response to palmitoleic acid. We have shown that orally administered palmitoleic acid induced satiety, enhanced the release of satiety hormones in rats.
    Appetite 01/2013; 65. DOI:10.1016/j.appet.2013.01.009 · 2.69 Impact Factor
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    • "Changes in blood lipid and lipoprotein concentrations did not differ between the four groups. Most previous literature suggests that regular nut consumption in hypercholesterolemic individuals results in significant reductions in TC and LDL-C [21, 25, 60–64] with some showing increases in HDL-C [25, 62, 63] whilst others do not [21, 60, 61, 64]. It is likely that we did not observe an improvement in blood lipoproteins with regular nut consumption due to the low baseline TC (4.8 mmol/L) and LDL-C (2.9 mmol/L) and relatively high HDL-C (1.3 mmol/L) concentrations of this study population. "
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    ABSTRACT: Previous studies have reported that regular nut consumption reduces cardiovascular disease (CVD) risk and does not promote weight gain despite the fact that nuts are energy-dense. However, no studies have investigated the body composition of those regularly consuming nuts compared to similar intakes of other snacks of equal energy density. This parallel study (n = 118) examined the effects of providing daily portions (~1100 kJ/d) of hazelnuts, chocolate, or potato crisps compared to a control group receiving no snacks for twelve weeks. Effects on body weight and composition, blood lipids and lipoproteins, resting metabolic rate (RMR), appetite indices, and dietary quality were compared. At week 12, there was no significant difference in any of the outcome measurements between the groups except for dietary quality, which improved significantly in the nut group. Nuts can be incorporated into the diet without adversely affecting body weight and can improve diet quality.
    Journal of nutrition and metabolism 08/2011; 2011(2090-0724):357350. DOI:10.1155/2011/357350
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    • "Palmitoleic acid (C16:1) is an omega-7 monounsaturated fatty acid that is abundant in plant and marine sources [4-6]. It has been demonstrated that palmitoleic acid prevents beta-cell apoptosis induced by glucose or saturated fatty acids [7,8], and diets rich in palmitoleic acid improve circulating lipid profile in both animal model [9] and human subjects [10,11]. Furthermore, a recent report demonstrated that palmitoleic acid functions as an adipose tissue-derived lipid hormone that stimulates muscle insulin action and suppresses hepatosteatosis in mice deficient in fatty acid binding protein [12]. "
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    ABSTRACT: Studies have demonstrated the beneficial effect of palmitoleic acid (C16:1 n-7) on reducing muscle insulin resistance and preventing beta-cell apoptosis. However, the effect of palmitoleic acid on diabetes remains to be elucidated. The aim of this study was to examine the antidiabetic effect of palmitoleic acid in KK-Ay mice, a spontaneous model for studies of obese type 2 diabetes with low insulin sensitivity. KK-Ay mice were orally administered vehicle, 300 mg/kg of palmitoleic acid, or 300 mg/kg of palmitic acid (C16:0) on a daily basis for 4 weeks. Palmitoleic acid reduced body weight increase, ameliorated the development of hyperglycemia and hypertriglyceridemia, and improved insulin sensitivity. In addition, hepatic characteristics were significantly affected, as weight of the liver and hepatic triglyceride levels were lower in the palmitoleic acid group when compared to the control (vehicle and palmitic acid groups). Oil red O staining clearly indicated reduced hepatic lipid accumulation in response to palmitoleic acid. Furthermore, palmitoleic acid down-regulated mRNA expressions of proinflammatory adipocytokine genes (TNFα and resistin) in white adipose tissue and lipogenic genes (SREBP-1, FAS, and SCD-1) in liver. These results suggest that palmitoleic acid improves hyperglycemia and hypertriglyceridemia by increasing insulin sensitivity, in part owing to suppressing proinflammatory gene expressions and improving hepatic lipid metabolism in diabetic mice.
    Lipids in Health and Disease 07/2011; 10(1):120. DOI:10.1186/1476-511X-10-120 · 2.22 Impact Factor
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