The alpha linolenic acid content of flaxseed is associated with an induction of adipose leptin expression.

Dietary flaxseed has cardioprotective effects that may be achieved through its rich content of the omega-3 fatty acid, alpha linolenic acid (ALA). Because ALA can be stored in adipose tissue, it is possible that some of its beneficial actions may be due to effects it has on the adipose tissue. We investigated the effects of dietary flaxseed both with and without an atherogenic cholesterol-enriched diet to determine the effects of dietary flaxseed on the expression of the adipose cytokines leptin and adiponectin. Rabbits were fed one of four diets: a regular (RG) diet, or a regular diet with added 0.5% cholesterol (CH), or 10% ground flaxseed (FX), or both (CF) for 8 weeks. Levels of leptin and adiponectin expression were assessed by RT-PCR in visceral adipose tissue. Consumption of flaxseed significantly increased plasma and adipose levels of ALA. Leptin protein and mRNA expression were lower in CH animals and were elevated in CF animals. Changes in leptin expression were strongly and positively correlated with adipose ALA levels and inversely correlated with levels of en face atherosclerosis. Adiponectin expression was not significantly affected by any of the dietary interventions. Our data demonstrate that the type of fat in the diet as well as its caloric content can specifically influence leptin expression. The findings support the hypothesis that the beneficial cardiovascular effects associated with flaxseed consumption may be related to a change in leptin expression.

The α-linolenic acid content of flaxseed can prevent the atherogenic effects of dietary trans fat.

Dietary intake of industrially hydrogenated trans fatty acids (TFA) has been associated with coronary heart disease. Dietary flaxseed can inhibit atherosclerosis induced by dietary cholesterol. The aim of this study was to determine whether supplementing the diet with flaxseed could protect against atherosclerosis induced by a diet enriched in TFA. Low-density lipoprotein receptor-deficient (LDLr(-/-)) mice were fed 1 of 14 experimental diets for 14 wk containing one of two fat sources [regular (pork/soy) or trans fat] at two concentrations (4 or 8%) and supplemented with or without dietary cholesterol (2%), whole ground flaxseed, or one of the components of flaxseed [α-linolenic acid (ALA), defatted fiber, or lignan]. Adding flaxseed to the diet partially mitigated the rise in circulating cholesterol levels induced by the cholesterol-enriched diet. Atherosclerosis was stimulated by TFA and/or cholesterol. Including milled flaxseed to an atherogenic diet significantly reduced atherosclerosis compared with the groups that consumed cholesterol and/or TFA. ALA was the only component within flaxseed that could inhibit the atherogenic action of cholesterol and/or TFA on its own. Dietary flaxseed protects against atherosclerotic development induced by TFA and cholesterol feeding through its content of ALA.

Dietary vaccenic acid has antiatherogenic effects in LDLr-/- mice.

Epidemiological evidence has associated dietary trans fatty acids (TFA) with heart disease. TFA are primarily from hydrogenated fats rich in elaidic acid, but dairy products also contain naturally occurring TFA such as vaccenic acid. Our purpose in this study was to compare the effects of consuming a commercially hydrogenated vegetable shortening rich in elaidic TFA (18:1t9) or a butter rich in vaccenic TFA (18:1t11) in the absence and presence of dietary cholesterol on atherosclerosis. LDL receptor deficient (LDLr(-/-)) mice were fed 1 of 8 experimental diets for 14 wk with the fat content replaced by: regular (pork/soy) fat (RG), elaidic shortening (ES), regular butter (RB), vaccenic butter (VB), or an atherogenic diet containing 2% cholesterol with RG (CH+RG), ES (CH+ES), RB (CH+RB), or VB (CH+VB). Serum cholesterol levels were elevated with cholesterol feeding (P < 0.001), whereas serum triglyceride levels were higher only in the CH+RB (P < 0.001) and CH+VB (P < 0.001) groups compared with the other 6 groups. Serum cholesterol and triglyceride levels were significantly lower in the CH+VB group than in the CH+RB group (P < 0.001). Atherosclerosis was stimulated by dietary ES compared with RG (P = 0.021), but CH+ES did not stimulate atherosclerosis beyond CH+RG alone. In contrast, VB did not induce an increase in atherosclerotic plaque formation compared with the RG and RB diets and the CH+VB diet reduced atherosclerosis compared with the other diets containing cholesterol (P < 0.01). In summary, consuming a hydrogenated elaidic acid-rich diet stimulates atherosclerosis, whereas a vaccenic acid-rich butter protects against atherosclerosis in this animal model.

Trans-fatty acids in the diet stimulate atherosclerosis.

Epidemiological evidence has associated dietary trans-fatty acids (TFAs) with coronary heart disease. It is assumed that TFAs stimulate atherosclerosis, but this has not been proven. The purpose of this study was to determine the effects of consuming 2 concentrations of TFAs obtained from commercially hydrogenated vegetable shortening on atherosclerotic development in the presence or absence of elevated dietary cholesterol. Low-density lipoprotein receptor-deficient mice were fed 1 of 7 experimental diets for 14 weeks: low regular fat (LR), low trans-fat (LT), regular high fat, high trans-fat (HT), or a diet containing 2% cholesterol with low regular fat (C + LR), low trans-fat (C + LT), or high trans-fat (C + HT). The extent of lesion development was quantified by en face examination of the dissected aortae. Dietary cholesterol supplementation significantly elevated serum cholesterol levels. Surprisingly, this rise was partially attenuated by the addition of TFAs (C + LT and C + HT) in the diet. Serum triglyceride levels were elevated with the higher-fat diets and with the combination of trans-fat and cholesterol. Animals consuming TFAs in the absence of dietary cholesterol developed a significantly greater extent of aortic atherosclerotic lesions as compared with control animals (LT > LR and HT > regular high fat). Atherosclerotic lesions were more extensive after cholesterol feeding, but the addition of TFAs to this atherogenic diet did not advance atherosclerotic development further. In summary, TFAs are atherogenic on their own; but they do not stimulate further effects beyond the strongly atherogenic effects of dietary cholesterol.

Nutrition as a vehicle for cardiovascular translational research.

It is becoming increasingly evident that poor nutrition plays an important role in inducing cardiovascular disease. Just as importantly, data now support the contention that appropriate nutritional interventions may have just as important an effect in preventing or delaying the appearance of cardiovascular disease. If this is indeed true, then it is critical that these advances in our knowledge of the effects of nutritional interventions be translated into effective strategies to combat cardiovascular disease. It is argued in this paper, with a few specific examples, that the translation of nutritional interventions can provide powerful approaches to alleviating the clinical challenges currently facing us today in the cardiovascular field. Furthermore, the value-added economic advantages of translating nutritional strategies on a wide scale into the public become another intriguing argument to further support investigations in this growing field.