Plasma Lipid Fatty Acids

Gas-liquid chromatographic analyses of fatty acids from various plasma lipid fractions of normal fasting subjects were compared with the same analyses done on plasmas taken after eating.     

Alteration of Yolk Fatty Acids

Conditions have been defined by which the polyunsaturated fatty acid content of egg yolks can be varied within considerable ranges.     

Consequences of Essential Fatty Acids

Essential fatty acids (EFA) are nutrients that form an amazingly large array of bioactive mediators that act on a large family of selective receptors. Nearly every cell and tissue in the human body expresses at least one of these receptors, allowing EFA-based signaling to influence nearly every aspect of human physiology. In this way, the health consequences of specific gene-environment interactions with these nutrients are more extensive than often recognized. The metabolic transformations have similar competitive dynamics for the n-3 and n-6 homologs when converting dietary EFA from the external environment of foods into the highly unsaturated fatty acid (HUFA) esters that accumulate in the internal environment of cells and tissues. In contrast, the formation and action of bioactive mediators during tissue responses to stimuli tend to selectively create more intense consequences for n-6 than n-3 homologs. Both n-3 and n-6 nutrients have beneficial actions, but many common health disorders are undesired consequences of excessive actions of tissue n-6 HUFA which are preventable. This review considers the possibility of preventing imbalances in dietary n-3 and n-6 nutrients with informed voluntary food choices. That action may prevent the unintended consequences that come from eating imbalanced diets which support excessive chronic actions of n-6 mediators that harm human health. The consequences from preventing n-3 and n-6 nutrient imbalances on a nationwide scale may be very large, and they need careful evaluation and implementation to avoid further harmful consequences for the national economy.     

Trans Fatty Acids and Cancer

Despite a general lack of evidence for the carcinogenic effects of trans fatty acids, some recent research and popular media have suggested a possible association. The available scientific data do not support this relationship and are reviewed so as to put this issue in perspective.     

Rat Brain Fatty Acids In Essential Fatty Acid Deficiency

Brain lipid composition was studied in rats depleted in essential fatty acids (EFA) from birth through one year, as well as in rats depleted for various periods up to 90 days and then refed EFA. Brain EFA were reduced in the depleted animals. Refeeding with EFA restored brain EFA pattern, brain weight, and body weight to normal. Thus, the fatty acid composition of brain con be altered by diet even in relatively mature rats.     

Short-Chain Fatty Acids in Ulcerative Colitis

Short-chain fatty acids (SCFA), a by-product of anaerobic fermentation of undigested carbohydrates within the colon, are an important energy source for colonic epithelial cells. It has been proposed that ulcerative colitis, a chronic inflammatory condition of the colon, may result from a metabolic defect in SCFA oxidation in the colon and that this defect may be corrected by supraphysiologic luminal levels of SCFA in the colon. Clinical trials published to date suggest that topical SCFA provide an effective primary and/or adjunctive treatment in patients with mild to moderate distal ulcerative colitis at substantial cost savings and without significant side effects.     

Unsaturated Fatty Acids In Trout Diets

Linoienic acid and fatty acids of the linolenic series appear to be the essential fatty acids in the nutrition of the trout (Salmo gairdneri). whereas fatty acids of the linoleic series are not essential. Some of the symptoms of linolcnate deficiency observed are similar to several conditions reported in trout raised on commercial diets, which previously have been rich in linoleic acid and low in linolenic acid.     

The Science of Fatty Acids and Inflammation

Inflammation is believed to play a central role in many of the chronic diseases that characterize modern society. In the past decade, our understanding of how dietary fats affect our immune system and subsequently our inflammatory status has grown considerably. There are compelling data showing that high-fat meals promote endotoxin [e.g., lipopolysaccharide (LPS)] translocation into the bloodstream, stimulating innate immune cells and leading to a transient postprandial inflammatory response. The nature of this effect is influenced by the amount and type of fat consumed. The role of various dietary constituents, including fats, on gut microflora and subsequent health outcomes in the host is another exciting and novel area of inquiry. The impact of specific fatty acids on inflammation may be central to how dietary fats affect health. Three key fatty acid–inflammation interactions are briefly described. First, the evidence suggests that saturated fatty acids induce inflammation in part by mimicking the actions of LPS. Second, the often-repeated claim that dietary linoleic acid promotes inflammation was not supported in a recent systematic review of the evidence. Third, an explanation is offered for why omega-3 (n–3) polyunsaturated fatty acids are so much less anti-inflammatory in humans than in mice. The article closes with a cautionary tale from the genomic literature that illustrates why extrapolating the results from inflammation studies in mice to humans is problematic.     

A Cytoplasmic Protein Which Binds Fatty Acids

Two studies describe the binding of long chain fatty acids to a low molecular weight protein present in the cytosol of many tissues. A role for this protein in the cellular transport and metabolism of fatty acids is suggested.     

Postprandial Lipid Metabolism in Normolipidemic Subjects and Patients with Mild to Moderate Hypertriglyceridemia: Effects of Test Meals Containing Saturated Fatty Acids,Mono-Unsaturated Fatty Acids,or Medium-Chain Fatty Acids

Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25–30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients: p = 0.003, controls: p = 0.03 compared to MCFA) and MUFA (patients: p = 0.001; controls: p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mg*h/dL, controls iAUC = 247 mg*h/dL, p = 0.02; MUFA: patients iAUC = 962 mg*h/dL, controls iAUC = 248 mg*h/dL, p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.