Fatty Acids in Health Promotion: Recent Developments. See presentations by Marie-Pierre St. Onge, PhD, Edward Farnsworth, PhD, Sherma Zibadi, MD, PhD, Gunther Bodon, MD.
Fatty Acids in Corn Oil: Role in Heart Disease Prevention
By Marie-Pierre St-Onge, New York Obesity Research Center, St. Luke’s/Roosevelt Hospital, New York, NY, USA. Conference paper presented at the American Oil Chemists’ Society (AOCS) Symposium, May 2009. Theme: Fatty Acids in Health Promotion: Recent Developments. mk/r.
Low-fat diets have long been advocated for CVD (cardiovascular disease) risk reduction. However, emerging evidence points towards more liberal total fat intakes granted that the overall fat profile of the diet is low in saturated and trans fats. There is thus an emphasis on reducing dietary saturated (SFA) and trans fatty acids while increasing the intake of unsaturated fatty acids. Both high monosaturated fatty acid (MUFA) and high polyunsaturated fatty acid (PUFA) diets can lead to reductions in TC (total Cholesterol) and LDL-C concentrations without adversely affecting HDL-C and TG (triglycerides) concentrations but there remains some controversy, however, with respect to which unsaturated fats, PUFA or MUFA, can produce the most beneficial lipid profile for CVD risk reduction.
Corn oil, which is high in PUFA and also contains an appreciable amount of MUFA, is well positioned for creating beneficial effects for heart disease risk reduction. In fact, when compared to higher saturated and trans fat diets, diets rich in corn oil have been shown to produce beneficial effects on the lipid profile. These effects on cardiovascular disease risk profile may be due to the unique combination of PUFA and MUFA found in corn oil but may also be the result of corn oil’s other phytochemical components, such as phytosterols. This paper will review the evidence leading to the conclusion that corn oil consumption may play a role in heart disease prevention.
Effects of Dietary Fatty Acids on Human Microbes: Role in Health
By E. Farnworth, . D. Sène, and C.P. Champagne, Agriculture and Agri-Food Canada, Canada. Conference paper presented at the American Oil Chemists’ Society (AOCS) Symposium, May 2009. Theme: Fatty Acids in Health Promotion: Recent Developments.
The human gastrointestinal tract (GIT) is inhabited by a large number and variety of bacteria. Some of the bacteria are beneficial to the host, some are not. Intestinal bacteria aid in digestion of foods, produce vitamins, produce bacteriocins that kill other bacteria, communicate with the immune system, and cause disease and infection through the production of toxins and other metabolites. Good health depends on a proper balance between the beneficial and non-beneficial bacteria. The lipid requirements for bacteria are not well defined. The growth of different bacterial strains (including pathogens) can be stimulated or suppressed in vitro by the same fatty acid (FA) depending on its structure and concentration.
The bacteria that reside in the GIT utilize ingested dietary lipid as free FAs hydrolysed from dietary triglycerides. It has been speculated that changing dietary fat will change the intestinal bacterial population, and this will in turn impact on the development of certain diseases and metabolic disorders. Since much of the FAs are absorbed in the small intestine, this is where free FAs probably exert most of their effects of the GIT microbiota. Bacterial enzyme activity, and the generation of secondary bile acids by intestinal bacteria have been proposed as possible causes of colon and rectal cancer as a result of dietary fat intake. Clinical data to support these hypotheses is lacking. The microbial population in obese humans changes when they lose weight. Animal studies indicate that intestinal bacteria can influence the absorption, the storage, and utilization of dietary fat, which may in part contribute to obesity. Polyunsaturated FAs, as free FAs, have been shown to suppress growth of probiotic bacteria in vitro and to alter the ability of bacteria to adhere to the intestinal mucus. Short chain FAs generated during fermentation of carbohydrates by intestinal bacteria have been shown to have many effects on metabolism that have long term health consequences.
Good clinical data to show if, and how, dietary fat can change the GIT bacterial population and its function have yet to be published. As our understanding of the impact of diet on this important component of metabolism and health increases, the role of dietary fat on human health, through its effect on the GIT microbiota, will become clearer.
Leptin Regulation of Cardiac Remodeling Due to Obesity
By Sherma Zibadi (1,2), Felina Cordova2, Douglas Larson (1), and Ronald Watson (1,2), (1) Sarver Heart Center, School of Medicine, University of Arizona, Tucson, AZ, USA, (2) College of Public Health, University of Arizona, Tucson, AZ, USA. Conference paper presented at the American Oil Chemists’ Society (AOCS) Symposium, May 2009. Theme: Fatty Acids in Health Promotion: Recent Developments.
Obesity contributes to the onset and/or development of heart diseases. Obesity-induced remodeling of cardiac extracellular matrix (ECM) leads to myocardial fibrosis and stiffness, and ultimately diastolic dysfunction. Leptin, an adipokine over-produced in obesity, is emerging as a novel mechanistic link between obesity and heart diseases. Despite the known essential role of leptin in hepatic and renal fibrosis, effect of leptin on cardiac ECM remodeling remains unclear.
To provide proof that leptin is one of the key mediators of profibrogenic responses in the heart, we administrated leptin to 5 month-old C57BL/6 and leptin-deficient ob/ob mice at 0.1 µg/g, sc, 3 times/week for 8 wks. Leptin-deficient ob/ob mice demonstrated eccentric hypertrophy, associated with significant increase of pro-MMP-2 and -8, TIMP-1 and -3 mRNA level, all implicated in collagen degradation, marked increase in pro-MMP-2 activity, and a reduction in cardiac collagen, compared to C57BL/6 control.
Upon treatment with leptin, ob/ob mice displayed diastolic dysfunction and partial reversal of eccentric hypertrophy, coincided with significant increase in pro-Collagen I1 and III1, suppression of pro-MMP-8, TIMP-1 and -3 gene expressions, and increase in myocardial collagen, compared to ob/ob controls. These data indicate the profibrotic effects of leptin in the heart, through increased collagen synthesis/degradation rate.
Free Fatty Acids: Role in Insulin Resistance/Type 2 Diabetes and Cardiovascular Disease
By G. Boden, and L.H. Carnell, Temple University School of Medicine, Philadelphia, PA, USA. Conference paper presented at the American Oil Chemists’ Society (AOCS) Symposium, May 2009. Theme: Fatty Acids in Health Promotion: Recent Developments.
Obesity is tightly linked with elevated plasma FFA levels, insulin resistance, low grade inflammation, endoplasmic reticulum (ER) stress and a greatly increased risk for ASVD (heart attacks, strokes and peripheral vascular disease). There are many causes for this association some of which have recently been elucidated. Among those, FFA have emerged as a major link between obesity and insulin resistance and type 2 diabetes. Most obese people have elevated plasma FFA levels and FFAs cause insulin resistance in skeletal muscle (by decreasing insulin stimulated glucose uptake) and in the liver (by decreasing insulin inhibition of glycogenolysis). The mechanisms involved include intracellular accumulation of diacylglycerol, activation of several serine/threonine kinases (including PKC, JNK, IKK, p38 MAPK) and decreased tyrosine phosphorylation of IRS 1/2 which causes inhibition of insulin signaling.
FFA also activate the proinflammatory and proatherogenic NFkB pathway resulting in synthesis and release of inflammatory cytokines (including TNF-a, IL-1b, IL-6, MCP-1) and strongly activate the tissue factor pathway of blood coagulation and, via hyperinsulinemia, activate several matrix metalloproteinases (such as MMP2, MMP9, MT1-MMP) known to be involved in development of acute coronary events. In addition, FFA and high fat diets have recently been found to produce ER stress which also (via activation of JNK) can produce insulin resistance and inflammation.
In conclusion, considerable progress has been made during the past ten years in our understanding of the mechanisms responsible for the 2-5 fold increase in ASVD risk in obese people.
