Abstract
Current guidelines recommend reducing the daily intake of dietary fats for the prevention of ischemic cardiovascular diseases (CVDs). Avoiding saturated fats while increasing the intake of mono- or polyunsaturated fatty acids has been for long time the cornerstone of dietary approaches in cardiovascular prevention, mainly due to the metabolic effects of these molecules. However, recently, this approach has been critically revised. The experimental evidence, in fact, supports the concept that the pro- or anti-inflammatory potential of different dietary fats contributes to atherogenic or anti-atherogenic cellular and molecular processes beyond (or in addition to) their metabolic effects. All these aspects are hardly translatable into clinics when trying to find connections between the pro-/anti-inflammatory potential of dietary lipids and their effects on CVD outcomes. Interventional trials, although providing stronger potential for causal inference, are typically small sample-sized, and they have short follow-up, noncompliance, and high attrition rates. Besides, observational studies are confounded by a number of variables and the quantification of dietary intakes is far from optimal. A better understanding of the anatomic and physiological barriers for the absorption and the players involved in the metabolism of dietary lipids (e.g., gut microbiota) might be an alternative strategy in the attempt to provide a first step towards a personalized dietary approach in CVD prevention.
Highlights
The favorable transition from hominids to homo sapiens during evolution [1] prompted changes in the physiological functions and immune competences to adapt to the intake of high-energy containing foods, principally dietary fats [2]
The dominant genetic pathways evolved to favor the intake of calorie-rich diets and the storage of energy as fats in the adipose tissue are in some circumstances redundant, especially in affluent societies, giving rise to obesity, diabetes and cardiovascular disease (CVD)-comorbidities
Fatty acids deriving from the hydrolysis of dietary triglycerides and phospholipids in the intestinal lumen are chaperoned to the intracellular endoplasmic reticulum (ER); there, diacylglycerol O-acyltransferase 1 (DGAT1) promotes their re-incorporation in triglycerides which are transferred by the microsomial triglyceride transfer protein (MTTP) to nascent apolipoprotein B
Summary
The favorable transition from hominids to homo sapiens during evolution [1] prompted changes in the physiological functions and immune competences (including survival to pathogens and infections) to adapt to the intake of high-energy containing foods, principally dietary fats [2]. Ruminococcus bromii, which is reduced in subjects with atherosclerosis [32], metabolizes complex carbohydrates (that are present in low-fat foods, including pinto beans, whole grains, and nuts with considerable proportion of fats) into propionate This SCFA promotes insulin sensitivity and reduces the atherosclerotic burden in mice [33]. Fatty acids deriving from the hydrolysis of dietary triglycerides and phospholipids in the intestinal lumen are chaperoned to the intracellular endoplasmic reticulum (ER); there, diacylglycerol O-acyltransferase 1 (DGAT1) promotes their re-incorporation in triglycerides which are transferred by the microsomial triglyceride transfer protein (MTTP) to nascent apolipoprotein B In this way, chylomicrons are released by the enterocytes in their basolateral membrane.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
