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Plasma Free Fatty Acid Concentration as a Modifiable Risk Factor for Metabolic Disease.
Henderson, GC
Nutrients. 2021;(8)
Abstract
Plasma free fatty acid (FFA) concentration is elevated in obesity, insulin resistance (IR), non-alcoholic fatty liver disease (NAFLD), type 2 diabetes (T2D), and related comorbidities such as cardiovascular disease (CVD). Furthermore, experimentally manipulating plasma FFA in the laboratory setting modulates metabolic markers of these disease processes. In this article, evidence is presented indicating that plasma FFA is a disease risk factor. Elevations of plasma FFA can promote ectopic lipid deposition, IR, as well as vascular and cardiac dysfunction. Typically, elevated plasma FFA results from accelerated adipose tissue lipolysis, caused by a high adipose tissue mass, adrenal hormones, or other physiological stressors. Reducing an individual's postabsorptive and postprandial plasma FFA concentration is expected to improve health. Lifestyle change could provide a significant opportunity for plasma FFA reduction. Various factors can impact plasma FFA concentration, such as chronic restriction of dietary energy intake and weight loss, as well as exercise, sleep quality and quantity, and cigarette smoking. In this review, consideration is given to multiple factors which lead to plasma FFA elevation and subsequent disruption of metabolic health. From considering a variety of medical conditions and lifestyle factors, it becomes clear that plasma FFA concentration is a modifiable risk factor for metabolic disease.
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El papel de los ácidos grasos libres en la resistencia a la insulina.
Vázquez-Jiménez, JG, Roura-Guiberna, A, Jiménez-Mena, LR, Olivares-Reyes, JA
Gaceta medica de Mexico. 2017;(7):852-863
Abstract
Free fatty acids are essential nutritional components and recent studies identified them as signaling molecules in various physiological processes. It has now been shown that high levels of free fatty acids, particularly saturated fatty acids, may be associated with insulin resistance in obese patients with type 2 diabetes mellitus. Insulin resistance is important in clinical since it is related to various diseases including type 2 diabetes mellitus, dyslipidemia, and abnormalities at cardiovascular level. Recent studies have proposed different molecular mechanisms by which these lipids may alter the signaling pathway of insulin. The purpose of this review is to highlight recent advances in the study of the effect of free fatty acids as modulators of insulin response.
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Acidemia and blood free fatty acids: analysis of cardiovascular risk factors in a new context.
Reis, AH
Discovery medicine. 2017;(126):183-188
Abstract
Following a hypothesis developed in an earlier paper, here it is discussed how deviations of blood pH from the normal range (namely states of acidemia) together with high blood levels of free fatty acids (FFA) may offer a rationale for many important risk factors for cardiovascular diseases (CVD) by shaping a context for formation of fatty acid micelles and vesicles with an acidic core, which fuse with the endothelia, disrupt vital cell processes, and thereby may initiate atherosclerotic plaque formation. Acidemia may arise primarily from dysregulation of the systemic buffers that control blood pH, chronic diseases of kidneys and lungs, inappropriate diet, or may be induced by some common drugs. The level of free fatty acids may be increased and maintained high by chronic stress, and adrenergic shocks. Elevated concentrations of blood FFA in a context of acidemia allow to understand important cardiovascular aspects: the increased risk of menopausal women, the protective effects of physical exercise, the changes in vascular behavior characteristic of metabolic acidosis/acidemia, the role of diet in the pH balance, on how some known medicines like metformin, steroids, NSAIDS, proton pump inhibitors, and calcium supplements may influence CVD risk, and an explanation is offered for the role of statins.
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[Free Fatty Acid Receptor Family: A New Therapeutic Target for Metabolic Diseases].
Hirasawa, A
Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan. 2015;(6):769-77
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Abstract
Free fatty acids (FFAs) are not only essential nutritional components but they also act as signaling molecules in various physiological processes. A strategy to deorphanize G-protein-coupled receptors (GPCRs) identified a series of receptors for FFAs that play significant roles in nutrition regulation. In this free fatty acid receptor family, FFAR1 (GPR40) and FFAR4 (GPR120) are activated by long-chain FFAs. FFAR1 regulates insulin secretion in pancreatic β-cells, whereas FFAR4 promotes the secretion of glucagon-like peptide-1 (GLP-1) in the intestine, and also acts as a lipid sensor in adipose tissue to sense dietary fat and control energy balance. In this review, we discuss recent advances in the pharmacological characterization of FFAR1 and FFAR4, and we present a summary of current understandings of their physiological roles and their potential as drug targets.
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Non-alcoholic fatty liver disease (NAFLD) and its connection with insulin resistance, dyslipidemia, atherosclerosis and coronary heart disease.
Gaggini, M, Morelli, M, Buzzigoli, E, DeFronzo, RA, Bugianesi, E, Gastaldelli, A
Nutrients. 2013;(5):1544-60
Abstract
Non-alcoholic fatty liver disease is marked by hepatic fat accumulation not due to alcohol abuse. Several studies have demonstrated that NAFLD is associated with insulin resistance leading to a resistance in the antilipolytic effect of insulin in the adipose tissue with an increase of free fatty acids (FFAs). The increase of FFAs induces mitochondrial dysfunction and development of lipotoxicity. Moreover, in subjects with NAFLD, ectopic fat also accumulates as cardiac and pancreatic fat. In this review we analyzed the mechanisms that relate NAFLD with metabolic syndrome and dyslipidemia and its association with the development and progression of cardiovascular disease.
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Origins of metabolic complications in obesity: adipose tissue and free fatty acid trafficking.
Mittendorfer, B
Current opinion in clinical nutrition and metabolic care. 2011;(6):535-41
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Abstract
PURPOSE OF REVIEW Obesity is associated with a number of serious medical complications that are risk factors for cardiovascular disease (e.g., insulin resistance, dyslipidemia, and liver fat accumulation). Alterations in fatty acid trafficking, both between tissues and within cells, represent a key feature in the pathophysiology of the metabolic complications in obese patients. The ways by which fatty acid 're-routing' may affect metabolic function are summarized in this article. RECENT FINDINGS Ectopic fat accumulation (i.e., fat accumulation in nonadipose tissues) appears to be a key feature distinguishing metabolically healthy from metabolically abnormal patients. This observation has led to the belief that an imbalance in fatty acid trafficking away from adipose tissue toward nonadipose tissues is a primary cause for the development of metabolic alterations in obese patients. More recently, however, it has become apparent that fatty acid trafficking within nonadipose tissues cells (i.e., toward storage - in the form of triglycerides - and oxidation) may be equally important in determining a person's risk for development of metabolic disease. SUMMARY The pathophysiology of the metabolic alterations associated with obesity is probably multifactorial within a complex network of coordinated physiological responses. Only through the integration of multiple concepts, will it be possible to further our understanding in this area and to help prevent the metabolic alterations associated with obesity.