scholarly journals Omega-3 Fatty Acids and Insulin Resistance: Focus on the Regulation of Mitochondria and Endoplasmic Reticulum Stress

Nutrients ◽  
2018 ◽  
Vol 10 (3) ◽  
pp. 350 ◽  
Author(s):  
Marilena Lepretti ◽  
Stefania Martucciello ◽  
Mario Burgos Aceves ◽  
Rosalba Putti ◽  
Lillà Lionetti
2019 ◽  
Vol 38 (5) ◽  
pp. 2087-2097 ◽  
Author(s):  
Maricela Rodríguez-Cruz ◽  
Salvador Atilano-Miguel ◽  
Lourdes Barbosa-Cortés ◽  
Mariela Bernabé-García ◽  
Tomas Almeida-Becerril ◽  
...  

2019 ◽  
Vol 6 (1) ◽  
pp. 1796-1803
Author(s):  
Rashmi S. Chouthe ◽  
◽  
Santosh D Shelke ◽  
Rahul P. Kshirsagar ◽  
◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (1) ◽  
pp. 223
Author(s):  
Kassandra Lanchais ◽  
Frederic Capel ◽  
Anne Tournadre

Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by a high prevalence of death due to cardiometabolic diseases. As observed during the aging process, several comorbidities, such as cardiovascular disorders (CVD), insulin resistance, metabolic syndrome and sarcopenia, are frequently associated to RA. These abnormalities could be closely linked to alterations in lipid metabolism. Indeed, RA patients exhibit a lipid paradox, defined by reduced levels of total, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol whereas the CVD risk is increased. Moreover, the accumulation of toxic lipid mediators (i.e., lipotoxicity) in skeletal muscles can induce mitochondrial dysfunctions and insulin resistance, which are both crucial determinants of CVD and sarcopenia. The prevention or reversion of these biological perturbations in RA patients could contribute to the maintenance of muscle health and thus be protective against the increased risk for cardiometabolic diseases, dysmobility and mortality. Yet, several studies have shown that omega 3 fatty acids (FA) could prevent the development of RA, improve muscle metabolism and limit muscle atrophy in obese and insulin-resistant subjects. Thereby, dietary supplementation with omega 3 FA should be a promising strategy to counteract muscle lipotoxicity and for the prevention of comorbidities in RA patients.


2015 ◽  
Vol 36 (3) ◽  
pp. 245-271 ◽  
Author(s):  
Licio A. Velloso ◽  
Franco Folli ◽  
Mario J. Saad

Abstract Obesity is accompanied by the activation of low-grade inflammatory activity in metabolically relevant tissues. Studies have shown that obesity-associated insulin resistance results from the inflammatory targeting and inhibition of key proteins of the insulin-signaling pathway. At least three apparently distinct mechanisms–endoplasmic reticulum stress, toll-like receptor (TLR) 4 activation, and changes in gut microbiota–have been identified as triggers of obesity-associated metabolic inflammation; thus, they are expected to represent potential targets for the treatment of obesity and its comorbidities. Here, we review the data that place TLR4 in the center of the events that connect the consumption of dietary fats with metabolic inflammation and insulin resistance. Changes in the gut microbiota can lead to reduced integrity of the intestinal barrier, leading to increased leakage of lipopolysaccharides and fatty acids, which can act upon TLR4 to activate systemic inflammation. Fatty acids can also trigger endoplasmic reticulum stress, which can be further stimulated by cross talk with active TLR4. Thus, the current data support a connection among the three main triggers of metabolic inflammation, and TLR4 emerges as a link among all of these mechanisms.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Mardia López-Alarcón ◽  
Otilia Perichart-Perera ◽  
Samuel Flores-Huerta ◽  
Patricia Inda-Icaza ◽  
Maricela Rodríguez-Cruz ◽  
...  

Background.Low-grade inflammation is the link between obesity and insulin resistance. Because physiologic insulin resistance occurs at puberty, obese pubertal children are at higher risk for insulin resistance. Excessive diets in refined carbohydrates and saturated fats are risk factors for insulin resistance, but calcium, magnesium, vitamin-D, and the omega-3 fatty acids likely protect against inflammation and insulin resistance.Objective.To analyze interactions among dietary saturated fat, refined carbohydrates, calcium, magnesium, vitamin D, and omega-3 fatty acids on the risk of inflammation and insulin resistance in a sample of prepubertal and pubertal children.Methods.A sample of 229 children from Mexico City was analyzed in a cross-sectional design. Anthropometric measurements, 24 h recall questionnaires, and blood samples were obtained. Serum insulin, glucose, calcium, magnesium, 25-OHD3, C-reactive protein, leptin, adiponectin, and erythrocytes fatty acids were measured. Parametric and nonparametric statistics were used for analysis.Results.While mean macronutrients intake was excessive, micronutrients intake was deficient(P<0.01). Inflammation determinants were central obesity and magnesium-deficient diets. Determinants of insulin resistance were carbohydrates intake and circulating magnesium and adiponectin.Conclusions.Magnesium-deficient diets are determinants of inflammation, while high intake of refined carbohydrates is a risk factor for insulin resistance, independently of central adiposity.


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