Macronutrient intake induces oxidative and inflammatory stress: potential relevance to atherosclerosis and insulin resistance

Dandona, Paresh; Ghanim, Husam; Chaudhuri, Ajay; Dhindsa, Sandeep; Kim, Sung Soo

doi:10.3858/emm.2010.42.4.033

Cited by 132 publications

(88 citation statements)

References 72 publications

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“…Lean mice in the diet-induced model are significantly heavier than lean mice in the db/db model (22.2 6 0.9 g versus 32.1 6 0.9 g; P , 0.0001), suggesting that differences in weight might affect BAL neutrophilia even in the "lean" groups. Diet composition, which differs substantially between models, also has been shown to alter the inflammatory response (40) and may contribute to the differences seen between models. Although we do not find a significant correlation between airspace neutrophilia and mouse age in our lung injury model, age has been shown to impair neutrophil chemotaxis response in mice and humans, independent of weight, through unclear mechanisms (41)(42)(43)(44)(45), and this may augment the defect in DIO neutrophils independent of CXCR2 expression levels.…”

Section: Discussionmentioning

confidence: 99%

Obesity Is Associated with Neutrophil Dysfunction and Attenuation of Murine Acute Lung Injury

Kordonowy

Burg²,

Lenox³

et al. 2012

Am J Respir Cell Mol Biol

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Although obesity is implicated in numerous health complications leading to increased mortality, the relationship between obesity and outcomes for critically ill patients appears paradoxical. Recent studies have reported better outcomes and lower levels of inflammatory cytokines in obese patients with acute lung injury (ALI)/acute respiratory distress syndrome, suggesting that obesity may ameliorate the effects of this disease. We investigated the effects of obesity in leptin-resistant db/db obese and diet-induced obese mice using an inhaled LPS model of ALI. Obesity-associated effects on neutrophil chemoattractant response were examined in bone marrow neutrophils using chemotaxis and adoptive transfer; neutrophil surface levels of chemokine receptor CXCR2 were determined by flow cytometry. Airspace neutrophilia, capillary leak, and plasma IL-6 were all decreased in obese relative to lean mice in established lung injury (24 h). No difference in airspace inflammatory cytokine levels was found between obese and lean mice in both obesity models during the early phase of neutrophil recruitment (2-6 h), but early airspace neutrophilia was reduced in db/db obese mice. Neutrophils from uninjured obese mice demonstrated diminished chemotaxis to the chemokine keratinocyte cytokine compared with lean control mice, and adoptive transfer of obese mouse neutrophils into injured lean mice revealed a defect in airspace migration of these cells. Possibly contributing to this defect, neutrophil CXCR2 expression was significantly lower in obese db/db mice, and a similar but nonsignificant decrease was seen in diet-induced obese mice. ALI is attenuated in obese mice, and this blunted response is in part attributable to an obesity-associated abnormal neutrophil chemoattractant response.Keywords: adult respiratory distress syndrome; chemotaxis; cytokines; innate immunity Acute lung injury (ALI) and the acute respiratory distress syndrome (ARDS) are characterized by persistent, uncontrolled pulmonary inflammation that occurs in response to a wide range of insults, including pneumonia, sepsis, and trauma (1, 2). Alveolar recruitment of neutrophils is thought to be a central factor in the onset and progression of this syndrome (3, 4), and increases in airspace neutrophilia and plasma neutrophilic cytokine levels, including TNF-a, IL-1b, IL-6, and IL-8, are associated with increased morbidity and mortality from this disease (4-6). It is increasingly recognized that ALI pathogenesis and outcome are strongly influenced by host factors, including genetic polymorphisms and comorbid conditions (1, 2). Preliminary clinical evidence suggests that obesity may have an ameliorative effect on ALI outcome (7). Although ambiguity exists in smaller studies (8, 9), recent large cohort studies from our group and others, as well as several metaanalyses, have shown a reduction in mortality with rising body mass index in ALI and critical illness in general (7,(10)(11)(12)(13)(14)(15)(16). Such an association, though tentative, is surprising because obesity...

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Section: Discussionmentioning

confidence: 99%

Obesity Is Associated with Neutrophil Dysfunction and Attenuation of Murine Acute Lung Injury

Kordonowy

Burg²,

Lenox³

et al. 2012

Am J Respir Cell Mol Biol

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“…Excessive food intake increases the amount of energy and nutrients in the blood stream. 23 Lipoxidation products include malondialdehyde, glyoxal, acrolein, 4-hydroxy-nonenal (HNE), while the products generated from glycation include glyoxal and methyl glyoxal. These compounds bind to the amino grouping of amino acids, resulting in advanced glycation end-products (AGEs) and advanced lipoxidation end--products (ALEs), 24 which are highly reactive and participate in the development of other components of MetS.…”

Section: Metabolic Syndrome and Oxidative Stressmentioning

confidence: 99%

The role of oxidative stress on the pathophysiology of metabolic syndrome

Francisqueti

Chiaverini

Santos

et al. 2017

Rev. Assoc. Med. Bras.

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The role of oxidaTive sTress on The paThophysiology of meTabolic syndrome rev assoc Med Bras 2017; 63(1):85-91 85 REVIEW ARTICLEThe role of oxidative stress on the pathophysiology of metabolic syndrome Metabolic syndrome (MetS) has a high prevalence around the world. Considering the components used to classify MetS, it is clear that it is closely related to obesity. These two conditions begin with an increase in abdominal adipose tissue, which is metabolically more active, containing a greater amount of resident macrophages compared to other fat deposits. Abdominal adiposity promotes inflammation and oxidative stress, which are precursors of various complications involving MetS components, namely insulin resistance, hypertension and hyperlipidemia. One way to block the effects of oxidative stress would be through the antioxidant defense system, which offsets the excess free radicals. It is known that individuals with metabolic syndrome and obesity have high consumption of fats and sugars originated from processed foods containing high levels of sodium as well as low intake of fruits and vegetables, thus maintaining a state of oxidative stress, that can speed up the onset of MetS. Healthy eating habits could prevent or delay MetS by adding antioxidant-rich foods into the diet.

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“…Systemic inflammation linked to dietary fat intake may underlie these associations. [64][65][66] Omega-6 fatty acids, including arachidonic acid (20:4 n-6) and linoleic acid (18:2 n-6), mediate inflammation, 67 whereas omega-3 fatty acids, including eicosapentaenoic acid (20:5 n-3) and docosahexaenoic acid (22:6 n-3), Truncal adiposity and general adiposity were associated with reduced FRC, RV, and RV/TLC ratio.…”

Section: Diet and Asthmamentioning

confidence: 99%

Pediatric Obesity-Related Asthma: The Role of Metabolic Dysregulation

2016

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The burden of obesity-related asthma among children, particularly among ethnic minorities, necessitates an improved understanding of the underlying disease mechanisms. Although obesity is an independent risk factor for asthma, not all obese children develop asthma. Several recent studies have elucidated mechanisms, including the role of diet, sedentary lifestyle, mechanical fat load, and adiposity-mediated inflammation that may underlie the obese asthma pathophysiology. Here, we review these recent studies and emerging scientific evidence that suggest metabolic dysregulation may play a role in pediatric obesity-related asthma. We also review the genetic and epigenetic factors that may underlie susceptibility to metabolic dysregulation and associated pulmonary morbidity among children. Lastly, we identify knowledge gaps that need further exploration to better define pathways that will allow development of primary preventive strategies for obesity-related asthma in children.

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Macronutrient intake induces oxidative and inflammatory stress: potential relevance to atherosclerosis and insulin resistance

Cited by 132 publications

References 72 publications

Obesity Is Associated with Neutrophil Dysfunction and Attenuation of Murine Acute Lung Injury

Obesity Is Associated with Neutrophil Dysfunction and Attenuation of Murine Acute Lung Injury

The role of oxidative stress on the pathophysiology of metabolic syndrome

Pediatric Obesity-Related Asthma: The Role of Metabolic Dysregulation

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