Is omega-3 key to unlocking inflammation in obesity?

White, Phillip J.; Marette, André

doi:10.1007/s00125-006-0346-9

Cited by 26 publications

(19 citation statements)

References 30 publications

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“…In this regard, TNF-␣ reduces PPAR␥ activity while IL-6 increases PPAR␥ expression (35). Moreover, earlier studies had reported the anti-inflammatory effects of PPAR␥ (9,23,28,44), which also suppresses NF-B activation (4) and induces adiponectin expression and secretion (23,24). It is conceivable that increased levels of TNF-␣ in adipose tissue of obese subjects activates NF-B and at the same time downregulates PPAR␥-induced adiponectin production.…”

Section: Discussionmentioning

confidence: 95%

Regulation of adiponectin production by insulin: interactions with tumor necrosis factor-α and interleukin-6

Hajri

Huan

Wattacheril

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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Obesity is often associated with insulin resistance, low-grade systemic inflammation, and reduced plasma adiponectin. Inflammation is also increased in adipose tissue, but it is not clear whether the reductions of adiponectin levels are related to dysregulation of insulin activity and/or increased proinflammatory mediators. In this study, we investigated the interactions of insulin, tumor necrosis factor-α (TNF-α) and interleukin 6 (IL-6) in the regulation of adiponectin production using in vivo and in vitro approaches. Plasma adiponectin and parameters of insulin resistance and inflammation were assessed in a cohort of lean and obese insulin-resistant subjects. In addition, the effect of insulin was examined in vivo using the hyperinsulinemic-euglycemic clamp, and in adipose tissue (AT) cultures. Compared with lean subjects, the levels of total adiponectin, and especially the high-molecular-weight (HMW) isomer, were abnormally low in obese insulin-resistant subjects. The hyperinsulinemic clamp data confirmed the insulin-resistant state in the obese patients and showed that insulin infusion significantly increased the plasma adiponectin in lean but not obese subjects (P < 0.01). Similarly, insulin increased total adiponectin release from AT explants of lean and not obese subjects. Moreover, expression and secretion of TNF-α and IL-6 increased significantly in AT of obese subjects and were negatively associated with expression and secretion of adiponectin. In 3T3-L1 and human adipocyte cultures, insulin strongly enhanced adiponectin expression (2-fold) and secretion (3-fold). TNF-α, and not IL-6, strongly opposed the stimulatory effects of insulin. Intriguingly, the inhibitory effect of TNF-α was especially directed toward the HMW isomer of adiponectin. In conclusion, these studies show that insulin upregulates adiponectin expression and release, and that TNF-α opposes the stimulatory effects of insulin. A combination of insulin resistance and increased TNF-α production could explain the decline of adiponectin levels and alterations of isomer composition in plasma of obese insulin-resistant subjects.

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Section: Discussionmentioning

confidence: 95%

Regulation of adiponectin production by insulin: interactions with tumor necrosis factor-α and interleukin-6

Hajri

Huan

Wattacheril

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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“…Both clinical and experimental studies have shown that omega-3 PUFA have anti-inflammatory effects particularly on cardiovascular and gastrointestinal systems [24][25][26][27]. Fish oil exerts its anti-inflammatory function, at least in part, by altering serum leptin and adiponectin levels [28][29][30]. Thus, the aim of this study was to demonstrate the effect of fish oil on adipokine levels and pancreatitis severity.…”

Section: Introductionmentioning

confidence: 95%

Acute Pancreatitis in Obesity: Adipokines and Dietary Fish Oil

et al. 2011

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“…It was observed that treatment of obese subjects with n-3 PUFA led to reduced circulating levels of pro-inflammatory cytokines and acute phase proteins [14]. In vitro and in vivo studies have revealed that these positive actions of n-3 PUFA at least partially are connected with their influence on metabolism and secretory functions of adipose tissue [15].…”

Section: Introductionmentioning

confidence: 99%

The influence of EPA and DHA on markers of inflammation in 3T3-L1 cells at different stages of cellular maturation

et al. 2014

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BackgroundEPA and DHA have been reported to have anti-obesity and anti-inflammatory properties. Recent studies revealed that these positive actions of n-3 PUFA at least partially are connected with their influence on metabolism and secretory functions of the adipose tissue. However, their impact on old adipocytes is still poorly understood. Therefore the aim of the present study was to evaluate the influence of EPA and DHA on markers of inflammation in 3T3-L1 cells at different stages of cellular maturation.MethodsYoung, mature and old differentiated 3T3-L1 adipocytes were cultured for 48 h in the presence of 100 μM EPA, or 50 μM DHA complexed to albumin, whereas in control conditions only albumin was added to the medium. The Oil Red O staining was used to confirm adipocytes differentiation, and measure triglycerides content in cells. The concentration of adipokines (interleukin 6, adiponectin and leptin) in conditioned media was measured using mouse-specific ELISA kits.ResultsThe fat accumulation in 3T3-L1 adipocytes was positively correlated with their age; however, EPA and DHA did not affect lipid accumulation on any stage of maturation. EPA and DHA increased the concentration of secreted adiponectin when compared with control, but only in the case of young adipocytes (58% and 35%, respectively). Moreover, EPA supplementation increased interleukin 6 concentration in conditioned medium, while DHA exerted an opposite effect on all stages of cellular maturation. Furthermore, EPA treatment increased leptin release from young cells, while DHA did not affect the secretion of this adipokine. In mature 3T3-L1 adipocytes both experimental factors decreased synthesis of leptin; however, in old cells no impact of these PUFA was noted.ConclusionsIn summary, age is an important determinant of fat accumulation in adipocytes and affects adipokines secretion by these cells. Moreover, the impact of investigated fatty acids: EPA and DHA on fat cells varies depending on the stage of maturation, and seems to be stronger in young cells than in mature and old ones. Docosahexaenoic acid exerts an anti-inflammatory action; however, on the basis of the obtained data it was not possible to determine whether eicosapentaenoic acid shows anti- or pro-inflammatory properties.

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Is omega-3 key to unlocking inflammation in obesity?

Cited by 26 publications

References 30 publications

Regulation of adiponectin production by insulin: interactions with tumor necrosis factor-α and interleukin-6

Regulation of adiponectin production by insulin: interactions with tumor necrosis factor-α and interleukin-6

Acute Pancreatitis in Obesity: Adipokines and Dietary Fish Oil

The influence of EPA and DHA on markers of inflammation in 3T3-L1 cells at different stages of cellular maturation

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