Effect of weight loss on inflammatory and endothelial markers and FMD using two low-fat diets

Clifton, Peter M.; Keogh, Jennifer B.; Foster, Paul; Noakes, Manny

doi:10.1038/sj.ijo.0803039

Cited by 80 publications

(70 citation statements)

References 44 publications

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“…On the other hand, other studies have observed no effect or an increase in pro-inflammatory markers after a rapid and significant weight loss. 37,38,[47][48][49][50][51] These observations may, to some extent, explain why the smaller reductions in hs-CRP, IL-6 and fibrinogen after both periods with substantial body weight losses became more obvious when body weight was stabilized in the following maintenance period. An explanation for not finding clear evidence of an acute effect of weight loss may be that the positive effect of body fat reduction on hs-CPR, IL-6 and fibrinogen levels is counteracted by the negative energy balance, most likely due to an adverse effect on the liver of a high influx of portal-free fatty acids.…”

Section: Discussionmentioning

confidence: 84%

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

et al. 2009

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Aims:To dissociate the possible differential effects of negative energy balance and reduction in body fat mass (FM) on inflammatory markers: C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), haptoglobin, transferrin and the adipokines leptin and adiponectin. Methods: Thirty-three obese subjects (BMI: 34.0±3.1 kg/m 2 , age: 43.0±10.5 years, mean±s.d., 16 men) participated in a 20-week controlled dietary intervention divided into four periods. Weight reduction was induced by an 8-week low energy diet (3.4 MJ d À1 ) (LED-1) followed by a 4-week weight maintenance program (M-1). Subsequently participants underwent an additional 4-week LED (4.2 MJ d À1 ) (LED-2) followed by a final 4-week weight maintenance diet (M-2). Blood samples and anthropometrics were assessed at baseline and after LED-1, M-1, LED-2 and M-2. Results: Body weight was significantly reduced by 13% (13.7 ± 4.0 kg, Po0.0001) after LED-1. However, a reduction in highsensitive CRP (hs-CRP) by 35% (À1.1 (95% CI: À2.5:0.2) mg l À1 , P ¼ 0.02) only became apparent after LED-2, which produced an additional weight loss of 2.9 kg compared to baseline, and it was maintained after M-2 (À1.0 (À1.4:0.4) mg l À1 , P ¼ 0.02). Also IL-6 was reduced by 21% (À0.6 (À2.4:0.2) ng l À1 , P ¼ 0.02) after M-2. The reductions in hs-CRP and IL-6 were both associated with reduction in FM but not body weight. Haptoglobin, transferrin and leptin were significantly reduced after both LED-1 and LED-2, but increased during weight maintenance. Adiponectin was not significantly changed during the intervention. Conclusions: The results suggest that, whereas haptoglobin and transferrin respond more rapidly and are more susceptible to the acute change in energy balance, a reduction in hs-CRP and IL-6 seems to be achieved by a reduction in FM when a new steady state has been established.

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Section: Discussionmentioning

confidence: 84%

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

et al. 2009

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“…Previous studies have demonstrated that surgically induced weight loss is accompanied by an improvement of the endothelial function (18,19,21) and the proinflammatory state (18,(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). However, few studies have studied endothelial function and proinflammatory state together, and have considered different time-points to determine postsurgical changes.…”

Section: Introductionmentioning

confidence: 99%

“…Inflammation of the vascular wall causes endothelial cells to express a wide variety of endothelial adhesion molecules, including intracellular adhesion molecule-1. sICAM-1 can be regarded as a marker of both endothelial function and inflammation (11) that is associated with atherosclerotic progression (44) and its levels are increased in obesity (9,(14)(15)(16)(17)19). It has been suggested that sICAM-1 mediated endothelial dysfunction is stimulated by cytokines secreted by adipose tissue (45).…”

Section: All Data Are Presented As the Mean ± S Bmi Body Mass Indexmentioning

confidence: 99%

“…Disturbed endothelial function can be assessed by measuring the level of these molecules. The concentration of soluble intracellular adhesion molecule-1 (sICAM1) and plasminogen activator inhibitor 1 (PAI-1) have been shown to be the earliest markers of endothelial dysfunction (6,7) and there is evidence that these substances are increased in obese patients (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

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Obesity, endothelial function and inflammation: the effects of weight loss after bariatric surgery

Gómez¹,

Ortega²,

Aragón‐Alonso³

et al. 2016

Nutr Hosp

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Palabras clave:Obesidad. Cirugía bariátrica. Infl amación. Función endotelial. Resistencia a la insulina. ResumenObjetivo: la obesidad está asociada con un aumento del riesgo de enfermedad cardiovascular. Se ha propuesto una relación causal entre obesidad, infl amación, resistencia a la insulina, y disfunción endotelial. El objetivo de este estudio fue valorar marcadores de insulinorresistencia, infl amación y disfunción endotelial en pacientes con obesidad mórbida antes y después de la pérdida de peso por cirugía bariátrica. Métodos: se midieron las concentraciones séricas de moléculas solubles de adhesión intercelular tipo 1 (sICAM-1), inhibidor del activador del plasminógeno tipo 1 (PAI-1), proteína C reactiva de alta sensibilidad (hs-PCR) e interleucina 6 (IL-6) en 79 pacientes con obesidad mórbida antes y a los 3, 6 y 12 meses de la realización de un by-pass gástrico. También se evaluaron índices de resistencia a la insulina. Resultados: a los 12 meses de la cirugía disminuyeron los niveles de sICAM1 (p < 0,001), PAI-1 (p < 0,05), hs-CRP (p < 0,001), IL-6 (p < 0,001) y el índice homeostasis model assessment (HOMA) (p < 0,001) y aumentó el índice McAuley (p < 0,001). Los niveles basales de hs-PCR estaban correlacionados con los de sICAM-1 (r = 0,450, p < 0,01) y de IL-6 (r = 0,451, p < 0,01). También existía correlación entre el descenso de los niveles de PAI-1 y el descenso de hs-PCR (r = 0,425, p < 0,01) y triglicéridos (r = 0,351, p < 0,01). Conclusiones: en pacientes con obesidad mórbida una importante pérdida de peso por cirugía bariátrica se acompaña de una mejora signifi cativa de marcadores infl amatorios, de función endotelial e insulinorresistencia, lo que puede suponer una disminución del riesgo cardiovascular. Existe una relación entre mejora del perfi l infl amatorio y función endotelial. AbstractObjective: Obesity is associated with a high risk for atherosclerotic cardiovascular disease. There is a causal association between obesity, infl ammation, insulin resistance (IR) and endothelial dysfunction. The aim of this study was to evaluate changes in IR, proinfl ammatory state and markers of endothelial dysfunction in morbidly obese patients after weight loss following bariatric surgery. Methods: In this study, we measured the levels of soluble intracellular adhesion molecule-1 (sICAM1), plasminogen activator inhibitor 1 (PAI-1), high-sensitivity C-reactive protein (hs-CRP), and interleukin-6 (IL-6) in 79 morbidly obese patients at baseline and 3, 6 and 12 months after gastric bypass. Also, we evaluated changes in IR. Results: Twelve months after surgery, there was a signifi cant decrease in plasma levels of sICAM1 (p < 0.001), PAI-1 (p < 0.05), hs-CRP (p < 0.001), IL-6 (p < 0.001) and homeostasis model assessment (HOMA) (p < 0.001) and a signifi cant increase of McAuley index (McAuley) (p < 0.001). Baseline levels of hs-PCR were positively correlated with sICAM-1 (r = 0.450, p < 0.01) and IL-6 (r = 0.451, p < 0.01). Signifi cant correlations were also found between the decrease of PAI-1 and the ...

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“…Few studies to date have used biochemical assessment of endothelial activation (54,(56)(57)(58) , and although the limited available data suggest that even modest weight loss (7 . 3%) is accompanied by significant decreases in intercellular adhesion molecule, this clearly requires further confirmation.…”

Section: Weight Loss and Endothelial Functionmentioning

confidence: 99%

Endothelial dysfunction associated with obesity and the effect of weight loss interventions

et al. 2011

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Endothelial damage is central to the initiation and progression of atherosclerosis, while in addition vascular endothelial cells secrete several anti-atherogenic substances including the potent vasodilator nitric oxide. Increased adhesion molecule expression, in response to pathophysiological stimuli is perhaps the earliest indicator of compromised endothelial integrity. Obesity and adiposity are associated with an increased risk of CVD, influencing disease progression via a number of mechanisms, including enhanced endothelial activation. This review discusses possible mechanisms linking adiposity and more specifically regional fat depots with endothelial function and evaluates studies investigating the effect of weight loss on endothelial function, assessed by biochemical and physiological measurements. Overall, the research to date suggests that visceral adiposity is a stronger predictor of endothelial activation than overall adiposity, possibly mediated via the action of NEFA in circulation. While in general there is a suggestion that weight loss is associated with significant improvements in endothelial function, this is not apparent in all interventions and published literature to date provides less than convincing evidence for the effects of weight loss on endothelial activation.

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Effect of weight loss on inflammatory and endothelial markers and FMD using two low-fat diets

Cited by 80 publications

References 44 publications

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

Effect of diet-induced energy deficit and body fat reduction on high-sensitive CRP and other inflammatory markers in obese subjects

Obesity, endothelial function and inflammation: the effects of weight loss after bariatric surgery

Endothelial dysfunction associated with obesity and the effect of weight loss interventions

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