Effects of Lifestyle Measures, Antiobesity Agents, and Bariatric Surgery on Serological Markers of Inflammation in Obese Patients

Τζιόμαλος, Κωνσταντίνος; Dimitroula, Hariklia; Katsiki, Niki; Savopoulos, Christos; Hatzitolios, Apostolos

doi:10.1155/2010/364957

Cited by 26 publications

(14 citation statements)

References 196 publications

(300 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nevertheless, significant weight reduction via change in diet (Breum et al , 2003) or bariatric surgery (Brandacher et al , 2006) has not been shown to restore tryptophan balance. This in part may be related to a relative lack of change in inflammatory factors after rapid weight loss (Brandacher et al , 2006), although more delayed responses may be seen (Tziomalos et al , 2010). Therefore, the immune activation found in obesity may contribute to the same diversion of tryptophan metabolism from serotonin to kynurenine, which could contribute to depression.…”

Section: 0 Inflammation and Depressionmentioning

confidence: 99%

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

Shelton

Miller

2010

Progress in Neurobiology

212

148

View full text Add to dashboard Cite

Obesity and related metabolic conditions are of epidemic proportions in most of the world, affecting both adults and children. The accumulation of lipids in the body in the form of white adipose tissue in the abdomen is now known to activate innate immune mechanisms. Lipid accumulation causes adipocytes to directly secrete the cytokines interleukin (IL) 6 and tumor necrosis factor α (TNFα), but also monocyte chemoattractant protein 1 (MCP-1), which results in the accumulation of leukocytes in fat tissue. This sets up a chronic inflammatory state which is known to mediate the association between obesity and conditions such as cardiovascular disease, type 2 diabetes, and cancer. There is also a substantial literature linking inflammation with risk for depression. This includes the observations that: 1. People with inflammatory diseases such as multiple sclerosis, cardiovascular disease, and psoriasis have elevated rates of depression; 2. Many people administered inflammatory cytokines such as interferon α develop depression that is indistinguishable from depression in non-medically ill populations; 3. A significant proportion of depressed persons show upregulation of inflammatory factors such as IL-6, C-reactive protein, and TNFα; and 4) Inflammatory cytokines can interact with virtually every pathophysiologic domain relevant to depression, including neurotransmitter metabolism, neuroendocrine function, and synaptic plasticity. While many factors may contribute to the association between inflammatory mediators and depression, we hypothesize that increased adiposity may be one causal pathway. Mediational analysis suggests a bi-directional association between adiposity and depression, with inflammation possibly playing an intermediary role.

show abstract

Section: 0 Inflammation and Depressionmentioning

confidence: 99%

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

Shelton

Miller

2010

Progress in Neurobiology

212

148

View full text Add to dashboard Cite

show abstract

“…90 Inflammatory mediators (hs-CRP, IL-6, IL-18) As mentioned above, obese PCOS patients have high levels of proinflammatory mediators, such as high sensitive C-reactive protein (hs-CRP), interleukin 6 (IL-6) and IL-18, which make them vulnerable to an increased risk of non-alcoholic fatty liver disease (NAFLD). 91 C-reactive protein (hs-CRP), one of the acute phase proteins known as a vascular inflammatory marker, rises dramatically in response to inflammation due to an increase in the circulating level of interleukin 6 (IL-6), which is produced mainly by macrophages and adipocytes. The level of hs-CRP is significantly elevated in PCOS patients.…”

Section: Leukotriene Metabolism Related Genes Alox15 Fem1a Fem1bmentioning

confidence: 99%

“…91 C-reactive protein (hs-CRP), one of the acute phase proteins known as a vascular inflammatory marker, rises dramatically in response to inflammation due to an increase in the circulating level of interleukin 6 (IL-6), which is produced mainly by macrophages and adipocytes. The level of hs-CRP is significantly elevated in PCOS patients.…”

mentioning

confidence: 99%

Systematic review: association of polycystic ovary syndrome with metabolic syndrome and non-alcoholic fatty liver disease

Baranova

Tran

Birerdinc

et al. 2011

Alimentary Pharmacology &Amp; Therapeutics

131

View full text Add to dashboard Cite

Aliment Pharmacol Ther 2011; 33: 801–814 Summary Background Polycystic ovary syndrome (PCOS) is a common disorder for women of child‐bearing age and is associated with metabolic syndrome (MS). Aim To assess the literature for associations between polycystic ovary syndrome and non‐alcholic fatty liver disease (NAFLD). Methods We performed a systematic review using PubMed‐search for peer‐reviewed articles related to polycystic ovary syndrome and NAFLD. Articles were summarised and grouped according to different sections defining interactions of polycystic ovary syndrome with metabolic syndrome and non‐alcholic fatty liver disease as well as risk factors, pathogenic pathways and treatment options. Results Obesity is a common factor involved in both polycystic ovary syndrome and non‐alcholic fatty liver disease. Obesity causes non‐alcholic fatty liver disease and aggravates hirsutism and menstrual disorders in polycystic ovary syndrome. Insulin resistance, a hallmark of metabolic syndrome is observed in 50–80% of women with polycystic ovary syndrome and patients with non‐alcholic fatty liver disease. Recent findings suggest that women with polycystic ovary syndrome may be at risk for developing non‐alcholic fatty liver disease and conversely, non‐alcholic fatty liver disease may be a risk for polycystic ovary syndrome. Based on the association of polycystic ovary syndrome and other metabolic abnormalities, such as insulin resistance, hyperandrogenism, obesity and non‐alcholic fatty liver disease, the candidate genes have been speculated for polycystic ovary syndrome. Closer scrutiny of these genes placed most of their proteins at the crossroads of three highly inter‐related conditions: metabolic syndrome, obesity and non‐alcholic fatty liver disease. In most studies, the prevalence of both polycystic ovary syndrome and non‐alcholic fatty liver disease rises proportionally to the degree of insulin resistance and increases in the mass of adipose tissue. Conclusions Non‐alcholic fatty liver disease is considered as the hepatic manifestation of metabolic syndrome. Similarly, it seems appropriate to consider polycystic ovary syndrome as the ovarian manifestation of metabolic syndrome. Both these conditions can co‐exist and may respond to similar therapeutic strategies.

show abstract

“…obesity reviews Adipose tissue, triglycerides and atherosclerosis A. P. van de Woestijne et al 835 lifestyle factors such as diet, physical activity and weight reduction, is of vital importance in these patients. Besides lifestyle measures, anti-obesity agents and bariatric surgery have all been reported to reduce inflammatory markers, indicating improved adipose tissue function (79).…”

Section: Management Of Obesity-induced Hypertriglyceridemiamentioning

confidence: 99%

Adipose tissue dysfunction and hypertriglyceridemia: mechanisms and management

et al. 2011

View full text Add to dashboard Cite

Elevated plasma triglyceride levels, as often seen in obese subjects, are independently associated with an increased risk of cardiovascular diseases. By secreting adipokines (such as adiponectin and leptin) and other proteins (such as lipoprotein lipase and cholesteryl ester transferase protein), adipose tissue affects triglyceride metabolism. In obesity, adipocyte hypertrophy leads to many changes in adipocyte function and production of anti- and pro-inflammatory cytokines. Furthermore, free fatty acids are released into the circulation contributing to insulin resistance. Adipose tissue dysfunction will eventually lead to abnormalities in lipid metabolism, such as hypertriglyceridemia (due to increased hepatic very-low-density lipoprotein production and decreased triglyceride hydrolysis), small dense low-density lipoprotein particles, remnant lipoproteins and low high-density lipoprotein cholesterol levels, all associated with a higher risk for the development of cardiovascular diseases. The clinical implications of elevated plasma triglycerides are still a matter of debate. Understanding the pathophysiology of adipose tissue dysfunction in obesity, which is becoming a pandemic condition, is essential for designing appropriate therapeutic interventions. Lifestyle changes are important to improve adipose tissue function in obese patients. Pharmacological interventions to improve adipose tissue function need further evaluation. Although statins are not very potent in reducing plasma triglycerides, they remain the mainstay of therapy for cardiovascular risk reduction in high-risk patients.

show abstract

Effects of Lifestyle Measures, Antiobesity Agents, and Bariatric Surgery on Serological Markers of Inflammation in Obese Patients

Cited by 26 publications

References 196 publications

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

Eating ourselves to death (and despair): The contribution of adiposity and inflammation to depression

Systematic review: association of polycystic ovary syndrome with metabolic syndrome and non-alcoholic fatty liver disease

Adipose tissue dysfunction and hypertriglyceridemia: mechanisms and management

Contact Info

Product

Resources

About