Effect of weight loss with or without orlistat treatment on adipocytokines, inflammation, and oxidative markers in obese women

Bougoulia, Maria; Triantos, A.; Koliakos, George

doi:10.14310/horm.2002.11190

Cited by 80 publications

(75 citation statements)

References 61 publications

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“…Increased adiposity is associated with lower adiponectin levels and greater inflammation and insulin resistance, and reduction in adipose tissue mass reverses the changes (65)(66)(67)(68)(69). However, reduction of adipose tissue and preventing its regain are challenging.…”

Section: Discussionmentioning

confidence: 99%

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

et al. 2008

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OBJECTIVE-Experimental infection of rats with human adenovirus type 36 (Ad-36) promotes adipogenesis and improves insulin sensitivity in a manner reminiscent of the pharmacologic effect of thiozolinediones. To exploit the potential of the viral proteins as a therapeutic target for treating insulin resistance, this study investigated the ability of Ad-36 to induce metabolically favorable changes in human adipose tissue. RESEARCH DESIGN AND METHODS-We determinedwhether Ad-36 increases glucose uptake in human adipose tissue explants. Cell-signaling pathways targeted by Ad-36 to increase glucose uptake were determined in the explants and human adipose-derived stem cells. Ad-2, a nonadipogenic human adenovirus, was used as a negative control. As a proof of concept, nondiabetic and diabetic subjects were screened for the presence of Ad-36 antibodies to ascertain if natural Ad-36 infection predicted improved glycemic control.RESULTS-Ad-36 increased glucose uptake by adipose tissue explants obtained from nondiabetic and diabetic subjects. Without insulin stimulation, Ad-36 upregulated expressions of several proadipogenic genes, adiponectin, and fatty acid synthase and reduced the expression of inflammatory cytokine macrophage chemoattractant protein-1 in a phosphotidylinositol 3-kinase (PI3K)-dependent manner. In turn, the activation of PI3K by Ad-36 was independent of insulin receptor signaling but dependent on Ras signaling recruited by Ad-36. Ad-2 was nonadipogenic and did not increase glucose uptake. Natural Ad-36 infection in nondiabetic and diabetic subjects was associated with significantly lower fasting glucose levels and A1C, respectively. CONCLUSIONS-Ad-36 proteins may provide novel therapeutic targets that remodel human adipose tissue to a more metabolically favorable profile.

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Section: Discussionmentioning

confidence: 99%

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

et al. 2008

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“…It has been shown consistently that insulin resistance, leptin and TNF-α levels decreased (17,43) and adiponectin increased (27) with weight reduction. Also, levels of CRP, a low grade inflammatory marker, fall with weight reduction obtained by a non-pharmaceutical approach (44).…”

Section: Discussionmentioning

confidence: 99%

“…Obese subjects typically are in proinflammatory state that may predispose them to acute cardiovascular morbidity and mortality (16)(17)(18). Elevated circulating levels of cytokines and inflammatory markers, such as interleukin-6 (IL-6), C-reactive protein (hsCRP) and tumor necrosis factor-alpha (TNF-α) have been implicated to play role in the obesity (16,19,21,22).…”

Section: Introductionmentioning

confidence: 99%

Cardiac valve evaluation and adipokine levels in obese women treated with sibutramine

Sarac¹,

Saraç²

2010

Anadolu Kardiyol Derg

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Cardiac valve evaluation and adipokine levels in obese women treated with sibutramine ABS TRACTObjective: The aims of present study were 1) to evaluate cardiac valve characteristics, 2) to determine the plasma concentrations of fibrinogen, high sensitivity C-reactive protein (hsCRP), adiponectin, and tumor necrosis factor-α (TNF-α) in the obese women before and after 19 months sibutramine treatment in the obese women. Methods: Sixty obese women were enrolled in this prospective, randomized study. Thirty women received 10 mg once daily dose of sibutramine for 19 months. The rest of the obese women received 15 mg once daily dose of sibutramine for 19 months. All patients were evaluated with echocardiography. Plasma levels of adiponectin and TNF-α were measured by enzyme-linked immunosorbent assay (ELISA) and hsCRP by immunoturbimetric assay. Student paired and unpaired t tests were used to compare the 10 mg or 15 mg dose sibutramine effects either in groups or between the groups. Results: There were no signs of significant regurgitation or thickening of the mitral and aortic valves on echocardiographic evaluation performed after 19 months of treatment. Parameters of systolic function after 10 or 15 mg treatment were not different from pretreatment characteristics. Minimal tricuspid regurgitation was found in one (1/27) patient treated with 10 mg sibutramine after 19 months. Among obese patients treated with 15 mg sibutramine one patient (1/28) had minimal mitral valve regurgitation and 2 patients (2/28) had minimal aortic insufficiency. Stage II diastolic dysfunction in the 15 obese treated with 15 mg regressed to stage I diastolic dysfunction (50%). Stage II diastolic dysfunction in the 10 obese treated with 10 mg regressed to stage I diastolic dysfunction (33.3%). Mean levels of TNF-α(p=0.04), fibrinogen (p=0.03) and hsCRP (p=0.04)i decreased and adiponectin (p=0.03) levels increased in the obese treated with 10 mg sibutramine. Likewise, in the patients treated with 15 mg sibutramine, mean levels of TNF-α(p=0.01), fibrinogen (p= 0.02), and hsCRP (p= 0.04) decreased and adiponectin (p= 0.02) levels increased. Conclusion: Nineteen months of sibutramine treatment does not affect heart valve and systolic functions, however, diastolic dysfunction severity reduced with sibutramine treatment. Also In addition, mean levels of adiponectin, TNF-α, fibrinogen and hs-CRP change with 19 months sibutramine treatment. (Anadolu Kardiyol Derg 2010; 10: 226-32)

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“…TNF-α promotes prooncogenic pathways, which specifically involve nuclear factor kB, c-Jun amino acid-terminal kinase (JNK), and mammalian target of rapamycin complex (mTOR) [25,26] . Obesity is associated with increased IL-6 levels, while weight loss reduces levels of TNF-α and IL-6, resulting in a decreased inflammatory and potentially carcinogenic response [27] . Prolonged upregulation of the IL-6/STAT3 axis results in an increased probability that hepatocytes that have already acquired oncogenic mutations from exposure to carcinogens will continue malignant transformation [28] .…”

Section: Mechanisms Underlying Nash-related Hccmentioning

confidence: 99%

Advances in hepatocellular carcinoma: Nonalcoholic steatohepatitis-related hepatocellular carcinoma

Khan

Perumpail

Wong

et al. 2015

WJH

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An increase in the prevalence of obesity and diabetes mellitus has been associated with the rise in non alcoholic fatty liver disease (NAFLD). Twothirds of the obese and diabetic populations are estimated to develop NAFLD. Currently, NAFLD is the most common etiology for chronic liver disease globally. The clinical spectrum of NAFLD ranges from simple steatosis, an accumulation of fat greater than 5% of liver weight, to nonalcoholic steatohepatitis (NASH), a more aggressive form with necroinflammation and fibrosis. Among the patients who develop NASH, up to 20% may advance to cirrhosis and are at risk for complications of endstage liver disease. One of the major complications observed in patients with NASHrelated cirrhosis is hepatocellular carcinoma (HCC), which has emerged as the sixth most common cancer and second leading etiology of cancerrelated deaths worldwide. The incidence of HCC in the United States alone has tripled over the last three decades. In addition, emerging data are suggesting that a small proportion of patients with NAFLD may be at higher risk for HCC in the absence of cirrhosis implicating obesity and diabetes mellitus as potential risk factors for HCC. Core tip: The worldwide rise in overweight and obesity has been associated with increasing rates of nonalcoholic fatty liver disease (NAFLD), which is now the most common etiology of chronic liver disease.

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Effect of weight loss with or without orlistat treatment on adipocytokines, inflammation, and oxidative markers in obese women

Cited by 80 publications

References 61 publications

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Metabolically Favorable Remodeling of Human Adipose Tissue by Human Adenovirus Type 36

Cardiac valve evaluation and adipokine levels in obese women treated with sibutramine

Advances in hepatocellular carcinoma: Nonalcoholic steatohepatitis-related hepatocellular carcinoma

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