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      Quantitative Assessment of Visceral Obesity and Postoperative Colon Cancer Outcomes

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          Abstract

          <div class="section"> <a class="named-anchor" id="S1"> <!-- named anchor --> </a> <h5 class="section-title" id="d9413007e179">Background</h5> <p id="P1">Quantitative computed tomography (CT) assessment of visceral adiposity may be superior to body mass index (BMI) as a predictor of surgical morbidity. We sought to examine the association of CT measures of obesity and BMI with short-term post-operative outcomes in colon cancer patients. </p> </div><div class="section"> <a class="named-anchor" id="S2"> <!-- named anchor --> </a> <h5 class="section-title" id="d9413007e184">Methods</h5> <p id="P2">In this retrospective study, 110 patients treated with colectomy for Stage I–III colon cancer were classified as obese or non-obese by pre-operative CT-based measures of adiposity or BMI. [Obese: BMI≥30kg/m <sup>2</sup>, visceral fat area (VFA) to subcutaneous fat area ratio (V/S) ≥0.4 and VFA&gt;100cm <sup>2</sup>)]. Post-operative morbidity and mortality rates were compared. </p> </div><div class="section"> <a class="named-anchor" id="S3"> <!-- named anchor --> </a> <h5 class="section-title" id="d9413007e195">Results</h5> <p id="P3">Obese patients, by V/S and VFA but not BMI, were more likely to be male and have pre-existing hypertension and diabetes. The overall complication rate was 25.5% and there were no mortalities. Obese patients by VFA (with a trend for VS but not BMI) were more likely to develop postoperative complications as compared to patients classified as non-obese; VFA (30.5% vs.10.7%, <i>p</i>= 0.03), VS (29.2% vs. 9.5%, <i>p</i>=0.05) and BMI (32.4% vs. 21.9%, <i>p</i>=0.23). </p> </div><div class="section"> <a class="named-anchor" id="S4"> <!-- named anchor --> </a> <h5 class="section-title" id="d9413007e209">Conclusions</h5> <p id="P4">Elevated visceral obesity quantified by CT is associated with the presence of key metabolic comorbidities and increased post-operative morbidity and may be superior to BMI for risk stratification. </p> </div>

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          Intra-abdominal fat is a major determinant of the National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome.

          The underlying pathophysiology of the metabolic syndrome is the subject of debate, with both insulin resistance and obesity considered as important factors. We evaluated the differential effects of insulin resistance and central body fat distribution in determining the metabolic syndrome as defined by the National Cholesterol Education Program (NCEP) Adult Treatment Panel III. In addition, we determined which NCEP criteria were associated with insulin resistance and central adiposity. The subjects, 218 healthy men (n = 89) and women (n = 129) with a broad range of age (26-75 years) and BMI (18.4-46.8 kg/m2), underwent quantification of the insulin sensitivity index (Si) and intra-abdominal fat (IAF) and subcutaneous fat (SCF) areas. The metabolic syndrome was present in 34 (15.6%) of subjects who had a lower Si [median: 3.13 vs. 6.09 x 10(-5) min(-1)/(pmol/l)] and higher IAF (166.3 vs. 79.1 cm2) and SCF (285.1 vs. 179.8 cm2) areas compared with subjects without the syndrome (P < 0.001). Multivariate models including Si, IAF, and SCF demonstrated that each parameter was associated with the syndrome. However, IAF was independently associated with all five of the metabolic syndrome criteria. In multivariable models containing the criteria as covariates, waist circumference and triglyceride levels were independently associated with Si and IAF and SCF areas (P < 0.001). Although insulin resistance and central body fat are both associated with the metabolic syndrome, IAF is independently associated with all of the criteria, suggesting that it may have a pathophysiological role. Of the NCEP criteria, waist circumference and triglycerides may best identify insulin resistance and visceral adiposity in individuals with a fasting plasma glucose <6.4 mmol/l.
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            Obesity and cancer risk: evidence, mechanisms, and recommendations

            Obesity, a growing health problem worldwide, has been associated with the metabolic syndrome, diabetes, cardiovascular disease, hypertension, and other chronic diseases. Recently, the obesity–cancer link has received much attention. Epidemiological studies have shown that obesity is also associated with increased risk of several cancer types, including colon, breast, endometrium, liver, kidney, esophagus, gastric, pancreatic, gallbladder, and leukemia, and can also lead to poorer treatment and increased cancer-related mortality. Biological mechanisms underlying the relationship between obesity and cancer are not well understood. They include modulation of energy balance and calorie restriction, growth factors, multiple signaling pathways, and inflammatory processes. Key among the signaling pathways linking obesity and cancer is the PI3K/Akt/mTOR cascade, which is a target of many of the obesity-associated factors and regulates cell proliferation and survival. Understanding the molecular and cellular mechanisms of the obesity–cancer connection is important in developing potential therapeutics. The link between obesity and cancer underscores the recommendation to maintain a healthy body weight throughout life as one of the most important ways to protect against cancer.
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              The metabolic syndrome: A high-risk state for cancer?

              The metabolic syndrome is composed of cardiovascular risk factors including increased body mass index/waist circumference, blood pressure, plasma glucose, and triglycerides, as well as decreased high-density lipoprotein cholesterol. The essence of the metabolic syndrome lies in the clustering of these risk factors, which are associated with cardiovascular disease. Interestingly, most of the components of the metabolic syndrome have individually been linked in some way to the development of cancer. However, epidemiological studies linking the metabolic syndrome to cancer are scarce. Nevertheless, two such studies indicate that the clustering of metabolic syndrome components significantly increases the risk of colon cancer mortality compared with the individual components. The purpose of this review is to further explore the potential relationship between the metabolic syndrome and cancer risk. Specifically, we examine the hypothesis that individual components of the metabolic syndrome contribute to the development of several processes, including insulin resistance, aromatase activity, adipokine production, angiogenesis, glucose utilization, and oxidative stress/DNA damage, which can work together to increase cancer risk beyond that of the individual components alone. We propose that the metabolic syndrome be considered as a high-risk state for certain types of cancer and that this relationship should be systematically explored across cancer types.
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                Author and article information

                Journal
                Journal of Gastrointestinal Surgery
                J Gastrointest Surg
                Springer Science and Business Media LLC
                1091-255X
                1873-4626
                March 2017
                January 18 2017
                March 2017
                : 21
                : 3
                : 534-542
                Article
                10.1007/s11605-017-3362-9
                5560865
                28101721
                d291afc0-f594-4316-9f3e-794fc7a6724c
                © 2017

                http://www.springer.com/tdm

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