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      The impact of obesity towards prostate diseases

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          Abstract

          Evidence has supported obesity as a risk factor for both benign prostate hyperplasia (BPH) and prostate cancer (PCa). Obesity causes several mechanisms including increased intra-abdominal pressure, altered endocrine status, increased sympathetic nervous activity, increased inflammation process, and oxidative stress, all of which are favorable in the development of BPH. In PCa, there are several different mechanisms, such as decreased serum testosterone, peripheral aromatization of androgens, insulin resistance, and altered adipokine secretion caused by inflammation, which may precipitate the development of and even cause high-grade PCa. The role of obesity in prostatitis still remains unclear. A greater understanding of the pathogenesis of prostate disease and adiposity could allow the development of new therapeutic markers, prognostic indicators, and drug targets. This review was made to help better understanding of the association between central obesity and prostate diseases, such as prostatitis, BPH, and PCa.

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          Abdominal visceral and subcutaneous adipose tissue compartments: association with metabolic risk factors in the Framingham Heart Study.

          Caroline S. Fox, Joseph Massaro, Udo Hoffmann … (2007)
          Visceral adipose tissue (VAT) compartments may confer increased metabolic risk. The incremental utility of measuring both visceral and subcutaneous abdominal adipose tissue (SAT) in association with metabolic risk factors and underlying heritability has not been well described in a population-based setting. Participants (n=3001) were drawn from the Framingham Heart Study (48% women; mean age, 50 years), were free of clinical cardiovascular disease, and underwent multidetector computed tomography assessment of SAT and VAT volumes between 2002 and 2005. Metabolic risk factors were examined in relation to increments of SAT and VAT after multivariable adjustment. Heritability was calculated using variance-components analysis. Among both women and men, SAT and VAT were significantly associated with blood pressure, fasting plasma glucose, triglycerides, and high-density lipoprotein cholesterol and with increased odds of hypertension, impaired fasting glucose, diabetes mellitus, and metabolic syndrome (P range < 0.01). In women, relations between VAT and risk factors were consistently stronger than in men. However, VAT was more strongly correlated with most metabolic risk factors than was SAT. For example, among women and men, both SAT and VAT were associated with increased odds of metabolic syndrome. In women, the odds ratio (OR) of metabolic syndrome per 1-standard deviation increase in VAT (OR, 4.7) was stronger than that for SAT (OR, 3.0; P for difference between SAT and VAT < 0.0001); similar differences were noted for men (OR for VAT, 4.2; OR for SAT, 2.5). Furthermore, VAT but not SAT contributed significantly to risk factor variation after adjustment for body mass index and waist circumference (P < or = 0.01). Among overweight and obese individuals, the prevalence of hypertension, impaired fasting glucose, and metabolic syndrome increased linearly and significantly across increasing VAT quartiles. Heritability values for SAT and VAT were 57% and 36%, respectively. Although both SAT and VAT are correlated with metabolic risk factors, VAT remains more strongly associated with an adverse metabolic risk profile even after accounting for standard anthropometric indexes. Our findings are consistent with the hypothesized role of visceral fat as a unique, pathogenic fat depot. Measurement of VAT may provide a more complete understanding of metabolic risk associated with variation in fat distribution.
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            Adipose tissue, adipokines, and inflammation.

            Giamila Fantuzzi (2005)
            White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-alpha, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
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              Waist circumference and not body mass index explains obesity-related health risk.

              Ian Janssen, Peter Katzmarzyk, Robert Ross (2004)
              The addition of waist circumference (WC) to body mass index (BMI; in kg/m(2)) predicts a greater variance in health risk than does BMI alone; however, whether the reverse is true is not known. We evaluated whether BMI adds to the predictive power of WC in assessing obesity-related comorbidity. Subjects were 14 924 adult participants in the third National Health and Nutrition Examination Survey, grouped into categories of BMI and WC in accordance with the National Institutes of Health cutoffs. Odds ratios for hypertension, dyslipidemia, and the metabolic syndrome were compared for overweight and class I obese BMI categories and the normal-weight category before and after adjustment for WC. BMI and WC were also included in the same regression model as continuous variables for prediction of the metabolic disorders. With few exceptions, overweight and obese subjects were more likely to have hypertension, dyslipidemia, and the metabolic syndrome than were normal-weight subjects. After adjustment for WC category (normal or high), the odds of comorbidity, although attenuated, remained higher in overweight and obese subjects than in normal-weight subjects. However, after adjustment for WC as a continuous variable, the likelihood of hypertension, dyslipidemia, and the metabolic syndrome was similar in all groups. When WC and BMI were used as continuous variables in the same regression model, WC alone was a significant predictor of comorbidity. WC, and not BMI, explains obesity-related health risk. Thus, for a given WC value, overweight and obese persons and normal-weight persons have comparable health risks. However, when WC is dichotomized as normal or high, BMI remains a significant predictor of health risk.
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                Author and article information

                Contributors
                Rainy Umbas
                Journal
                Journal ID (nlm-ta): Prostate Int
                Journal ID (iso-abbrev): Prostate Int
                Title: Prostate International
                Publisher: Asian Pacific Prostate Society
                ISSN (Print): 2287-8882
                ISSN (Electronic): 2287-903X
                Publication date PMC-release: 24 November 2015
                Publication date (Print): March 2016
                Publication date (Electronic): 24 November 2015
                Volume: 4
                Issue: 1
                Pages: 1-6
                Affiliations
                [1]Department of Urology, Faculty of Medicine, Universitas Indonesia, Cipto Mangunkusumo Hospital, Jakarta, Indonesia
                Author notes
                [∗ ]Corresponding author. Department of Urology, Cipto Mangunkusumo Hospital, Universitas Indonesia, Diponegoro Number 71, Central Jakarta, DKI Jakarta, 10430, Indonesia. rizalhamid.urology@ 123456gmail.com
                Article
                Publisher ID: S2287-8882(15)30074-X
                DOI: 10.1016/j.prnil.2015.08.001
                PMC ID: 4789344
                PubMed ID: 27014656
                SO-VID: 1b1b75c5-779a-46cb-9b30-0311340753b0
                Copyright © Copyright © 2015 Asian Pacific Prostate Society, Published by Elsevier.
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 31 July 2015
                Date accepted : 13 August 2015
                Categories
                Subject: Review Article

                Keywords: benign prostate hyperplasia,obesity,prostate cancer,prostatitis
                Data availability:
                Keywords: benign prostate hyperplasia, obesity, prostate cancer, prostatitis

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