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      Abdominal Obesity, Adipokines and Non-communicable Diseases

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          Highlights

          • Our article reviews relationship between abdominal obesity and non-communicable diseases generally observed in South Asians. Abdominal obesity may be defined as excess deposits of fat in the abdominal region and is a common health condition seen in South Asians. It is being positively related to non-communicable diseases (NCDs).

          • It is independent of body mass index and measured by raised waist circumference for men≥90 cm and women≥80 cm.

          • The reason for its prevalence being common in Indians finds its root from pregnancy- during fetal period. It has emerged as a concept of ‘Thin Fat Indian’. Malnutrition in such a critical period of growth has consequences in the form of reduced basal metabolic rate (BMR), reduced blood flow to growing tissues, reduced functional ability of vital organs, endocrine changes and reduced capacity of primary adipose tissue.

          • However, excess of visceral fat facilitates high dosage of adipokines in the portal vein to liver and other body tissues having serious implications seen in the form NCDs like diabetes, hypertension, heart diseases, non-alcoholic fatty liver diseases, kidney disorders, cancer and other health problems.

          • Abdominal obesity should be addressed before it has progressed further to defined health issues by exercise and diet, so that people can live a quality life.

          Abstract

          Abdominal obesity may be defined as excess deposits of fat in the abdominal region. It is a common health condition seen in South Asians and is positively related to non-communicable diseases (NCDs). It is independent of body mass index and measured by raised waist circumference for men≥90 cm and women≥80 cm. The reason for its prevalence being common in Indians finds its root from pregnancy, during fetal period and has emerged as a concept of ‘Thin Fat Indian’. Malnutrition in such a critical period of growth has consequences in the form of reduced basal metabolic rate (BMR), reduced blood flow to growing tissues, reduced functional ability of vital organs, endocrine changes and reduced capacity of primary adipose tissue. However, excess of visceral fat facilitates high dosage of adipokines in the portal vein to liver and other body tissues having serious implications seen in the form NCDs like diabetes, hypertension, heart diseases, non-alcoholic fatty liver diseases, kidney disorders, cancer and other health problems. Abdominal obesity should be addressed before it has progressed further to defined health issues by exercise and diet, so that people can live a quality life.

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          Most cited references51

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          Waist circumference and not body mass index explains obesity-related health risk.

          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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            In utero programming of chronic disease.

            1. Many human fetuses have to adapt to a limited supply of nutrients. In doing so they permanently change their structure and metabolism. 2. These 'programmed' changes may be the origins of a number of diseases in later life, including coronary heart disease and the related disorders stroke, diabetes and hypertension. 3. This review examines the evidence linking these diseases to fetal undernutrition and provides an overview of previous studies in this area.
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              Tumor necrosis factor-alpha induces skeletal muscle insulin resistance in healthy human subjects via inhibition of Akt substrate 160 phosphorylation.

              Most lifestyle-related chronic diseases are characterized by low-grade systemic inflammation and insulin resistance. Excessive tumor necrosis factor-alpha (TNF-alpha) concentrations have been implicated in the development of insulin resistance, but direct evidence in humans is lacking. Here, we demonstrate that TNF-alpha infusion in healthy humans induces insulin resistance in skeletal muscle, without effect on endogenous glucose production, as estimated by a combined euglycemic insulin clamp and stable isotope tracer method. TNF-alpha directly impairs glucose uptake and metabolism by altering insulin signal transduction. TNF-alpha infusion increases phosphorylation of p70 S6 kinase, extracellular signal-regulated kinase-1/2, and c-Jun NH(2)-terminal kinase, concomitant with increased serine and reduced tyrosine phosphorylation of insulin receptor substrate-1. These signaling effects are associated with impaired phosphorylation of Akt substrate 160, the most proximal step identified in the canonical insulin signaling cascade regulating GLUT4 translocation and glucose uptake. Thus, excessive concentrations of TNF-alpha negatively regulate insulin signaling and whole-body glucose uptake in humans. Our results provide a molecular link between low-grade systemic inflammation and the metabolic syndrome.
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                Author and article information

                Contributors
                Journal
                J Steroid Biochem Mol Biol
                J. Steroid Biochem. Mol. Biol
                The Journal of Steroid Biochemistry and Molecular Biology
                Elsevier Ltd.
                0960-0760
                1879-1220
                18 August 2020
                18 August 2020
                : 105737
                Affiliations
                [a ]Department of Dietetics and Applied Nutrition, Amity University, Haryana, Gurgaon, India
                [b ]Department of Food science and Nutrition, Banasthali Vidyapith, Rajasthan, India
                Author notes
                [* ]Corresponding author at: Department of Dietetics and Applied Nutrition, Amity University, Haryana, Gurgaon, India. deepikadhawan10@ 123456gmail.com
                Article
                S0960-0760(20)30262-4 105737
                10.1016/j.jsbmb.2020.105737
                7431389
                32818561
                882914ed-66ab-4e7f-81b2-ceab528b75fb
                © 2020 Elsevier Ltd. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                : 8 May 2020
                : 1 July 2020
                : 12 August 2020
                Categories
                Article

                Biochemistry
                abdominal obesity,non-communicable diseases,adipokines,visceral fat
                Biochemistry
                abdominal obesity, non-communicable diseases, adipokines, visceral fat

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