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      Salivary Leptin Level in Young Adult Males and its Association with Anthropometric Measurements, Fat Distribution and Muscle Mass

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          Abstract

          Aims: 1) To assess salivary leptin levels in normal-underweight versus overweight and obese healthy adult males aged 18–25 years old. 2) The relative contribution of anthropometric measurements, fat percentage, fat distribution (visceral versus subcutaneous) and total as well as regional muscle mass in arms, trunk and legs respectively in predicting salivary leptin levels. Methods: A total of 92 adult males were classified into two groups based on their body mass index (BMI): normal-underweight, BMI <24.9 kg/m 2 (n=51); overweight-obese, BMI >25 kg/m 2 (n=41). Anthropometric measurements such as BMI, waist circumference (WC), hip circumference (HC) and waist-hip ratio (WHR) were measured through standardised methods. Fat percentage, visceral fat level, subcutaneous fat and muscle mass (total and regional) were measured using Karada scan bioelectrical impedance method. Fasting saliva samples were collected and used for assessing salivary leptin concentrations using enzyme-linked immunosorbent assay. Results: Statistical analysis of the data showed a significant difference between the two groups in all of the parameters measured except height and salivary leptin levels. Multiple regression analysis showed that HC, WC and WHR were good predictors for salivary leptin levels in normal-underweight group. However, in the overweight-obese group, height was the most important independent variable that could predict salivary leptin levels as a dependent variable. Conclusions: Predictors for salivary leptin levels in adult healthy males are different in normal-underweight subjects from overweight-obese subjects. The most important predictor for salivary leptin levels is HC in normal weight subjects, while it is height in overweight and obese healthy adult males.

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          Most cited references39

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          Adapting to obesity with adipose tissue inflammation

          Adipose tissue inflammation is an adaptive response to overnutrition in the early stages of obesity, but later becomes maladaptive. Here, Reilly and Saltiel review the cellular and molecular mechanisms of obesity-induced inflammation in adipose tissue and discuss potential therapeutic approaches.
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            Associations of visceral and abdominal subcutaneous adipose tissue with markers of cardiac and metabolic risk in obese adults

            Visceral (VAT) and abdominal subcutaneous (SAT) adipose tissues contribute to obesity but may have different metabolic and atherosclerosis risk profiles. Among obese participants in the Dallas Heart Study, we examined the cross-sectional associations of abdominal VAT and SAT mass, assessed by magnetic resonance imaging (MRI) and indexed to body surface area (BSA), with circulating biomarkers of insulin resistance, dyslipidemia, and inflammation (n=942); and with aortic plaque and liver fat by MRI and coronary calcium by computed tomography (n=1200). Associations of VAT/BSA and SAT/BSA were examined after adjustment for age, sex, race, menopause, and body mass index. In multivariable models, VAT significantly associated with the homeostasis model assessment of insulin resistance (HOMA-IR), lower adiponectin, smaller LDL and HDL particle size, larger VLDL size, and increased LDL and VLDL particle number (p<0.001 for each). VAT also associated with prevalent diabetes, metabolic syndrome, hepatic steatosis, and aortic plaque (p<0.001 for each). VAT independently associated with C-reactive protein but not with any other inflammatory biomarkers tested. In contrast, SAT associated with leptin and inflammatory biomarkers, but not with dyslipidemia or atherosclerosis. Associations between SAT and HOMA-IR were significant in univariable analyses but attenuated after multivariable adjustment. In conclusion, VAT associated with an adverse metabolic, dyslipidemic, and atherogenic obesity phenotype. In contrast, SAT demonstrated a more benign phenotype, characterized by modest associations with inflammatory biomarkers and leptin, but no independent association with dyslipidemia, insulin resistance, or atherosclerosis in obese individuals. These findings suggest that abdominal fat distribution defines distinct obesity sub-phenotypes with heterogeneous metabolic and atherosclerosis risk.
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              Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons.

              Despite high leptin levels, most obese humans and rodents lack responsiveness to its appetite-suppressing effects. We demonstrate that leptin modulates NPY/AgRP and alpha-MSH secretion from the ARH of lean mice. High-fat diet-induced obese (DIO) mice have normal ObRb levels and increased SOCS-3 levels, but leptin fails to modulate peptide secretion and any element of the leptin signaling cascade. Despite this leptin resistance, the melanocortin system downstream of the ARH in DIO mice is over-responsive to melanocortin agonists, probably due to upregulation of MC4R. Lastly, we show that by decreasing the fat content of the mouse's diet, leptin responsiveness of NPY/AgRP and POMC neurons recovered simultaneously, with mice regaining normal leptin sensitivity and glycemic control. These results highlight the physiological importance of leptin sensing in the melanocortin circuits and show that their loss of leptin sensing likely contributes to the pathology of leptin resistance.
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                Author and article information

                Journal
                Eur Endocrinol
                Eur Endocrinol
                EE
                European Endocrinology
                Touch Medical Media
                1758-3772
                1758-3780
                September 2018
                10 September 2018
                : 14
                : 2
                : 94-98
                Affiliations
                [1 ] Physiology Department, Faculty of Medicine, MAHSA University, Kuala Lumpur, Malaysia
                [2 ] Faculty of Medicine, Minia University, Egypt
                Author notes
                Corresponding author: Mona Mohamed Ibrahim Abdalla, Level 7, Main Building, Bandar Saujana Putra, 42610 Jenjarom, Selangor, Malaysia. E: monaalbetar@ 123456yahoo.com ; dr.mona@ 123456mahsa.edu.my

                Disclosure: Mona Mohamed Ibrahim Abdalla and Soon Siew Choo have nothing to disclose in relation to this article.

                Article
                10.17925/EE.2018.14.2.94
                6182931
                30349601
                35ccf5ad-2119-4c47-9674-d4e4d8dd80ca
                © The Author(s) 2018

                This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. © The Authors 2018.

                Compliance with Ethics: The study design and consent forms were approved by the Research Management Committee of MAHSA University, Malaysia. All procedures were followed in accordance with the responsible committee on human experimentation and with the Helsinki Declaration of 1975 and subsequent revisions, and informed consent was received from the participants involved in this study.

                Authorship: All named authors meet the criteria of the International Committee of Medical Journal Editors for authorship for this manuscript, take responsibility for the integrity of the work as a whole and have given final approval for the version to be published.

                Review Process: Double-blind peer review

                History
                : 16 April 2018
                : 11 June 2018
                Page count
                Pages: 5
                Funding
                Support: This article was funded by a grant from MAHSA University, Malaysia.
                Categories
                Obesity

                visceral fat,subcutaneous fat,obesity,muscle mass,salivary leptin,body mass index

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