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UCP2, SHBG, Leptin, and T3 Levels are Associated with Resting Energy Expenditure in Obese Women

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Objective: The aim of this study was to investigate the association of Sex Hormone Binding Globulin (SHBG) with leptin, Triidothyronine (T3), and Uncoupling Protein 2 (UCP2) in obese women with low and normal Resting Energy Expenditure (REE) and to determine the role of these factors in the regulation of REE in obese women.

Method: A total 49 subjects (25-50 years old) were selected. Anthropometric and body composition parameters and resting energy expenditure were measured. Fasting circulating leptin, T3, SHBG and UCP2 levels were measured. Subjects were divided into three groups: Group I (BMI>30 and low resting energy expenditure, 16 subjects), group II (BMI>30 and normal resting energy expenditure, 17 subjects), and group III (control group, 16 non-obese subjects).

Result: It was found that obese subjects who had higher SHBG and leptin levels were at risk for high levels of UCP2. A significant association was found between T3 and REE. Obese subjects with higher concentrations of UCP2 and SHBG had decreased resting energy expenditure. A significant association was observed between SHBG and leptin in group I (r=0.90, p<0.0001) and group II (r=0.83, p<0.0001). Moreover, a significant association was found between T3 and SHBG in group I (r=-0.69, P=0.003).

Conclusion: Changes of the UCP2, leptin, and thyroid hormone (T3) levels may be related to SHBG levels. Thus, lower leptin and T3 levels may decrease SHBG in obese women. Therefore, lower SHBG, leptin, T3 and UCP2 levels may decrease the REE level in obese women.

Keywords: Obesity; UCP2; body mass index; leptin; resting energy expenditure; sex hormone binding globulin

Document Type: Research Article

Publication date: 01 March 2020

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  • This journal is devoted to timely reviews of experimental and clinical studies in the field of endocrine, metabolic, and immune disorders. Specific emphasis is placed on humoral and cellular targets for natural, synthetic, and genetically engineered drugs that enhance or impair endocrine, metabolic, and immune parameters and functions. Topics related to the neuroendocrine-immune axis are given special emphasis in view of the growing interest in stress-related, inflammatory, autoimmune, and degenerative disorders.
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