Dataset Information

Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning.

ABSTRACT: Obesity, characterized by excessive fat mass, has been emerging as a major global epidemic and contributes to the increased risk of morbidity around the world. Thus, the necessity to find effective therapy and specific regulatory mechanisms is increasing for controlling obesity. Lately, many researchers have been interested in the linkage between obesity and adipokines/myokines, particularly adiponectin and brain-derived neurotrophic factor (BDNF). However, the role of adiponectin and BDNF in adiposity has not been clearly defined yet. We examined the association of adiposity with adiponectin and BDNF through human study (observational study) with Korean women and in vitro experiments. In the human study, we found a negative relationship between adiposity and circulating adiponectins but irregular patterns in the relationship between adiposity and circulating BDNFs. In the in vitro study using 3T3-L1 adipocytes, adiponectin treatment strongly promoted adipocyte differentiation and the fat browning process, whereas BDNF treatment attenuated adipocyte differentiation and the fat browning process in differentiated adipocytes. Our results demonstrate that adiponectin and BDNF play an important role in regulating fat mass and the expression of fat-browning markers in different ways, and also suggest that circulating adiponectin may be used as an important monitoring index for obesity status.

SUBMITTER: Jo D

PROVIDER: S-EPMC7794779 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning.

Jo Danbi D Son Yujeong Y Yoon Gwangho G Song Juhyun J Kim Oh Yoen OY

Journal of clinical medicine 20201226 1

Obesity, characterized by excessive fat mass, has been emerging as a major global epidemic and contributes to the increased risk of morbidity around the world. Thus, the necessity to find effective therapy and specific regulatory mechanisms is increasing for controlling obesity. Lately, many researchers have been interested in the linkage between obesity and adipokines/myokines, particularly adiponectin and brain-derived neurotrophic factor (BDNF). However, the role of adiponectin and BDNF in ad ...[more]

PMID: 33375318

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Project description:This study had two main objectives: To examine the association between body fat distribution and non-alcoholic fatty liver disease (NAFLD) and liver fat content, and to determine whether the relationship between NAFLD and regional body fat distribution, with respect to liver fat content in youths with excess adiposity, is independent of cardiorespiratory fitness (CRF) and a healthy diet. Liver fat content (controlled attenuation parameter (CAP)), body fat distribution (body mass index (BMI) z-score, waist circumference, waist-to-height ratio, fat mass/height, body fat percentage, total fat mass, android-to-gynoid fat mass ratio, visceral adipose tissue (VAT), and lean mass index, determined by dual-energy X-ray absorptiometry (DXA)), CRF (20-m shuttle-run test), and healthy diet (adherence to the Mediterranean diet by KIDMED questionnaire) were measured in 126 adolescents (66% girls) aged between 11 and 17 years. Participants were assigned to two groups according to the presence or absence of hepatic steatosis (CAP values ?225 dB/m or <225 dB/m of liver fat, respectively). Considering the similar total fat values for the two groups (>30% by DXA), youths with NAFLD had higher fat distribution parameters than those without NAFLD, regardless of sex, age, puberty stage, lean mass index, CRF, and healthy diet (p < 0.01). In the non-NAFLD group, the association between hepatic fat and fat distribution parameters presented a similar pattern, although the association was statistically insignificant after adjusting for a potential confounding variable (ps > 0.05), except for the case of VAT. Body fat distribution parameters were higher in youths with NAFLD compared to those without NAFLD. Additionally, body fat distribution showed a significant association with liver fat content as assessed by CAP in youths with NAFLD independent of CRF and adherence to the Mediterranean diet, supporting the notion that upper body fat distribution might play a pivotal role in the development of NAFLD in adolescents. These results may have implications for the clinical management of youths with excess adiposity given the high prevalence of NAFLD in children and young adults.

Project description:Aims/hypothesisDespite a similar fat storing function, visceral (intra-abdominal) white adipose tissue (WAT) is detrimental, whereas subcutaneous WAT is considered to protect against metabolic disease. Recent findings indicate that thermogenic genes, expressed in brown adipose tissue (BAT), can be induced primarily in subcutaneous WAT. Here, we investigate the hypothesis that the Wilms tumour gene product (WT1), which is expressed in intra-abdominal WAT but not in subcutaneous WAT and BAT, suppresses a thermogenic program in white fat cells.MethodsHeterozygous Wt1 knockout mice and their wild-type littermates were examined in terms of thermogenic and adipocyte-selective gene expression. Glucose tolerance and hepatic lipid accumulation in these mice were assessed under normal chow and high-fat diet conditions. Pre-adipocytes isolated from the stromal vascular fraction of BAT were transduced with Wt1-expressing retrovirus, induced to differentiate and analysed for the expression of thermogenic and adipocyte-selective genes.ResultsExpression of the thermogenic genes Cpt1b and Tmem26 was enhanced and transcript levels of Ucp1 were on average more than tenfold higher in epididymal WAT of heterozygous Wt1 knockout mice compared with wild-type mice. Wt1 heterozygosity reduced epididymal WAT mass, improved whole-body glucose tolerance and alleviated severe hepatic steatosis upon diet-induced obesity in mice. Retroviral expression of WT1 in brown pre-adipocytes, which lack endogenous WT1, reduced mRNA levels of Ucp1, Ppargc1a, Cidea, Prdm16 and Cpt1b upon in vitro differentiation by 60-90%. WT1 knockdown in epididymal pre-adipocytes significantly lowered Aldh1a1 and Zfp423 transcripts, two key suppressors of the thermogenic program. Conversely, Aldh1a1 and Zfp423 mRNA levels were increased approximately five- and threefold, respectively, by retroviral expression of WT1 in brown pre-adipocytes.Conclusion/interpretationWT1 functions as a white adipocyte determination factor in epididymal WAT by suppressing thermogenic genes. Reducing Wt1 expression in this and other intra-abdominal fat depots may represent a novel treatment strategy in metabolic disease.

Dataset Information

Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning.

Publications

Role of Adiponectin and Brain Derived Neurotrophic Factor in Metabolic Regulation Involved in Adiposity and Body Fat Browning.

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