Mapping research in the obesity, adipose tissue, and microRNA field: a bibliometric analysis

Recent studies have investigated the control of adipose tissue expansion and inflammatory process by microRNAs (miRNAs). These two processes are of great interest because both are associated with obesity and metabolic syndrome. However, despite the great relevance of the role of miRNAs in obesity and adipose tissue, no qualitative and quantitative analysis on the subject has been performed. Thus, we aimed to examine global research activity and current trends with respect to the interaction between obesity, adipose tissue and miRNAs through a bibliometric analysis. This research was performed on the Scopus database for publications containing miRNA, obesity, and adipose tissue keyword combinations. In total, 898 articles were analyzed and the most frequently occurring keywords were selected and clustered into three well-defined groups. As a result, first group of keywords pointed to the research area on miRNAs expressed in obesity-associated diseases. The second group demonstrated the regulation of the adipogenesis process by miRNAs, while the third group highlighted brown adipose tissue and thermogenesis as one of the latest global research trends related to the theme. The studies selected in this paper describe the expression and performance of different miRNAs in obesity and comorbidities. Most studies have focused on identifying miRNAs and signaling pathways associated with obesity, type 2 diabetes mellitus, and cardiovascular disease. Thus, the miRNA profile for these diseases may be used as biomarkers and therapeutic targets in the prevention and treatment of obesity-associated diseases812CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP132365/2018-9sem informação17/09602-4; 2017/19504-

Exercise training induces depot-specific adaptations to white and brown adipose tissue

Exercise affects whole-body metabolism through adaptations to various tissues, including adipose tissue (AT). Recent studies investigated exercise-induced adaptations to AT, focusing on inguinal white adipose tissue (WAT), perigonadal WAT, and interscapular brown adipose tissue (iBAT). Although these AT depots play important roles in metabolism, they account for only ∼50% of the AT mass in a mouse. Here, we investigated the effects of 3 weeks of exercise training on all 14 AT depots. Exercise induced depot-specific effects in genes involved in mitochondrial activity, glucose metabolism, and fatty acid uptake and oxidation in each adipose tissue (AT) depot. These data demonstrate that exercise training results in unique responses in each AT depot; identifying the depot-specific adaptations to AT in response to exercise is essential to determine how AT contributes to the overall beneficial effect of exercise11425439This work was supported by National Institutes of Health grants R01-HL138738 and K01-DK105109 (to K.I.S.), R01-DK099511 (to L.J.G.), and 5P30 DK36836 (Joslin Diabetes Center DRC). The authors thank Nathan Makarewicz for editorial contribution

Lifelong exercise practice and immunosenescence : master athletes cytokine response to acute exercise

The study aimed to analyze the effects of aging and lifelong training on the main pro- and anti-inflammatory cytokines, and the impact of acute exercise on the expression of these cytokines. Thirty-nine participants were allocated into 3 groups: young (31.8 +/- 3.00 yrs.), middle-aged (54.2 +/- 5.9 yrs.) and master athletes (53.1 +/- 8.8 yrs.) and performed a maximal incremental test on a cycle ergometer. Blood samples were obtained before (Pre), 10 min post-exercise (Post) and 1 h post-exercise (Post 1 h). Mean VO2max was similar for master athletes and youngers and higher compared to the middle-aged group. Resting values of the IL-1 ra, IL-1 beta, IL-4, and IL-8 were higher in master athletes compared to the young and middle-aged groups (P < 0.01), while the highest values of IL-10 and IL-17 were observed for the youngers (29.49 +/- 18.00 pg/mL and 66.24 +/- 23.23 pg/mL, respectively) with the middle-aged group showing the lowest values (2.13 +/- 1.40 pg/mL). Acute exercise effects (Post) were observed for IL-1 beta in the master athletes group, IL-6 in the young group and IL-4 for both groups (P < 0.05). No Post effects were observed for the middle-age group for all cytokines. The TNF-alpha/IL-10 ratio was higher in all moments for the middle-aged (P < 0.05). In conclusion, lifelong training helps to maintain the balance of pro- and anti-inflammatory cytokines, together with IL-10 levels close to those found in young adults11517COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPES1417/13-4Firstly, the authors would like to thank all the master athletes that volunteered to participate in this study. The Faculty of Sport Sciences and Physical Education, University of Coimbra funded the study. The present manuscript was accomplished with support from CAPES, Coordination for the Improvement of Higher Education Personnel, Brazil (grants numbers 1417/13-4

Acute physical exercise increases APPL1/PI3K signaling in the hypothalamus of lean mice

Adiponectin is an adipokine that acts in the control of energy homeostasis. The adaptor protein containing the pleckstrin homology domain, phosphotyrosine-binding domain, and leucine zipper motif 1 (APPL1) is a key protein in the adiponectin signaling. The APPL1 mediates a positive effect on the insulin signaling through the interaction with the phosphoinositide 3-kinase (PI3K). Thus, the present study aimed to explore the effects of an acute physical exercise session on the hypothalamic adiponectin signaling. Firstly, using bioinformatics analysis, we found a negative correlation between hypothalamic APPL1 mRNA levels and food consumption in several strains of genetically diverse BXD mice. Also, the mice and the human database revealed a positive correlation between the levels of APPL1 mRNA and PI3K mRNA. At the molecular level, the exercised mice showed increased APPL1 and PI3K (p110) protein contents in the hypothalamus of Swiss mice. Furthermore, the exercise increases co-localization between APPL1 and PI3K p110 predominantly in neurons of the arcuate nucleus of hypothalamus (ARC). Finally, we found an acute exercise session reduced the food intake 5 hr after the end of fasting. In conclusion, our results indicate that physical exercise reduces the food intake and increases some proteins related to adiponectin pathway in the hypothalamus of lean mice50731813190CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP306535/2017-32016/18488-

Short-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice

The consumption of saturated fatty acids is one of the leading risk factors for Alzheimer's Disease (AD) development. Indeed, the short-term consumption of a high-fat diet (HFD) is related to increased inflammatory signals in the hippocampus; however, the potential molecular mechanisms linking it to AD pathogenesis are not fully elucidated. In our study, we investigated the effects of short-term HFD feeding (within 3, 7 and 10 days) in AD markers and neuroinflammation in the hippocampus of mice. The short period of HFD increased fasting glucose and HOMA-IR. Also, mice fed HFD increased the protein content of beta-Amyloid, pTau, TNF alpha, IL1 beta, pJNK, PTP1B, peIF2 alpha, CHOP, Caspase3, Cleaved-Caspase3 and Alzheimer-related genes (Bax, PS1, PEN2, Aph1b). At 10 days, both neuronal (N2a) and microglial (BV2) cells presented higher expression of inflammatory and apoptotic genes when stimulated with palmitate. These findings suggest that a short period of consumption of a diet rich in saturated fat is associated with activation of inflammatory, ER stress and apoptotic signals in the hippocampus of young mice79284293COORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP306535/2017-3; 309339/2016-2; 462410/2014-52016/18488-8Obesity and Comorbidities Research Center - OCRC; CNPqNational Council for Scientific and Technological Development (CNPq) [306535/2017-3, 309339/2016-2, 462410/2014-5]; FAPESPFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [2016/18488-8