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 diseases.

Can low-level laser therapy (LLLT) associated with an aerobic plus resistance training change the cardiometabolic risk in obese women? A placebo-controlled clinical trial.

INTRODUCTION: Obesity is one of the most important link factors to coronary artery disease development mainly due to the pro-inflammatory and pro-thrombotic states favoring atherosclerosis progression. The LLLT acts in the cellular metabolism and it is highly effective to improve inflammation. The same occur in response to different kinds of exercise. However, we have not known the associate effects using LLLT therapies with aerobic plus resistance training as strategy specifically with target at human obesity control and its comorbidities. OBJECTIVE: Investigate the effects of the LLLT associated with aerobic plus resistance training on cardiometabolic risk factors in obese women. METHODOLOGY: Women aged 20-40 years (BMI ≥ 30 kg/m(2)), were divided into 2 groups: Phototherapy (PHOTO) and Placebo. They were trained aerobic plus resistance exercises (in a concurrent mode), 1h, 3 times/week during 16 weeks. Phototherapy was applied after each exercise session for 16 min, with infrared laser, wavelength 808 nm, continuous output, power 100 mW, and energy delivery 50 J. The body composition was measured with bioimpedance. Inflammatory mark concentrations were measured using a commercially available multiplex. RESULTS: LLLT associated with aerobic plus resistance training was effective in decrease neck (P=0.0003) and waist circumferences (P=0.02); percentual of fat (P=0.04); visceral fat area (P=0.02); HOMA-IR (P=0.0009); Leptin (P=0.03) and ICAM (P=0.03). Also, the reduction in leptin (P=0.008) and ICAM-1 (0, 05) was much more expressive in the phototherapy group in comparison to placebo group when analyzed by delta values. CONCLUSION: LLLT associated with concurrent exercise (aerobic plus resistance training) potentiates the exercise effects of decreasing the cardiometabolic risk factors in obese woman. These results suggest the LLLT associated with exercises as a new therapeutic tool in the control of obesity and its comorbidities for obese people, targeting to optimize the strategies to control the cardiometabolic risk factors in these populations.

Food restriction and refeeding induces changes in lipid pathways and fat deposition in the adipose and hepatic tissues in rats with diet-induced obesity.

The aim of this study was to determine the effects of successive cycles of a moderately restrictive diet and refeeding with a high-fat diet on the metabolism of the adipose and hepatic tissues of obese rats. Rats were assigned to the following groups: a chow diet; a high-fat diet; a moderate caloric restriction; or a moderate caloric restriction plus refeeding. Some animals in each group were given [1-(14)C]triolein intragastrically, while others received an intraperitoneal injection of 3 mCi (3)H(2)O. All animals were killed by decapitation. The retroperitoneal, visceral epididymal and omental white adipose tissues, brown adipose tissue, liver and blood were immediately removed. The lipid uptake from the diet, in vivo rate of lipogenesis, percentage of fat, lipid profile and leptin concentration were analysed. The high-fat diet promoted an increase in fatty liver (P ≤ 0.05), adiposity mass (P ≤ 0.05) and the plasma concentration of leptin (P ≤ 0.05) and a decreased lipid uptake in white adipose tissue depots (P ≤ 0.05) in relation to the chow diet. The moderate caloric restriction did not reverse the changes promoted by the high-fat diet but induced a small decrease in adiposity, which was reversed after refeeding, and the animals maintained a dyslipidaemic profile and high fat deposition in the liver. We can conclude that the high-fat diet and subsequent moderate caloric restriction plus refeeding increased the risks of developing visceral obesity, dyslipidaemia and non-alcoholic fatty liver disease, which suggests that this type of experimental protocol can be used to study mechanisms related to the metabolic syndrome.

Caloric restriction and refeeding promoted different metabolic effects in fat depots and impaired dyslipidemic profile in rats.

OBJECTIVE: We investigated the effects of severe caloric restriction and refeeding with a high-fat diet on lipid uptake by visceral adipose fat and lipid profile in rats. METHODS: Rats were assigned to six groups: a chow diet (C), a high-fat diet (H), severe caloric restriction (SC and SH), and severe caloric restriction plus refeeding (SC-r and SH-r) during 8 wk. All animals were killed by decapitation 4 h after intragastric administration of [1-14C] triolein ( approximately 0.5 g, 0.3 muCi/rat). Liver; visceral retroperitoneal (RET), epididymal (EPI), and omental (VIS) white adipose tissues; brown adipose tissue; and intestine were immediately removed and weighed. The whole intestine was withdrawn and homogenized to determine lipid uptake. Total cholesterol, high-density lipoprotein (HDL), and triacylglycerol in plasma were determined enzymatically. RESULTS: The SC and SH groups showed reduced visceral adiposity, although this effect was more evident in the SC group. The SC group had greater lipid absorption in the VIS than the C group. The SH treatment increased RET and VIS lipid uptake in relation to the H group. The SH-r treatment increased RET and VIS adiposity. HDL cholesterol decreased with caloric restriction in the SC and SH groups. The SH-r treatment did not increase HDL cholesterol. CONCLUSION: Severe caloric restriction decreased visceral adiposity even in rats in the H group but did not reduce the risk of development of dyslipidemia. Therefore, food restriction plus refeeding with a high-fat diet increase the risk of development of visceral adiposity and dyslipidemia.