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Obesity is a multifactorial disease associated with metabolic dysfunction and the prevention and treatment of obesity are often unsatisfactory. Transcranial direct-current stimulation (tDCS) is a non-invasive brain stimulation technique that has proven promising in the treatment of eating disorders such as obesity. We investigate the effects of tDCS on locomotor and exploratory activities, anxiety-like and feeding behavior, and levels of brain-derived neurotrophic factor (BDNF), IL (interleukin)-10, IL-1β, and tumor necrosis factor-alpha (TNF-α) in the cerebral cortex of obese rats. A total of 40 adult male Wistar rats were used in our study. Animals were divided into groups of three or four animals per cage and allocated to four treatment groups: standard diet plus sham tDCS treatment (SDS), standard diet plus tDCS treatment (SDT), hypercaloric diet plus sham tDCS treatment (HDS), hypercaloric diet plus tDCS treatment (HDT). After 40 days on a hypercaloric diet and/or standard diet were to assessed the locomotor and exploratory activity and anxiety-like behavior to by the open field (OF) and elevated plus maze (EPM) tests respectively before and after exposure to tDCS treatment. The experimental groups were submitted to active or sham treatment tDCS during eight days. Palatable food consumption test (PFT) was performed 24 h after the last tDCS session under fasting and feeding conditions. Obese animals submitted to tDCS treatment showed a reduction in the Lee index, visceral adipose tissue weight, and food craving. In addition, bicephalic tDCS decreased the cerebral cortex levels of IL-1β and TNF-α in these animals. Exposure to a hypercaloric diet produced an anxiolytic effect, which was reversed by bicephalic tDCS treatment. These results suggest that, in accordance with studies in humans, bicephalic tDCS could modulate biometric and inflammatory parameters, as well as anxiety-like and feeding behavior, of rats subjected to the consumption of a hypercaloric diet., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Disruption of the circadian system can lead to metabolic dysfunction as a response to environmental alterations. This study assessed the effects of the association between obesity and chronic stress on the temporal pattern of serum levels of adipogenic markers and corticosterone in rats. We evaluated weekly weight, delta weight, Lee index, and weight fractions of adipose tissue (mesenteric, MAT; subcutaneous, SAT; and pericardial, PAT) to control for hypercaloric diet-induced obesity model efficacy. Wistar rats were divided into four groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD), and analyzed at three time points: ZT0, ZT12, and ZT18. Stressed animals were subjected to chronic stress for 1h per day, 5 days per week, during 80 days. The chronic exposure to a hypercaloric diet was an effective model for the induction of obesity and metabolic syndrome, increasing delta weight, Lee index, weight fractions of adipose tissue, and triglycerides and leptin levels. We confirmed the presence of a temporal pattern in the release of triglycerides, corticosterone, leptin, and adiponectin in naïve animals. Chronic stress reduced delta weight, MAT weight, and levels of triglycerides, total cholesterol, and leptin. There were interactions between chronic stress and obesity and serum total cholesterol levels, between time points and obesity and adiponectin and corticosterone levels, and between time points and chronic stress and serum leptin levels. In conclusion, both parameters were able to desynchronize the temporal pattern of leptin and triglyceride release, which could contribute to the development of metabolic diseases such as obesity and metabolic syndrome., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Obesity is a disease that has become a serious public health issue worldwide, and chronic stressors, which are a problem for modern society, cause neuroendocrine changes with alterations in food intake. Obesity and chronic stress are associated with the development of cardiovascular diseases and metabolic disorders. In this study, a rat model was used to evaluate the effects of a hypercaloric diet plus chronic restraint stress on the serum leptin and lipids levels and on the weight of specific adipose tissue (mesenteric, MAT; subcutaneous, SAT and visceral, VAT). Wistar rats were divided into the following 4 groups: standard chow (C), hypercaloric diet (HD), stress plus standard chow (S), and stress plus hypercaloric diet (SHD). The animals in the stress groups were subjected to chronic stress (placed inside a 25 cm × 7 cm plastic tube for 1h per day, 5 days per week for 6 weeks). The following parameters were evaluated: the weight of the liver, adrenal glands and specific adipose tissue; the delta weight; the Lee index; and the serum levels of leptin, corticosterone, glucose, total cholesterol, and triglycerides. The hypercaloric diet induced obesity in rats, increasing the Lee index, weight, leptin, triglycerides, and cholesterol levels. The stress decreased weight gain even in animals fed a hypercaloric diet but did not prevent a significant increase in the Lee index. However, an interaction between the independent factors (hypercaloric diet and stress) was observed, which is demonstrated by the increased serum leptin levels in the animals exposed to both protocols., (Copyright © 2012 Elsevier Inc. All rights reserved.)