Ana Beatriz Rezende Paula’s research while affiliated with Universidade Federal de Ouro Preto and other places

Exposure to cold promotes cardiac remodeling, characterized by deleterious effects on structure and function, contributing to increased mortality from cardiovascular diseases. The mechanisms associated with these changes are poorly understood. This review gathers the literature data on the main alterations and mechanisms associated with the adverse cardiac structural and functional remodeling induced by cold exposure in mice. Original studies were identified by searching PubMed, Scopus, and Embase databases from January 1990 to June 2022. This systematic review was conducted in accordance with the criteria established by PRISMA and registered in PROSPERO (CRD42022350637). The risk of bias was evaluated by the SYRCLE. Eligible studies included original papers published in English that evaluated cardiac outcomes in mice submitted to short- or long-time cold exposure and had a control group at room temperature. Seventeen original articles were included in this review. Cold exposure induces pathological cardiac remodeling, characterized by detrimental structural and functional parameters, changes in metabolism and autophagy process, and increases in oxidative stress, inflammation, and apoptosis. In addition, Nppa, AT1A, Fbp3, BECN, ETA, and MT, appear to play fundamental roles in regulating cardiac remodeling. We suggest that strategies that seek to minimize the CVD risk and adverse effects of cold exposure should target these agents.

Circadian rhythms play important roles in regulating physiological and behavioral processes. These are adjusted by environmental cues, such as diet, which acts by synchronizing or attenuating the circadian rhythms of peripheral clocks, such as the liver, intestine, pancreas, white and brown adipose tissue, lungs, kidneys, as well as the heart. Some studies point to the influence of diet composition, feeding timing, and dietary restriction on metabolic homeostasis and circadian rhythms at various levels. Therefore, this systematic review aimed to discuss studies addressing the effect of diet on the heart clock in animal models and, additionally, the chronodisruption of the clock and its relation to the development of cardiovascular disorders in the last 15 years. A search was conducted in the PubMed, Scopus, and Embase databases. The PRISMA guide was used to construct the article. Nineteen studies met all inclusion and exclusion criteria. In summary, these studies have linked the circadian clock to cardiovascular health and suggested that maintaining a robust circadian system may reduce the risks of cardiometabolic and cardiovascular diseases. The effect of time-of-day-dependent eating on the modulation of circadian rhythms of the cardiac clock and energy homeostasis is notable, among its deleterious effects predominantly in the sleep (light) phase and/or at the end of the active phase.

Abstract The present study investigated the effects of aerobic physical training on the femoral morphological, densitometric and biomechanical properties in growing male rats subjected to protein-based malnutrition. Four-week-old male Wistar rats were randomized into groups of 10 animals: Control Sedentary (CS), Control Trained (CT), Malnourished Sedentary (MS) and Malnourished Trained (MT). Control and malnourished animals received diets with 12% protein and 6% protein, respectively. The trained groups were submitted to a treadmill running program for 8 weeks. Total proteins and albumin were analyzed in the animals' blood plasma. Histological, densitometric and biomechanical analyzes were performed on the animals' femur. Body mass gain, physical performance, biochemical markers and the femoral morphological, densitometric and biomechanical properties were determined. Exercise tolerance increased in trained groups. Malnourished animals exhibited lower serum protein and albumin levels than controls. Porosity and trabecular bone density were not different between groups. The femoral maximum load, maximum load until fracture, resilience, stiffness, tenacity and densitometric properties were reduced by malnutrition. Physical training associated with malnutrition exacerbated the impairment in the femoral maximum load, maximum load until fracture, bone mineral content and density. Aerobic physical training worsens the damages induced by protein-based malnutrition in the femoral biomechanical and densitometric properties of growing male rats.

This paper reviews studies that addressed the influence of diet on circadian rhythmicity in mice and, in turn, circadian clock chronodisruption and its role in the development of metabolic disorders. Studies from the past 14 years were selected via a systematic search conducted using the PubMed electronic database. After applying the inclusion and exclusion criteria, 291 studies were selected, of which 13 were chosen using the following inclusion criteria: use of a high-fat diet for mice, evaluation of clock gene expression, and the association between chronodisruption and lipid metabolism disorders. These studies reported changes in animals' biological clock when they developed metabolic disorders by consuming a high-fat diet. It was also evident that some clock gene mutations or deletions triggered metabolic changes. Disturbances of clock gene machinery may play important roles in lipid metabolism and the development of atherosclerotic processes. However, many metabolic processes also affect the function of clock genes and circadian systems. In summary, this review's results may provide new insights into the reciprocal regulation of energy homeostasis and the biological clock.