Summary A growing body of research links traffic‐related environmental factors to childhood obesity; however, the evidence is still inconclusive. This review aims to fill this important research gap by systematically reviewing existing research on the relationship between traffic‐related environmental factors and childhood obesity. Based on the inclusion criteria, 39 studies are selected with environmental factors of interest, including traffic flow, traffic pollution, traffic noise, and traffic safety. Weight‐related behaviours include active travel/transport, physical activity (PA), and intake of a high trans‐fat diet or stress symptoms; weight‐related outcomes are mainly body mass index (BMI) or BMI z‐scores and overweight/obesity. Of 16 studies of weight‐related behaviours, significant associations are reported in 11 out of 12 studies on traffic flow (two positively and nine negatively associated with PA), five out of six studies on traffic safety (four positively and one negatively associated with PA), one study on traffic pollution (positively with unhealthy food consumption), and one study on traffic noise (negatively associated with PA). Among 23 studies of weight‐related outcomes, significant associations are reported in six out of 14 studies on traffic flow (five positively and one negatively associated with obesity outcome), seven out of 10 studies on traffic pollution (all positively associated with obesity outcome), and two out of five on traffic noise (all positively associated with obesity outcome). Our findings show that long‐term traffic pollution is weakly positively associated with children's BMI growth, and traffic flow, pollution, and noise could affect weight‐related behaviours. Associations between traffic density and noise and weight status are rather inconclusive.

<h4>Objective</h4>Obesity and cardiovascular disease are major global public health problems. Maternal obesity has been linked to multiple adverse health consequences for both mother and baby. Obesity during pregnancy may adversely alter the intrauterine environment, which has been hypothesised to predispose the offspring to poorer cardiovascular health throughout life. In this paper, we systematically review current literature examining the links between maternal obesity and offspring cardiovascular health.<h4>Methods</h4>This study is registered with PROSPERO (CRD42021278567) and was conducted in accordance with the PRISMA guidelines. A comprehensive systematic literature search was conducted, including two electronic databases (Ovid Medline, Embase), cross-referencing, author searching, and grey literature searches. We selected studies exploring the relationship between maternal obesity and offspring cardiovascular health, using pre-defined eligibility criteria. Studies were critically appraised using the ROBINS-I tool.<h4>Results</h4>From 1,214 results, 27 articles met the eligibility criteria. Multiple cardiovascular outcomes were considered, including congenital heart disease, cardiometabolic parameters, and cardiovascular diseases in neonates, children, and adults. In these studies, maternal obesity was consistently associated with congenital heart disease, several adverse cardiometabolic parameters throughout life including higher body mass index and insulin levels, and greater risk of cardiovascular disease in adulthood. Hypothesized underlying mechanisms are complex and multifactorial comprising genetic, environmental, and socioeconomic components, which can be difficult to quantify. Heterogeneity in study designs, highly selected study samples, and high risk of bias in some studies limit conclusions regarding causality.<h4>Conclusions</h4>We identified consistent evidence of links between maternal obesity and poorer offspring cardiovascular health throughout the lifecourse, extending from the neonatal period into adulthood. Although underlying mechanisms are unclear, our findings support consideration of targeted maternal obesity prevention for promotion of offspring cardiovascular health. This all-encompassing systematic review provides critical appraisal of the latest evidence, defines gaps and biases of existing literature, and may inform potential new public health strategies for cardiovascular disease prevention.<h4>Systematic review registration</h4>[https://www.crd.york.ac.uk/prospero], identifier PROSPERO (CRD42021278567).

Obesity has assumed epidemic proportions in many countries worldwide, including Brazil, where it has also been considered as a major public health problem. The disease is characterized by an undesired accumulation of fat in all the deposit sites. The etiology of obesity has factors whose origins may be linked to genetic, nutritional, endocrine, hypothalamic, pharmacological, behavioral and environmental (mainly physical inactivity), which are interrelated and feed off of each other. Currently, adipose tissue has been recognized as a multifunctional organ that produces and secretes a number of bioactive peptides and proteins, which are involved in inflammation and immune response. According to its location, the adipocyte has different metabolic characteristics, and the fat excess, mainly located in the abdominal region shows a higher risk for developing type 2 diabetes mellitus and cardiovascular disease. Concomitant with obesity, physical inactivity has been considered an independent risk factor for cardiovascular disease. Therefore, the systematic practice of aerobic and resistance exercise has been recommended as a major non-pharmacological intervention for prevention and treatment of obesity and * Endereco para correspondencia:

Understanding the developmental origins of health and disease is integral to overcome the global tide of obesity and its metabolic consequences, including atherosclerotic cardiovascular disease, type 2 diabetes, hyperlipidemia, and nonalcoholic fatty liver disease. The rising prevalence of obesity has been attributed, in part, to environmental factors including the globalization of the western diet and unhealthy lifestyle choices. In this review we argue that how and when such exposures come into play from conception significantly impact overall risk of obesity and later health outcomes. While the laws of thermodynamics dictate that obesity is caused by an imbalance between caloric intake and energy expenditure, the drivers of each of these may be laid down before the manifestation of the phenotype. We present evidence over the last half-century that suggests that the temporospatial evolution of obesity from intrauterine life and beyond is, in part, due to the conditioning of physiological processes at critical developmental periods that results in maladaptive responses to obesogenic exposures later in life. We begin the review by introducing studies that describe an association between perinatal factors and later risk of obesity. After a brief discussion of the pathogenesis of obesity, including the systemic regulation of appetite, adiposity, and basal metabolic rate, we delve into the mechanics of how intrauterine, postnatal and early childhood metabolic environments may co

Overweight and obesity represent the most common nutritional disorder in domestic cats and constitute a significant global health issue. In this review, we synthesize current knowledge on the determinants, diagnosis, pathophysiology, complications, and comprehensive management of feline obesity. Feline overweight and obesity have a complex and multifactorial pathogenesis, arising from an interplay of intrinsic factors (e.g., genetic predisposition, age, sex, neutering status) and extrinsic factors (e.g., environment, owner behavior). The condition is characterized by a state of chronic low-grade systemic inflammation, endocrine dysregulation, insulin resistance, and hyperlipidemia, which collectively elevate the risk of numerous comorbidities, including diabetes mellitus, osteoarthritis, urinary tract disorders, dermatopathies, cardiomyopathy, and respiratory diseases, ultimately compromising life expectancy. This means that early detection and examination of excess body weight are crucial to treatment and prevention; at the same time, weight loss should be centered around personalized nutritional intervention, combined with behavioral correction measures such as regular feeding schedules and increased physical exercise. Furthermore, maintaining good communication between clinicians and the pet owners, as well as continuous monitoring, is the key to achieving effective weight loss. Future research is needed to move beyond current reactive models and embrace a focus on metabolic health over weight, prediction over reaction, and pathogenesis over symptomatology, aiming for preemptive strategies that improve feline healthspan.

The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets. It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models. These animals can then be used to study in vivo obesity, obesity's comorbidities, and ot Mice are used by scientists as diet-induced obesity models in experiments because they have mammalian physiological systems similar to those in humans. They also can be bred or genetically engineered to be resistant to certain diseases, which can be important for studies of these diseases and/or their influence on other biological systems. Scientists used mice to study the effect of lymphotoxins on metabolism. Mice without lymphotoxin alpha, lymphotoxin beta, or a lymphotoxin beta receptor had poorly composed microbiota, which made them resistant to obesity. Mice without lymphotoxin alpha, lymphotoxin beta, or a lymphotoxin beta receptor gained less weight on a high-fat diet than wild type mice did, even after remaining on a high-fat diet for a prolonged period of time. Mice are used to study the significance of certain chemicals on obesity. For example, mice were put on a high-fat diet, but given either tap water, green tea, or Goishi tea to drink. The mice who drank Goishi tea gained less weight and had less sugar in their blood than the mice who drank tap water and green tea. The researchers found that Goishi tea prevented the growth of adipocytes and prevented changes caused by tumor necrosis factor alpha and interleukin 6 when the mice were on a high fat diet. Another chemical studied to find an effect on obesity was propolis. To study the effects of the fungus, scientists injected it into mice while they were on an unrestricted high-fat diet. The researchers found that the mice injected with propolis had less adipose tissue, glucose, and cholesterol than the mice who were not administered propolis. Similar effects were seen in mice who were slowly introduced to propolis while on the high-fat diet. Some species of mice are used in research because they have specific traits important for a study rather than for similarity to humans. For example, Apodemus chevrieri is used in studies of metabolism because the length of the day determines their metabolism instead of their diet. In studies with A. chevrieri, scientists found that even if metabolism is controlled by day length, the mice could still gain weight with a high-fat diet.

Abstract Metabolic diseases such as obesity and diabetes are often thought to be caused by reduced energy expenditure, which poses a serious threat to human health. Cold exposure, exercise and caloric restriction have been shown to promote adipose tissue browning and thermogenesis. These physiological interventions increase energy expenditure and thus have emerged as promising strategies for mitigating metabolic disorders. However, that increased adipose tissue browning and thermogenesis elevate thermogenic consumption is not a reasonable explanation when humans and animals confront energetic challenges imposed by these interventions. In this review, we collected numerous results on adipose tissue browning and whitening and evaluated this bi‐directional conversion of adipocytes from the perspective of energy homeostasis. Here, we propose a new interpretation of the role of adipose tissue browning under energetic challenges: increased adipose tissue browning and thermogenesis under energy challenge is not to enhance energy expenditure, but to reestablish a more economical thermogenic pattern to maintain the core body temperature. This can be achieved by enhancing the contribution of non‐shivering thermogenesis (adipose tissue browning and thermogenesis) and lowering shivering thermogenesis and high intensity shivering. Consequently, the proportion of heat production in fat increases and that in skeletal muscle decreases, enabling skeletal muscle to devote more energy reserves

are both physiological and psychological and the solution or output is both physiological and psychological … food is easily available is not adaptive. Obesity is caused by eating too much. Obese people have higher … weakness. 2. Immune dysfunction. CFS is caused by immune disturbance caused by infection (Landay et al., 1991;