Epidemiological evidence show that shift work can contribute to increased body weight. This study aims to map the prevalence of obesity and overweight among health professionals who work in shifts and analyse the factors that contribute to weight gain. A scoping review was conducted, following the proposal of the Joanna Briggs Institute. The Population, Concept, and Context strategy was used to formulate the guiding question. The proposed question was: "What is the prevalence of overweight and obesity among health professionals with shift work schedules?" After excluding duplicate articles, analysing titles and abstracts, and excluding articles that did not answer the guiding question, 20 articles remained and were included in this review. The studies have shown that the main factors that could influence weight gain among health professionals that are shift workers, are hormonal dysregulation, eating unhealthy meals, and low rates of physical activities practice. This scoping review showed that shift work can be an important risk factor for the development of overweight and obesity among these professionals. This implies the need of developing and implementing health policies aimed at reducing the excessive exposure of these workers to shift schedules and encouraging healthier and long-lasting changes in their lifestyles, both at workplace and outside of it.

Obesity-induced metabolic disorders can cause chronic inflammation in the whole body, activating the nuclear factor kappa B (NF-κB) pathway and inducing apoptosis. Therefore, anti-inflammatory strategies may be effective in preventing obesity-related renal injury. Tabersonine (Tab) has been used pharmacologically to alleviate inflammation-related symptoms. This study evaluated the therapeutic effect of Tab on obesity-related renal injury and explored the pharmacological mechanism. Tab (20 mg/kg) relieved HFD-induced renal structural disorder and alleviated renal functional decline in mice, including improvement of renal tissue fibrosis, reducing renal cell apoptosis and inflammation in renal tissues. Mechanistically, we demonstrated that Tab inhibited the activation of NF-κB signaling pathway both in vivo and in vitro, thereby improving the renal tissue lesions in the mice with obesity-related renal injury. In both the obese mouse model and the mouse glomerular mesangial cell model, the natural compound Tab ameliorated HFD- and saturated fatty acid-induced renal cell injury by inhibiting the activation of NF-κB signaling pathway. Our data suggest that Tab may become a potential candidate for the prevention and treatment of obesity-related renal injury.

Cardiovascular diseases (CVDs), the leading cause of death worldwide, share in common mitochondrial dysfunction, in specific a dysregulation of Ca2+ uptake dynamics through the mitochondrial Ca2+ uniporter (MCU) complex. In particular, Ca2+ uptake regulates the mitochondrial ATP production, mitochondrial dynamics, oxidative stress, and cell death. Therefore, modulating the activity of the MCU complex to regulate Ca2+ uptake, has been suggested as a potential therapeutic approach for the treatment of CVDs. Here, it is presented the role and implications of the MCU complex in CVDs are presented, followed by a review of the evidence for MCU complex modulation, genetically and pharmacologically. While most approaches have aimed within the MCU complex for the modulation of the Ca2+ pore channel, the MCU subunit, its intra- and extra- mitochondrial implications, including Ca2+ dynamics, oxidative stress, post-translational modifications, and its repercussions in the cardiac function, highlight that targeting the MCU complex has the translational potential for novel CVDs therapeutics.

Background Severe uncontrolled asthma in the pediatric population is a complicated disease and is considered a major challenge for pediatricians. Severe bronchial asthma in the pediatric population is related to significant morbidity and mortality. Children with complicated asthma are at a higher risk for unfavorable outcomes, including medication-associated adverse effects, severe life-threatening exacerbations, and poor quality of life. Methodology A cohort study was conducted at National Guard Health Affairs Hospital in Riyadh, Saudi Arabia. Data were collected using the chart review method utilizing a data collection sheet. A total of 363 charts of children aged one month to 14 years who visited the emergency room (ER) due to asthma exacerbation at NGHA were reviewed, from January 2016 to May 2022, to extract the variables. Variables included demographic data, comorbidities, and asthma-related variables which included the number of asthma exacerbations, hospital admission, ER visit, medication use (non-steroidal anti-inflammatory drugs and steroids), and the presence of allergic rhinitis and eczema. Results A total of 363 patients were analyzed, with 229 (63.1%) males and 134 (36.9%) females. The mean age was 4.9 years (SD = 3.5 years). Overall, 8.5% of patients had congenital heart disease, 4.1% had gastroesophageal reflux disease, 2.2% had diabetes mellitus, 1.9% had obstructive sleep apnea, and 0.6% had hypertension. Most patients presented with a cough at 88.2% (n = 320), followed by shortness of breath at 59% (n = 214) and fever at 46% (n = 167). Male asthmatics visited ER more than females. Forty-four patients were admitted to the hospital. Inhaled steroids were associated with fewer emergency department visits and night symptoms. Most asthmatic patients presented in the winter and fall seasons. Conclusions Asthma is a common pediatric respiratory disease that could be a burden if not controlled well. Unfortunately, the frequency of hospital admissions and pediatric ER visits due to asthma exacerbation is increasing. Comorbidities such as obesity and gastroesophageal reflux disease play a significant role in asthma control.

Background Cardiovascular disease (CVD) is still the leading cause of death globally. Alterations in the arterial wall architecture predict CVD morbidity and mortality and are associated with other CVD risk factors. Aortic wall thickness is closely linked to short- and long-term CVD morbidity and mortality, even without pronounced atherosclerotic changes. Obesity increases the risk of a broad spectrum of pathologies with vascular manifestation, which are often pathogenically associated with chronic oxidative stress and inflammatory response. Hence, as an antioxidant and anti-inflammatory agent, the pineal gland hormone melatonin is expected to have vasoprotective effects. This study evaluated the effects of melatonin supplementation on aortic wall thickness by assessing the cross-sectional associations of abdominal obesity with aortic intima-media thickness in a diet-induced obesity rat model. Methodology The model comprised of male Wistar rats that were on a high-fructose diet (HFD) (20% glucose-fructose corn syrup) for 12 weeks; the rats were divided into four groups (n = 8): control, HFD, HFD and melatonin supplementation (per os - 4 mg/kg/24h), and control and melatonin supplementation. All rats received a standard rodent diet and tap water. Zoometric measurements and the Lee index were calculated. Morphometric analysis of the abdominal aorta was performed by staining with hematoxylin-eosin and measuring the thickness of the abdominal aortic wall. For this, we used the Aperio Image Scope software. To evaluate the functional properties of the abdominal aorta, the modified Kernogan's index (KI) was employed. Results The results showed significantly elevated body weight (Lee index), KI, and wall thickness of the aorta abdominalis with morphometric changes in the vessel wall in HFD rats compared to the control group. Melatonin supplementation prevented these changes. Conclusions The administration of HFD to Wistar rats led to pathomorphological and morphometric changes in their abdominal aorta, which constitute the main diagnostic criteria of endothelial dysfunction. Melatonin supplementation regressed vascular wall remodeling and restored its functional capacity.

The polycystic ovarian syndrome affects many women today. Previous research has demonstrated a direct link between it and serious ailments such as type 2 diabetes, heart disease, and infertility. Originally thought to be a reproductive disorder, polycystic ovarian syndrome (PCOS) is now understood to be a metabolic and psychological disorder. Women of reproductive age suffering from PCOS undergo hormonal imbalances in which progesterone, insulin, and testosterone are produced in excess. PCOS exhibits a variety of characteristics as well as a heterogeneity of symptoms, including acne, hirsutism, androgenic alopecia, irregular menstruation, infertility, obesity, and mood disorders like despair and anxiety. Chronic anovulation, hyperandrogenism, type 2 diabetes, dyslipidemia, and an elevated threat of coronary artery disease are some of its defining characteristics. PCOS develops due to interacting genetic and environmental factors. From a gynaecological curiosity, it grew into a multisystem endocrinopathy. It is fascinating to learn how hormonal issues result in gynaecological problems. Insulin resistance, compensatory hyperinsulinism, and an increase in ovarian androgenic hyperresponsiveness to circulating insulin are all directly related to hyperandrogenism and anovulation. Independent of weight, insulin resistance is more common with PCOS and plays a crucial role in the syndrome's metabolic and reproductive complications. Anovulation, polycystic ovaries, and elevated luteinizing hormones, which increase circulating androgen, are all caused by a reduction in follicle-stimulating hormone. High androgen levels cause hyperinsulinemia, which leads cells to become insulin resistant and makes PCOS patients more likely to develop diabetes mellitus. Later research established that women with polycystic ovarian shape and persistent anovulation are the only ones susceptible to insulin resistance. Insulin resistance is thus a distinct characteristic of the condition. The purpose of this review paper is to investigate how PCOS ultimately results in type 2 diabetes mellitus.

A 58-year-old man without any personal or familial cardiac history presented to the emergency department with complaints of worsening left-sided chest pain that began at rest, described as a burning sensation and escalating to a 9/10 severity. He denied any personal or familial cardiac history but admitted that he had not been medically evaluated in approximately five years. His physical examination was notable for obesity, xerosis, macroglossia, and bilateral lower extremity edema. His initial labs demonstrated critical troponin levels that peaked at 11.5 ng/mL and he was diagnosed with a myocardial infarction and underwent cardiac catheterization with percutaneous stenting of the left anterior descending artery. His post-operative period was complicated by prolonged lethargy that was determined to be myxedema coma two days later when his thyroid stimulating hormone level was found to be 78 mIU/mL.

Obesity remains a public health concern, and intermittent fasting (IF) is a popular strategy for weight loss that has gained considerable scientific and popular attention. However, weight control can affect body image. Poor body image and its impact on psychological well-being are linked to obesity in many individuals. Body appreciation is a crucial characteristic of positive body image. However, there is a lack of studies assessing these relationships in Saudi adults.

Background: Obesity is one of the major public health problems worldwide and contributes to the onset of many diseases, especially the ones related to the metabolic syndrome. The new Dietary Guidelines for the Brazilian population bring a new food classification based on food processing and prioritizes the consumption of fresh or minimally processed foods. Aim: This study analyzed the effects of an educational intervention on obese women, on their weight loss, quality of life, components of the metabolic syndrome and pain. Methods: Randomized controlled pilot study, including 40 obese women, randomized into 2 groups: control group and intervention group. An educational intervention with 5 biweekly meetings of 90 min based on the Dietary Guidelines for the Brazilian population (2014) was carried out involving the intervention group. Parameters related to weight loss, quality of life (SF-36), pain (McGill), bioelectrical impedance analysis, cardiorespiratory fitness, and serum and clinical components of metabolic syndrome, as well as serum concentrations of cytokines were assessed. Results: Significantly decrease of body mass, waist and hip circumferences, basal metabolic rate, extracellular water, body capacitance, and body cell mass were observed in the intervention group after 3 months. Reduction of pain and improvement in quality of life and cardiorespiratory fitness were also observed in the intervention group. There were reductions in waist circumference and glycemia, components of metabolic syndrome. Conclusions: This study showed that the educational intervention can be associated with weight loss, increase in quality of life, reduction of pain, and better metabolic syndrome parameters in obese women.

Purpose: In the last decades we have seen an increase in sedentary behaviors and a decrease in physical activity in children when compared to past generations. This lifestyle is commonly associated with the development of clustering risk factors that define metabolic syndrome (MetS). Knowing that motor competence (MC) development can influence lifelong physical activity habits, it is reasonable to assume that children's MC will directly link to clustered cardiometabolic health outcomes. The aim of this study was to analyze the role of MC in MetS risk factors. Methods: Seventy children with a mean age of 7.49 (SD = 1.28) years were evaluated on motor competence (MCA-Motor Competence Assessment instrument), cardiovascular fitness (PACER test), upper body strength (UBS; handgrip), and the components of MetS, hypertriglyceridemia, hypertension, abdominal obesity, low concentration of high-density lipoprotein cholesterol, and high fasting blood glucose. The composite value of MetS was calculated according to Burns et al. (2017). Multiple standard regressions were performed to explore the effect of different variables on MetS. Motor competence and health-related fitness (cardiovascular fitness and relative upper body strength) were used as independent variables (predictors) and MetS as dependent variable. Results: Overall, the results showed that motor competence (β = -.072; p < .05) is a significant predictor and this model explained 7,1% of the variance in MetS. Conclusion: Although more studies are needed, our results indicate that MC seems to have a positive role in children's health markers.

The topic of obesity is gaining increasing popularity globally. From an evolutionary genetic perspective, it is believed that the main cause of the high obesity rate is the mismatch between environment and genes after people have shifted toward a modern high-calorie diet. However, it has been debated for over 60 years about how obesity-related genes become prevalent all over the world. Here, we review the three most influential hypotheses or viewpoints, i.e., the thrifty gene hypothesis, the drifty gene hypothesis, and the maladaptation viewpoint. In particular, genome-wide association studies in the recent 10 years have provided rich findings and evidence to be considered for a better understanding of the evolutionary genetic mechanisms of obesity. We anticipate this brief review to direct further studies and inspire the future application of precision medicine in obesity treatment.

Metabolic diseases, such as obesity, metabolic syndrome (MetS) and type 2 diabetes (T2D), are now a widespread pandemic in the developed world. These pathologies show sex differences in their development and prevalence, and sex steroids, mainly estrogen and testosterone, are thought to play a prominent role in this sexual dimorphism. The influence of sex hormones on these pathologies is not only reflected in differences between men and women, but also between women themselves, depending on the hormonal changes associated with the menopause. The observed sex differences in gut microbiota composition have led to multiple studies highlighting the interaction between steroid hormones and the gut microbiota and its influence on metabolic diseases, ultimately pointing to a new therapy for these diseases based on the manipulation of the gut microbiota. This review aims to shed light on the role of sexual hormones in sex differences in the development and prevalence of metabolic diseases, focusing on obesity, MetS and T2D. We focus also the interaction between sex hormones and the gut microbiota, and in particular the role of microbiota in aspects such as gut barrier integrity, inflammatory status, and the gut-brain axis, given the relevance of these factors in the development of metabolic diseases.

Endometrial cancer (EC) is a common gynecological cancer that endangers women health. Although substantial progresses of EC management have been achieved in recent years, the incidence of EC still remains high. Obesity has been a common phenomenon worldwide that increases the risk of EC. However, the mechanism associating obesity and EC has not been fully understood. Metabolic reprogramming as a remarkable characteristic of EC is currently emerging. As the primary factor of metabolic syndrome, obesity promotes insulin resistance, hyperinsulinemia and hyperglycaemia. This metabolic disorder remodels systemic status, which increases EC risk and is related with poor prognosis. Glucose metabolism in EC cells is complex and mediated by glycolysis and mitochondria to ensure energy requirement. Factors that affect glucose metabolism may have an impact on EC initiation and progression. In this study, we review the glucose metabolic reprogramming of EC not only systemic metabolism but also inherent tumor cell metabolism. In particular, the role of glucose metabolic regulation in malignant properties of EC will be focused. Understanding of metabolic profile and glucose metabolism-associated regulation mechanism in EC may provide novel perspective for treatment.

Mesenchymal stem cell (MSC) therapy is an emerging treatment strategy to counteract metabolic syndromes, including obesity and its comorbid disorders. However, its effectiveness is challenged by various factors in the obese environment that negatively impact MSC survival and function. The identification of these detrimental factors will provide opportunities to optimize MSC therapy for the treatment of obesity and its comorbidities. Dysregulated production of adipokines, a group of cytokines and hormones derived from adipose tissue, has been postulated to play a pivotal role in the development of obesity-associated complications. Intriguingly, adipokines have also been implicated in the modulation of viability, self-renewal, proliferation, and other properties of MSC. However, the involvement of adipokine imbalance in impaired MSC functionality has not been completely understood. On the other hand, treatment of obese individuals with MSC can restore the serum adipokine profile, suggesting the bidirectionality of the adipokine-MSC relationship. In this review, we aim to discuss the current knowledge on the central role of adipokines in the crosstalk between obesity and MSC dysfunction. We also summarize recent advances in the use of MSC for the treatment of obesity-associated diseases to support the hypothesis that adipokines modulate the benefits of MSC therapy in obese patients.