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The origin of breast cancer (BC) is widely considered to be a result of multiple factors, including both genetic and dietary influences. Dietary patterns shaped by calorie restriction—defined as reduced energy intake without inducing malnutrition, and varying ratios of the three major nutrients are thought to influence tumorigenesis. However, the complex interplay between caloric restriction, carbohydrate intake ratios, and genetic predisposition in influencing BC risk remains inadequately understood. This study aimed to explore these relationships in greater depth. A prospective cohort study which included 139,829 participants aged 40–72 years was conducted. We evaluated the association between dietary carbohydrate ratio under caloric restriction and the BC risk in a genetic risk group by using Cox proportional hazards regression models. The analysis also included a calculation of polygenic risk score (PRS) based on 304 breast cancer-associated genetic loci. A high dietary carbohydrate ratio pattern under caloric restriction was significantly associated with a 21% reduction in BC risk, respectively (HRG4 VS G1 = 0.80, 95% CI 0.66–0.97, P = 0.021), whereas a low PRS (lowest tertile) was associated with 0.84-fold decrease in risk (HRlow VS high = 0.84, 95%CI 0.72–0.98, P = 0.032). Compared with other participants, those at intermediate genetic risk with low carbohydrate ratio above caloric restriction showed a higher risk of BC (HR = 1.39, 95% CI 1.01–1.90, P = 0.041). In this cohort study, a diet pattern characterized by a high ratio of carbohydrates under conditions of caloric restriction may attenuate the impact of genetic factors on BC risk in individuals of European ancestry. [ABSTRACT FROM AUTHOR]

[Display omitted] • Caloric Restriction Mimetics (CRMs) are the chemicals that mimic the effects of Caloric Restriction (CR). • CRMs mimic CR effects via the mTOR, insulin, and sirtuin pathways, aiding cellular health and longevity. • CRMs such as resveratrol, metformin, and rapamycin enhance autophagy, benefiting Alzheimer's and Parkinson's diseases. • Clinical trials on CRMs have shown mixed results, but ongoing studies hold promise for improved outcomes. • Reconsidering the trial parameters, inclusion criteria, and dosages can optimize CRMs efficacy and synergistic mechanisms. Neurodegenerative disorders (NDDs) have been prevalent for more than a decade, and the number of individuals affected per year has increased exponentially. Among these NDDs, Alzheimer's disease, which causes extreme cognitive impairment, and Parkinson's disease, characterized by impairments in motor activity, are the most prevalent. While few treatments are available for clinical practice, they have minimal effects on reversing the neurodegeneration associated with these debilitating diseases. Lifestyle modifications and dietary choices are emerging and promising approaches to combat these disorders. Of the lifestyle changes that one could adopt, a major habit is caloric restriction. Caloric restriction (CR) is a lifestyle modification in which the amount of calories ingested is reduced to a significant amount without resulting in malnutrition. However, maintaining such a lifestyle is challenging. As alternatives, certain compounds have been recognized to mimic the effects produced by CR. These compounds are called caloric restriction mimetics (CRMs). Among these compounds, some have been designated established CRMs, namely, resveratrol, metformin, and rapamycin, whereas several other candidates are termed potential CRMs because of a lack of conclusive evidence of their effects. The potential CRMs discussed in this review are quercetin, chrysin, astragalin, apigenin, curcumin, epigallocatechin-3-gallate, and NAD+ precursors. This review aims to provide an overview of these CRMs' effectiveness in preventing neurodegenerative disorders associated with aging. Moreover, we highlight the clinical relevance of these compounds by discussing in detail the results of clinical trials on them. [ABSTRACT FROM AUTHOR]

Androgen exposure (AE) poses a profound health threat to women, yet its transgenerational impacts on male descendants remain unclear. Here, employing a large-scale mother-child cohort, we show that maternal hyperandrogenism predisposes sons to β-cell dysfunction. Male offspring mice with prenatal AE exhibited hyperglycemia and glucose intolerance across three generations, which were further exacerbated by aging and a high-fat diet. Mechanistically, compromised insulin secretion underlies this transgenerational susceptibility to diabetes. Integrated analyses of methylome and transcriptome revealed differential DNA methylation of β-cell functional genes in AE-F1 sperm, which was transmitted to AE-F2 islets and further retained in AE-F2 sperm, leading to reduced expression of genes related to insulin secretion, including Pdx1, Irs1, Ptprn2, and Cacna1c. The methylation signatures in AE-F1 sperm were corroborated in diabetic humans and the blood of sons with maternal hyperandrogenism. Moreover, caloric restriction and metformin treatments normalized hyperglycemia in AE-F1 males and blocked their inheritance to offspring by restoring the aberrant sperm DNA methylations. Our findings highlight the transgenerational inheritance of impaired glucose homeostasis in male offspring from maternal AE via DNA methylation changes, providing methylation biomarkers and therapeutic strategies to safeguard future generations' metabolic health. [ABSTRACT FROM AUTHOR]

Background/Objectives: To evaluate the impact of maximal fat oxidation intensity exercise combined with calorie restriction intervention on lipid-related parameters in a hypercholesterolemic population, and to determine if an optimal range of calorie restriction exists for effectively enhancing blood lipid profiles. Methods: A 4-week intervention study combined exercise and calorie restriction for 64 patients aged 18–60 with secondary hypercholesterolemia. Ultimately, 43 participants completed the study. The dietary intervention adhered to the principles of a balanced diet, with meal plans designed to provide three meals per day for the duration of the study. Each subject's daily calorie intake was set to match their individual resting energy expenditure (REE) plus varying proportions of physical activity (PA) calories. Participants were divided into four groups based on these proportions: REE only, REE + PA33%, REE + PA67%, and REE + PA100%. FATmax exercises were conducted 5 times per week, lasting 1 h each. Results: 1) Compared with baseline, subjects' body weight, fat mass and body fat rate decreased significantly; fat-free mass also decreased significantly in the REE, REE + PA33%, and REE + PA67% groups. 2) Subjects' serum TC decreased significantly; serum LDL-C and ApoB decreased significantly in the REE, REE + PA33%, and REE + PA67% groups; there were no significant changes in serum HDL-C and ApoA1. 3) Serum PCSK9 was significantly decreased in the REE and the REE + PA 67% groups; serum LDLR was significantly decreased in all groups of subjects. 4) Between the groups, the rate of change in serum LDL-C was significantly different. Conclusion: FATmax exercise combined with proper proportions of calorie restriction can significantly decrease serum cholesterol levels and fat mass in hypercholesterolemic patients. Nevertheless, it is misleading to assume that a drastic reduction in calorie intake invariably results in superior outcomes. Optimal cost-effectiveness may be achieved within a calorie restriction range of REE + PA33-67%. [ABSTRACT FROM AUTHOR]

AbstractBackgroundObjectivesMethodsResultsConclusionThe gluten-free diet (GFD) may aid weight loss, but its effects on non-celiac individuals are not well-studied.This pilot study compared the GFD’s effectiveness to a low-calorie diet (LCD) for weight loss in non-celiac Iranian women over an 8-week exercise program.A total of 126 women participated, 61 followed the LCD with exercise and therapies, while 65 adhered to the GFD with the same exercises. Data on demographics and body measurements were gathered via a survey.The GFD group showed significant reductions in body weight (p = 0.04), waist circumference (p = 0.006), and abdominal circumference (p = 0.0004). In contrast, the LCD group exhibited a significant reduction in waist circumference only (p = 0.03). A significant inverse correlation was found between non-alcoholic fatty liver disease (NAFLD) and the rate of weight reduction (r = −0.33, p = 0.006).Combining the GFD with exercise and therapies may effectively promote weight loss, especially in Iranian women. [ABSTRACT FROM AUTHOR]

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) reduce bodyweight and blood glucose. Extensive evidence from randomized controlled trials has indicated that GLP-1RAs have benefits well beyond weight loss and glucose control, extending from reductions in cardiovascular mortality to reductions in prostate cancer risk. Notably, some benefits of GLP-1RAs for the cardiovascular–kidney–metabolic (CKM) system arise before weight loss occurs for reasons that are not entirely clear but are key to patient care and drug development. Here, we hypothesize that GLP-1RAs act by inducing calorie restriction and by activating adenosine monophosphate-activated protein kinase (AMPK), which not only provides an explanation for the unique effectiveness of GLP-1RAs but also indicates a common mechanism shared by effective CKM therapies, including salicylates, metformin, statins, healthy diet, and physical activity. Whether AMPK activation is obligatory for effective CKM therapies should be considered. As such, we propose a mechanism of action for GLP-1RAs and explain how it provides an overarching framework for identifying means of preventing and treating cardiovascular, kidney, metabolic and related diseases, as well as informing the complementary question as to the components of a healthy lifestyle. [ABSTRACT FROM AUTHOR]

Background: Chronic stress and chronic pain are closely linked by the capacity to exacerbate each other, sharing common roots in the brain and in the gut. The strict intersection between these two neurological diseases makes important to have a therapeutic strategy aimed at preventing both to maintain mental health in patients. Diet is an modifiable lifestyle factor associated with gut-brain axis diseases and there is growing interest in its use as adjuvant to main therapies. Several evidence attest the impact of specific diets or nutrients on chronic stress-related disorders and pain with a good degree of certainty. A daily adequate intake of foods containing micronutrients such as amino acids, minerals and vitamins, as well as the reduction in the consumption of processed food products can have a positive impact on microbiota and gut health. Many nutrients are endowed of prebiotic, anti-inflammatory, immunomodulatory and neuroprotective potential which make them useful tools helping the management of chronic stress and pain in patients. Dietary regimes, as intermittent fasting or caloric restriction, are promising, although further studies are needed to optimize protocols according to patient's medical history, age and sex. Moreover, by supporting gut microbiota health with diet is possible to attenuate comorbidities such as obesity, gastrointestinal dysfunction and mood disorders, thus reducing healthcare costs related to chronic stress or pain. Objective: This review summarize the most recent evidence on the microbiota-mediated beneficial effects of macro- and micronutrients, dietary-related factors, specific nutritional regimens and dietary intervention on these pathological conditions. [ABSTRACT FROM AUTHOR]

Background/Objectives: Elevated body temperature is a well-established biomarker of infection, increased disease risk, and adverse health outcomes. However, the relationship between resting body temperature and long-term survival in older individuals is complex. Emerging evidence suggests that higher basal body temperature is associated with reduced survival and accelerated aging in non-obese older adults. This study aimed to compare body temperatures across different age groups in hospitalized older adults. Methods: Data were retrospectively collected from 367 physically healthy residents of a mental health center. Longitudinal data from 142 individuals (68 men and 74 women), aged 45 to 70 years and monitored continuously over 25 years, were compared with cross-sectional data from 225 individuals (113 men and 112 women) who underwent periodic clinical examinations with temperature measurements. The cross-sectional sample was stratified into four survival categories. Resting oral temperatures were measured under clinical conditions to ensure protocol consistency. Age-related changes in both sexes were evaluated using standard regression analysis, Student's t-tests, ANOVA, and Generalized Linear Models. Results: Longitudinal analysis revealed an increase in body temperature with age among women, while cross-sectional analysis showed that long-lived residents generally had lower body temperatures compared to their shorter-lived counterparts. Conclusions: These findings support the hypothesis that lower lifetime steady-state body temperature is associated with greater longevity in physically healthy older adults. However, further research is needed to determine whether the lower body temperature observed in long-lived individuals is linked to specific health advantages, such as enhanced immune function, absence of detrimental factors or diseases, or a reduced metabolic rate potentially influenced by caloric restriction. [ABSTRACT FROM AUTHOR]

Drunkorexia refers to high-risk behaviors that involve the intersection of disordered eating behaviors and risky alcohol consumption. This study utilized the extended Theory of Planned Behavior (TPB) to identify potential psychosocial factors that contribute to drunkorexia among students (484 undergraduate students) from a midwestern Mid-sized university. This cross-sectional study used online surveys designed to measure various drunkorexia-related behaviors including alcohol consumption, calorie restriction, excessive exercise, and purging utilizing antecedents of the TPB. About one-fourth of participants reported engagement in drunkorexia. The extended TPB model reported strong predictive validity for intention for calorie restriction, excessive exercise, and purging with instrumental attitudes and capacity being significant predictors for all three behaviors. Findings provide more profound insight regarding patterns of drunkorexia that could inform future theory-based interventions to address drunkorexia among college students. • Drunkorexia is becoming more common as college drinkers reported participating/practicing 1.04 days per week on average. • The least common compensatory behavior for drunkorexia was purging. • Instrumental attitudes were the strongest predictor of intentions to engage in any drunkorexia behavior. [ABSTRACT FROM AUTHOR]

Context Proneurotensin (pNT) is associated with obesity and type 2 diabetes (T2D), but the effects of Roux-en-Y gastric bypass (RYGB) on postprandial pNT levels are not well studied. Objective This work aimed to assess the effects of RYGB vs a very low-energy diet (VLED) on pNT levels in response to mixed-meal tests (MMTs), and long-term effects of RYGB on fasting pNT. Methods Cohort 1: Nine normoglycemic (NG) and 10 T2D patients underwent MMT before and after VLED, immediately post RYGB and 6 weeks post RYGB. Cohort 2: Ten controls with normal weight and 10 patients with obesity and T2D, who underwent RYGB or vertical sleeve gastrectomy (VSG), underwent MMTs and glucose-dependent insulinotropic polypeptide (GIP) infusions pre surgery and 3 months post surgery. Glucagon-like peptide-1 (GLP-1) infusions were performed in normal-weight participants. Cohort 3: Fasting pNT was assessed pre RYGB (n = 161), 2 months post RYGB (n = 92), and 1year post RYGB (n = 118) in NG and T2D patients. pNT levels were measured using enzyme-linked immunosorbent assay. Results Reduced fasting and postprandial pNT were evident after VLED and immediately following RYGB. Reintroduction of solid food post RYGB increased fasting and postprandial pNT. Prior to RYGB, all patients lacked a meal response in pNT, but this was evident post RYGB/VSG. GIP or GLP-1 infusion had no effect on pNT levels. Fasting pNTs were higher 1-year post RYGB regardless of glycemic status. Conclusion RYGB causes a transient reduction in pNT as a consequence of caloric restriction. The RYGB/VSG-induced rise in postprandial pNT is independent of GIP and GLP-1, and higher fasting pNTs are maintained 1 year post surgically. [ABSTRACT FROM AUTHOR]

This study investigates the cardioprotective effects of intense caloric restriction (ICR) from birth in ovariectomized rats, a model of estrogen deficiency mimicking menopause. Our findings demonstrate that ICR significantly improved both basal and post-ischemic cardiac function, even in the absence of estrogens. The restricted animals exhibited enhanced cardiac contractility and relaxation, particularly after ischemia/reperfusion (I/R) injury, with superior functional recovery compared to control groups. Notably, ICR reduced key cardiometabolic risk factors, including blood pressure, heart rate, and adiposity, while improving glucose tolerance and insulin sensitivity. Additionally, while mitochondrial biogenesis remained unaffected, ICR preserved mitochondrial integrity by reducing the number of damaged mitochondria. This was linked to a reduction in oxidative stress, as evidenced by lower reactive oxygen species (ROS) production in the hearts of restricted animals. These results suggest that ICR offers a protective effect against cardiovascular dysfunction induced by estrogen depletion, potentially through enhanced antioxidant defenses and mitochondrial protection. [ABSTRACT FROM AUTHOR]

Obesity results from a disproportionate accumulation of fat and has become a global health concern. The increase in adipose tissue is responsible for several systemic and testicular changes including hormone levels (leptin, adiponectin, testosterone, estrogen), inflammatory cytokines (increase in TNF-α and IL-6 and decrease in IL-10), and redox state (increase in reactive oxygen species and reduction in antioxidant enzymes). This results in poor sperm quality and compromised fertility in men with obesity. Lifestyle modifications, particularly diet transition to caloric restriction and physical exercise, are reported to reverse these negative effects. Nevertheless, precise mechanisms mediating these benefits, including how they modulate testicular oxidative stress, inflammation, and metabolism, remain to be fully elucidated. The main pathway described by which these lifestyle interventions reverse obesity-induced oxidative damage is the Nrf2-SIRT1 axis, which modulates the overexpression of antioxidant defenses. Of note, some of the detrimental effects of obesity on the testis are inherited by the descendants of individuals with obesity, and while caloric restriction reverses some of these effects, no significant work has been carried out regarding physical exercise. This review discusses the consequences of obesity-induced testicular oxidative stress on adult and pediatric populations, emphasizing the therapeutic potential of lifestyle to mitigate these detrimental effects. [ABSTRACT FROM AUTHOR]

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The global increase in human life expectancy, coupled with an unprecedented rise in the prevalence of obesity, has led to a growing clinical and socioeconomic burden of heart failure with preserved ejection fraction (HFpEF). Mechanistically, the molecular and cellular hallmarks of aging are omnipresent in HFpEF and are further exacerbated by obesity and associated metabolic diseases. Conversely, weight loss strategies, particularly caloric restriction, have shown promise in improving health status in patients with HFpEF and are considered the gold standard for promoting longevity and healthspan (disease-free lifetime) in model organisms. In this review, we implicate fundamental mechanisms of aging in driving HFpEF and elucidate how caloric restriction mitigates the disease progression. Furthermore, we discuss the potential for pharmacologically mimicking the beneficial effects of caloric restriction in HFpEF using clinically approved and emerging caloric restriction mimetics. We surmise that these compounds could offer novel therapeutic avenues for HFpEF and alleviate the challenges associated with the implementation of caloric restriction and other lifestyle modifications to reduce the burden of HFpEF at a population level. [ABSTRACT FROM AUTHOR]

Objectives: Epithelial ovarian cancer is a significant contributor to cancer-related mortality in women, frequently recurring post-treatment, often accompanied by chemotherapy resistance. Dietary interventions have demonstrated influence on cancer progression; for instance, caloric restriction has exhibited tumor growth reduction and enhanced survival in animal cancer models. In this study, we calculated a transcriptomic signature based on caloric-restriction for ovarian cancer patients and explored its correlation with ovarian cancer progression. Methods: We conducted a literature search to identify proteins modulated by fasting, intermittent fasting or prolonged caloric restriction in human females. Based on the gene expression of these proteins, we calculated a Non-Fasting Genomic Signature score for each ovarian cancer sample sourced from the Cancer Genome Atlas (TCGA) database. Subsequently, we examined the association between this genomic profile and various clinical characteristics. Results: The non-fasting genomic signature, comprising eight genes, demonstrated higher prevalence in primary ovarian tumors compared to normal tissue. Patients with elevated signature expression exhibited reduced overall survival and increased lymphatic invasion. The mesenchymal subtype, associated with chemotherapy resistance, displayed the highest signature expression. Multivariate analysis suggested the non-fasting genomic signature as a potential independent prognostic factor. Conclusions: Ovarian cancer tumors expressing a "non-fasting" transcriptional profile correlate with poorer outcomes, emphasizing the potential impact of caloric restriction in improving patient survival and treatment response. Further investigations, including clinical trials, are warranted to validate these findings and explore the broader applicability of non-fasting genomic signatures in other cancer types. [ABSTRACT FROM AUTHOR]

Age-related muscle wasting, sarcopenia is an extensive loss of muscle mass and strength with age and a major cause of disability and accidents in the elderly. Mechanisms purported to be involved in muscle ageing and sarcopenia are numerous but poorly understood, necessitating deeper study. Hence, we employed high-throughput RNA sequencing to survey the global changes in protein-coding gene expression occurring in skeletal muscle with age. Caloric restriction (CR) is a known prophylactic intervention against sarcopenia. Therefore, total RNA was isolated from the muscle tissue of both rats fed ad libitum and CR rats. RNA-seq data were subjected to Gene Ontology, pathway, co-expression, and interaction network analyses. This revealed the functional pathways most activated by both ageing and CR, as well as the key "hub" proteins involved in their activation. RNA-seq revealed 442 protein-coding genes to be upregulated and 377 to be downregulated in aged muscle, compared to young muscle. Upregulated genes were commonly involved in protein folding and immune responses; meanwhile, downregulated genes were often related to developmental biology. CR was found to suppress 69.7% and rescue 57.8% of the genes found to be upregulated and downregulated in aged muscle, respectively. In addition, CR uniquely upregulated 291 and downregulated 304 protein-coding genes. Hub genes implicated in both ageing and CR included Gc, Plg, Irf7, Ifit3, Usp18, Rsad2, Blm and RT1-A2, whilst those exclusively implicated in CR responses included Alb, Apoa1, Ambp, F2, Apoh, Orm1, Mx1, Oasl2 and Rtp4. Hub genes involved in ageing but unaffected by CR included Fgg, Fga, Fgb and Serpinc1. In conclusion, this comprehensive RNA sequencing study highlights gene expression patterns, hub genes and signalling pathways most affected by ageing in skeletal muscle. This data may provide the initial evidence for several targets for potential future therapeutic interventions against sarcopenia. [ABSTRACT FROM AUTHOR]

The 13th British Hernia Society Conference in 2024 featured presentations on various hernia-related topics, including the use of botulinum toxin in abdominal wall reconstruction and the experiences of patients with parastomal hernias. Studies also discussed surgical experience's impact on hernia rates and the use of lightweight mesh in repair. A case study from Brazil highlighted successful total abdominal wall reconstruction in a patient with a chronically infected mesh. Another study from the UK focused on reducing inappropriate hernia ultrasound requests to improve patient care and resource utilization. These findings emphasize the importance of thorough patient assessment and appropriate diagnostic practices in hernia management. [Extracted from the article]

Summary: Introduction: Obesity is characterized by chronic low‐grade inflammation. This study presents an updated systematic review and meta‐analysis on the effect of caloric restriction (CR) and intermittent fasting (IF) on plasma inflammatory biomarkers (C‐reactive protein [CRP], tumor necrosis factor [TNF]‐alpha, and interleukin [IL]‐6) in individuals with obesity/overweight compared with unrestricted or ad libitum feeding. Methods: PubMed, Web of Science, and SCOPUS databases were searched for randomized controlled trials (RCTs) reporting inflammatory biomarkers after at least 8 weeks of intervention. Standardized mean differences (SMDs) were calculated using a fixed effect model. Heterogeneity was determined using I2 statistics. Sensitivity analysis was conducted using the "leave‐one‐out" approach. Results: Relatively few RCTs have investigated the effect of IF on inflammatory biomarkers than with CR (6 vs. 15). Analysis of pooled data showed that CR was associated with a significant reduction in CRP with low heterogeneity (SMD −0.15 mg/L [95% CI −0.30 to −0.00], p = 0.04; I2 = 0%, p = 0.69) and IL‐6 with high heterogeneity (SMD −0.31 pg/mL [95% CI −0.51 to −0.10], p = 0.004; I2 = 73%, p = 0.001). IF was associated with a significant decrease in TNF‐alpha with moderate heterogeneity (SMD −0.32 pg/mL [95% CI −0.63 to −0.02], p = 0.04; I2 = 44%, p = 0.13). No associations were detected between IF and CRP or IL‐6 and CR and TNF‐alpha. Conclusion: CR may be more effective in reducing chronic low‐grade inflammation than IF. However, there were some concerns regarding the included studies' randomization and allocation sequence concealment process. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study is to nutritionally evaluate dams exposed to caloric restriction or cafeteria diets during the lactation period. Design/methodology/approach: Twenty-four female Wistar rats (n = 8/group) and their respective litters received during lactation: Control (CTRL) – received standard chow; Caloric restriction (CR) – received 50% of the ratio of the CTRL group; Cafeteria diet (CAF) – received cafeteria diet. Weighing of the mother rats and their respective litters occurred weekly and the diets were daily. At weaning, levels of glucose, total cholesterol, high-density lipoprotein, low-density lipoprotein (LDL) and triglycerides were evaluated. Abdominal adipose tissue was removed and weighed. Liver tissue was removed to determine the lipid profile. Findings: CR dams showed lower food (p < 0.01), caloric (p < 0.01) and all macronutrients (p < 0.01) intake. This group also observed intense weight loss (p < 0.01), in addition to low litter weight (p < 0.01). CAF dams had higher caloric intake (p < 0.05) and increased consumption of lipids (p < 0.01). The CAF group also reported greater accumulation of abdominal adipose tissue (p = 0.01), elevated levels of LDL (p < 0.01) and hepatic lipids (p < 0.01), as well as a litter with higher weaning weight (p < 0.01). Originality/value: Few studies have evaluated the effects of different models of malnutrition focusing on dams. CR dams showed severe weight loss, which may have caused their pups to be underweight. On the other hand, the CAF diet during lactation led to a higher consumption of lipids and accumulation of adipose tissue, which generated a high weight of the litter. [ABSTRACT FROM AUTHOR]

Introduction: Very low-calorie diets with hospitalization have demonstrated promise as a viable therapeutic option for severe obesity and its associated comorbidities. However, large studies providing a comprehensive longitudinal observation of patients undergoing this therapy are lacking. We evaluated the effectiveness of treating severe obesity in hospitalized patients, using very low-calorie diets and clinical support to develop lifestyle changes. Methods: This study was a retrospective cohort comparing exposure variables in a secondary data analysis with a pre-post treatment design. Data were obtained from medical records of patients with severe obesity (grade II or III) treated in a Brazilian obesity specialist hospital from 2016 to 2022. The patients underwent a very low-calorie diet (500–800 kCal/day) and immersive changes in lifestyle habits, monitored by a multidisciplinary team. At 3 months, 777 patients presented complete data and 402 presented complete data at 6 months. The study compared changes in bioimpedance and laboratory tests, between men and women and age groups. Results: Three months of hospitalization yielded significant reductions in weight, body mass index (BMI), body fat, skeletal muscle mass, glucose, inflammatory, and lipid parameters. These reductions were more pronounced after 6 months, nearly doubling those observed at 3 months. In women, BMI and fat mass reduced by 10.4% and 15.2% at 3 months and 20.4% and 31.3% at 6 months, respectively. In men, BMI and fat mass decreased by 12.9% and 25.3 at 3 months and 23.6% and 45.3% at 6 months, respectively. Elderly individuals (aged ≥ 60 years) had smaller reductions in BMI and fat mass than non-elderly individuals (aged < 60 years) but still presented significant improvements. Conclusion: This study suggests the viability of treating severe obesity by hospitalization with low-calorie diets and immersive lifestyle changes. This treatment modality significantly improves anthropometric measurements, glucose, lipids, and inflammatory markers, thereby reducing cardiovascular risk. [ABSTRACT FROM AUTHOR]

Aging is a complex multifactorial process that results in a general functional decline, including cognitive impairment. Caloric restriction (CR) can positively influence the aging processes and delay cognitive decline. There is a rhythmic variation in memory and learning processes throughout the day, indicating the involvement of the circadian clock in the regulation of these processes. Despite growing evidence on the efficacy of CR, it has not yet been fully determined whether starting this strategy at an advanced age is beneficial for improving quality of life and eventually, for protection against age-related diseases. Here, we investigated the effect of late-onset CR on the temporal organization of the molecular clock machinery, molecules related to cognitive processes and epigenetic regulation, in the hippocampus of old male rats maintained under constant darkness conditions. Our results evidenced the existence of a highly coordinated temporal organization of Bmal1 , Clock , Bdnf , Trkb , Dnmts , Sirt1 , and Pgc-1α in the hippocampus of young adult rats. We observed that aging led to cognitive deficits and loss of circadian oscillations of all the above variables. Interestingly, CR restored circadian rhythmicity in all cases and, in addition, improved the cognitive performance of the old animals. This work would highlight the importance of the circadian clock and its synchronization with feeding signals, as the basis of the beneficial effects of CR. Thus, lifestyle modifications, such as CR, might be a powerful intervention to preserve hippocampal circadian organization and cognitive health during aging. [ABSTRACT FROM AUTHOR]

Context The liver/foregut satiety hormone liver-expressed antimicrobial peptide 2 (LEAP2) is an inverse agonist at the acyl ghrelin receptor (GHSR), increasing after food intake and decreasing after bariatric surgery and short-term nonsurgical weight loss, but effects of long-term dietary weight loss are unknown. Objective The objective of this study was to examine and compare the effects of these interventions on fasting and postprandial plasma LEAP2 and investigate potential metabolic mediators of changes in plasma LEAP2. Methods Plasma LEAP2 was measured in a previously published 2-year trial comparing standard medical management (SMM) (including 600-kcal/day deficit) with duodenal-jejunal bypass liner (DJBL, Endobarrier) insertion (explanted after 1 year) in adults with obesity and inadequately controlled type 2 diabetes mellitus. Results In the SMM group (n = 25-37), weight decreased by 4.3%, 8.1%, 7.8%, and 6.4% at 2, 26, 50, and 104 weeks and fasting plasma LEAP2 decreased from baseline mean ± SD 15.3 ± 0.9 ng/mL by 1.7, 3.8, 2.1, and 2.0 ng/mL, respectively. Absolute/decreases in fasting plasma LEAP2 positively correlated with absolute/decreases in body mass index, glycated hemoglobin A1c, fasting plasma glucose, serum insulin, homeostatic model assessment for insulin resistance, and serum triglycerides. Despite greater weight loss in the DJBL group (n = 23-30) at 26 to 50 weeks (10.4%-11.4%), the decrease in fasting plasma LEAP2 was delayed and attenuated (vs SMM), which may contribute to greater weight loss by attenuating GHSR signaling. Plasma LEAP2 did not increase with weight regain from 50 to 104 weeks after DJBL explant, suggesting a new set point with weight loss maintenance. Increases in plasma LEAP2 after a 600-kcal meal (10.8%-16.1% at 1-2 hours) were unaffected by weight loss, improved glucose metabolism, or DJBL insertion (n = 9-25), suggesting liver rather than duodenum/jejunum may be the primary source of postprandial LEAP2 secretion. Conclusion These findings add to our understanding of the regulation and potential physiological role of plasma LEAP2. [ABSTRACT FROM AUTHOR]

Cellular senescence is a state of permanent cell cycle arrest accompanied by metabolic activity and characteristic phenotypic changes. This process is crucial for developing age-related diseases, where excessive calorie intake accelerates metabolic dysfunction and aging. Overnutrition disturbs key metabolic pathways, including insulin/insulin-like growth factor signaling (IIS), the mammalian target of rapamycin (mTOR), and AMP-activated protein kinase. The dysregulation of these pathways contributes to insulin resistance, impaired autophagy, exacerbated oxidative stress, and mitochondrial dysfunction, further enhancing cellular senescence and systemic metabolic derangements. On the other hand, dysfunctional endothelial cells and adipocytes contribute to systemic inflammation, reduced nitric oxide production, and altered lipid metabolism. Numerous factors, including extracellular vesicles, mediate pathological communication between the vascular system and adipose tissue, amplifying metabolic imbalances. Meanwhile, caloric restriction (CR) emerges as a potent intervention to counteract overnutrition effects, improve mitochondrial function, reduce oxidative stress, and restore metabolic balance. CR modulates pathways such as IIS, mTOR, and sirtuins, enhancing glucose and lipid metabolism, reducing inflammation, and promoting autophagy. CR can extend the health span and mitigate age-related diseases by delaying cellular senescence and improving healthy endothelial–adipocyte interactions. This review highlights the crosstalk between endothelial cells and adipocytes, emphasizing CR potential in counteracting overnutrition-induced senescence and restoring vascular homeostasis. [ABSTRACT FROM AUTHOR]

Summary Calorie‐restricted diets cause weight loss and can drive type 2 diabetes remission. However, many patients struggle to achieve clinically relevant weight loss, and the reasons are not well understood. Chemical exposure is associated with obesity and type 2 diabetes development, and some evidence from preclinical experiments suggests it can limit the clinical benefits of calorie restriction. We systematically reviewed the evidence for the effects of environmental chemical exposure on mass loss and glycemic control during diet‐induced weight management in humans (PROSPERO: CRD42022339993). Of 222 unique citations, only six papers directly examined this question. Only one targeted people with type 2 diabetes. One linked phthalates and parabens, but not bisphenols, with slower fat loss. Two showed per‐ and polyfluoroalkyl substances were not associated with mass loss, but with faster subsequent mass regain. One linked impaired adiposity improvements with air pollutants. Two papers reported weight loss‐induced elevation in plasma organochlorines associated with altered glycemic control. The risk of bias largely arose from the potential for deviation from the intended diet, and statistics and reporting. The role of chemical exposure in impeding the effectiveness of weight management programs needs to be better understood to provide suitable support to people living with obesity and type 2 diabetes. [ABSTRACT FROM AUTHOR]

Stem and progenitor cell mitosis is essential for tissue development and homeostasis. How these cells ensure proper chromosome segregation, and thereby maintain mitotic fidelity, in the complex physiological environment of a living animal is poorly understood. Here we use in situ live-cell imaging of C. elegans germline stem and progenitor cells (GSPCs) to ask how the signaling environment influences stem and progenitor cell mitosis in vivo. Through a candidate screen we identify a new role for the insulin/IGF receptor (IGFR), daf-2, during GSPC mitosis. Mitosis is delayed in daf-2/IGFR mutants, and these delays require canonical, DAF-2/IGFR to DAF-16/FoxO insulin signaling, here acting cell non-autonomously from the soma. Interestingly, mitotic delays in daf-2/IGFR mutants depend on the spindle assembly checkpoint but are not accompanied by a loss of mitotic fidelity. Correspondingly, we show that caloric restriction, which delays GSPC mitosis and compromises mitotic fidelity, does not act via the canonical insulin signaling pathway, and instead requires AMP-activated kinase (AMPK). Together this work demonstrates that GSPC mitosis is influenced by at least two genetically separable signaling pathways and highlights the importance of signaling networks for proper stem and progenitor cell mitosis in vivo. Author summary: Stem and progenitor cells drive tissue development and sustain adult tissue turnover by producing new daughter cells via cell division, the success of which depends on proper chromosome segregation during mitosis. Stem and progenitor cells perform mitosis in the complex environment of a living animal, yet relatively little is known about how events during mitosis are influenced by this in vivo context. In particular, whether signaling pathways that coordinate other aspects of stem and progenitor cell behavior with animal physiology also play a role during mitosis is poorly understood. Here we took advantage of the germline stem and progenitor cells of the model nematode C. elegans to address this question. Through live-cell imaging of germline stem and progenitor cell mitosis, we uncover a new role for the insulin signaling pathway. We find that reducing insulin signaling delays germline stem and progenitor cell mitosis, but, surprisingly, these delays are not accompanied by a loss of mitotic fidelity. In addition, we find that reducing insulin signaling in somatic tissues is sufficient to delay germline stem and progenitor mitosis, indicating that the pathway acts non-autonomously. Finally, while insulin signaling is known to link cell division with nutritional status in many species, we found that it did not mediate the effects of caloric restriction on germline stem and progenitor cell mitosis. Instead, caloric restriction acts via the conserved energy-sensing regulator AMPK. These results uncover new regulators of germline stem and progenitor cell mitosis and emphasize the importance of signaling pathways for proper stem and progenitor cell mitosis in vivo. [ABSTRACT FROM AUTHOR]

Calorie restriction (CR) and physical exercise (EX) are well‐established interventions known to extend health span and lifespan in animal models. However, their impact on human biological aging remains unclear. With recent advances in omics technologies and biological age (BioAge) metrics, it is now possible to assess the impact of these lifestyle interventions without the need for long‐term follow‐up. This study compared BioAge biomarkers in 41 middle‐aged and older adult long‐term CR practitioners, 41 age‐ and sex‐matched endurance athletes (EX), and 35 sedentary controls consuming Western diets (WD), through PhenoAge: a composite score derived from nine blood‐biomarkers. Additionally, a subset of participants (12 CR, 11 EX, and 12 WD) underwent multi‐omic profiling, including DNA methylation and RNAseq of colon mucosa, blood metabolomics, and stool metagenomics. A group of six young WD subjects (yWD) served as a reference for BioAge calculation using Mahalanobis distance across six omic layers. The results demonstrated consistently lower BioAge biomarkers in both CR and EX groups compared to WD controls across all layers. CR participants exhibited lower BioAge in gut microbiome and blood‐derived omics, while EX participants had lower BioAge in colon mucosa‐derived epigenetic and transcriptomic markers, suggesting potential tissue‐specific effects. Multi‐omic pathway enrichment analyses suggested both shared and intervention‐specific mechanisms, including oxidative stress and basal transcription as common pathways, with ether lipid metabolism uniquely enriched in CR. Despite limitations due to sample size, these findings contribute to the broader understanding of the potential anti‐aging effects of CR and EX, offering promising directions for further research. [ABSTRACT FROM AUTHOR]

Summary The endocrine consequences of weight loss by bariatric surgery (BS) and caloric restriction are not fully understood but contribute to variable improvements in insulin sensitivity and cardiometabolic health. This study compared changes in insulin sensitivity and plasma concentrations of gut peptides 8 weeks and 1 year after BS and a low‐calorie diet (LCD). Nineteen female patients with obesity self‐selected BS (gastric bypass [n = 5] or sleeve gastrectomy [n = 7]) or LCD (n = 7) in this parallel‐arm, prospective observational study. We assessed insulin sensitivity via a two‐step hyperinsulinemic–euglycemic clamp (20 and 80 mU/min/m2 insulin). Plasma glucose, insulin, and gut peptides were measured around a mixed meal tolerance test (400 kcal). Visual analogue scales (VAS) were used to rate subjective appetite sensations. All assessments were conducted at baseline and after 8 weeks and 1 year of intervention. Whole‐body insulin sensitivity was unchanged 8 weeks after the intervention. One year after surgery, insulin sensitivity at both 20 and 80 mU/m2/min insulin infusion doses increased with BS weight loss (−33.8% ± 1.4% body weight) but was unchanged in LCD with small weight loss (−3.7% ± 2.0% body weight). Postprandial total PYY increased more following BS while total and acylated ghrelin decreased more following BS compared to LCD. Hunger decreased and fullness increased with BS compared to LCD (p = .037; p = .010, respectively). Insulin sensitivity was improved only 1 year after BS, despite significant weight loss after 8 weeks. Changes in gut peptides after BS paralleled reduced hunger and increased fullness. Most improvements in cardiometabolic health were related to weight loss. [ABSTRACT FROM AUTHOR]

The global rise in obesity underscores the need for effective weight management strategies that address individual metabolic and hormonal variability, moving beyond the simplistic "calories in, calories out" model. Body types—ectomorph, mesomorph, and endomorph—provide a framework for understanding the differences in fat storage, muscle development, and energy expenditure, as each type responds uniquely to caloric intake and exercise. Variability in weight outcomes is influenced by factors such as genetic polymorphisms and epigenetic changes in hormonal signaling pathways and metabolic processes, as well as lifestyle factors, including nutrition, exercise, sleep, and stress. These factors impact the magnitude of lipogenesis and myofibrillar protein synthesis during overfeeding, as well as the extent of lipolysis and muscle proteolysis during caloric restriction, through complex mechanisms that involve changes in the resting metabolic rate, metabolic pathways, and hormonal profiles. Precision approaches, such as nutrigenomics, indirect calorimetry, and artificial-intelligence-based strategies, can potentially leverage these insights to create individualized weight management strategies aligned with each person's unique metabolic profile. By addressing these personalized factors, precision nutrition offers a promising pathway to sustainable and effective weight management outcomes. The main objective of this review is to examine the metabolic and hormonal adaptations driving variability in weight management outcomes and explore how precision nutrition can address these challenges through individualized strategies. [ABSTRACT FROM AUTHOR]

Introduction and purpose Obesity is a complex, chronic disease that has recently reached epidemic proportions. According to the World Health Organization, the prevalence of this disease tripled since 1975, reaching 13% of the global population in 2016. A body mass index (BMI) > 30 kg/m² is typically the reference point for obesity in adults, and the mortality risk associated with obesity increases by 100% at BMI > 40 kg/ m² compared to individuals with normal body weight. The aim of the article is to present the benefits of bariatric surgery, encompassing not only weight loss but also a range of other advantages for obese patients undergoing the procedure. Materials and methods The literature included in the PubMed databases is searched through the words such as obesity, bariatric surgery. Description of the state of knowledge: The literature review shows the breadth of the issue. Obesity constitutes a public health crisis and a significant risk factor for many diseases, including cardiovascular diseases, diabetes, cancer, and numerous others. Since in most cases, lifestyle optimization and low-calorie diet alone are not sufficient, pharmacological interventions as well as surgical interventions are often necessary. Bariatric surgery remains the most effective treatment option, as it has been demonstrated to not only reduce body weight but also decrease mortality from cardiovascular diseases and extend overall life expectancy. Conclusions The benefits, complications, and selection of the best surgical method for treating obesity are still under investigation. However, research demonstrates the long-term effectiveness of bariatric surgery in weight loss and the remission of comorbidities such as type 2 diabetes, as well as in preventing obesity-related cancers. [ABSTRACT FROM AUTHOR]

Objectives: The ketogenic diet (KD) has long been used as an alternative nonpharmacological therapy to manage pharmacoresistant epilepsy. The anticonvulsant mechanisms of KD have yet to be fully elucidated. The present study explored whether a KD could exert antioxidative effects by altering brain Klotho (Kl) gene expression.Methods: Thirty male rats were divided into three groups: the normal diet (ND) group received standard rat chow; the calorie-restricted diet (CRD) group was maintained at 90% of the calculated energy need; and the KD group received a diet composed of 8% protein, 2% carbohydrates, and 90% fat (per calorie macronutrient). The levels of β-hydroxybutyrate (BHB) in the serum, Kl gene expression in the brain, and Kl protein, malondialdehyde (MDA), and protein carbonyl (PC) levels in the serum and brain were evaluated by standard methods.Results: The serum BHB levels in the KD group were significantly greater than those in the ND and CRD groups (p < 0.001). The Kl expression in the brain was significantly greater in the KD group than in the ND group (p = 0.028). The brain MDA levels in the KD group were significantly lower than those in the ND group (p = 0.006). Elevated BHB was positively correlated with brain Kl expression (r = 0.668, p < 0.001). The brain MDA levels were negatively correlated with brain Kl expression (r = −0.531, p = 0.003) and serum BHB levels (r = 0.472, p = 0.020).Discussion: KD might exert antioxidative effects by increasing BHB and upregulating Kl in the brain. This could be considered a possible anticonvulsant mechanism of KD. [ABSTRACT FROM AUTHOR]

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Emerging evidence suggests the potential of rapamycin, an antibiotic from Streptomyces hygroscopicus that functions as a mechanistic target of rapamycin (mTOR) inhibitor, as a mimetic of caloric restriction (CR) for maintaining skeletal muscle health. Several studies showed that rapamycin administration (RAP) reduced appetite and energy intake. However, the physiological and molecular differences between RAP and CR in skeletal muscle are not fully understood. Here we observed the effects of 4 weeks of RAP administration and CR corresponding to the reduction in energy intake produced by RAP administration (PF, paired feeding) on fast glycolytic and slow oxidative muscle in young adult rats. We found that 4 weeks of RAP demonstrated low fast-glycolytic muscle mass with smaller type I and IIb/x myofiber size independent of the energy intake. In addition, PF improved the contractile function of the plantar flexor muscle, whereas RAP did not improve its function. The suppressing response of mTORC1 signaling to RAP is greater in slow-oxidative muscles than in fast-glycolytic muscles. In addition, systemic glucose tolerance was exacerbated by RAP, with reduced expression of Rictor and hexokinase in skeletal muscle. These observations imply that RAP may have a slight but significant negative impact and it obviously different to CR in young adult skeletal muscle. [ABSTRACT FROM AUTHOR]

Background: Aging is caused by the progressive accumulation of various changes in the body, which is associated with an increase in free radicals and oxidative stress (OS). The aim of this study was to investigate the potential of caloric restriction (CR) and quercetin (QUER) in alleviating OS in aging and the involvement of the NAD (P) H quinone oxidoreductase 1 (NQO1)/SIRT1 signaling pathway in these effects. Methods: Two age groups of male Wistar rats (eight and 20 weeks of age) were included in the study and subdivided into normal diet (ND), ND with QUER (15 mg Kg-1, IP), ND with CR, and ND with QUER and CR groups. The activities of catalase (CAT), paraoxonase (PON1), liver enzymes and lipid profiles, and the expression of SIRT1 and NQO1 genes were analyzed using the desired methods. Results: We showed higher liver enzymes (aspartate aminotransferase [AST], alanine transaminase [ALT], and alkaline phosphatase [ALP]), increased atherogenic lipids, and reduced PON1 activity in 20-week-old rats compared with eight-week-old rats, and the administration of QUER and CR restored these values to the normal range. The expression of NQO1 and SIRT1 is also affected by CR and QUER. CR alone and in combination with QUER significantly raised the expression of the NQO1 and SIRT1 genes. This effect was notable in SIRT1. Conclusions: QUER and CR together improved the detrimental effects of aging by modulating antioxidant signaling pathways, suggesting this combination is a complementary therapeutic regime for aging and age-related diseases. [ABSTRACT FROM AUTHOR]

Caloric intake can greatly affect many aspects of an organism's life. A deficiency of calories can lead to stress resulting in decreased fecundity, insufficient calories to maintain tissues and increased lifespan. Conversely, increasing caloric density increases fecundity and decreases lifespan. Despite decades of work exploring food quality and quantity on physiology in the model species Drosophila melanogaster Meigan 1830 (Diptera: Drosophilidae) and the melanogaster group in general, relatively little work explores the physiological responses to diet manipulation in other Drosophila species, like the obscura species group. Here, we looked at the effects of five different caloric densities (0.5×, 0.75×, 1.0×, 1.5× and 3.0×) on food intake, body weight, body fat, fecundity and longevity in D. pseudoobscura Frolova & Astaurov, 1929 (Diptera: Drosophilidae). Comparing longevity and fecundity across diets, we found that heavy caloric concentration (3.0×) decreases lifespan and that calorie restriction (0.5× and 0.75×) led to significant decreases in fecundity and body weight. However, calorie concentration did not significantly increase D. pseudoobscura body fat. By expanding our understanding of the physiological responses to diet stress to D. pseudoobscura, we establish the framework for comparative work across Drosophila species. With this information, we can then identify which physiological responses to diet manipulation might be most conserved and comparable across species. [ABSTRACT FROM AUTHOR]

Maternal caloric restriction during pregnancy significantly impacts kidney development, influencing susceptibility to chronic kidney disease in adulthood. This study explores DNA methylation changes in nephron progenitor cells resulting from caloric restriction and their implications for kidney health. Global DNA hypomethylation is observed in nephron progenitors from caloric-restricted embryos, with specific genomic regions displaying distinct methylation patterns, including hypomethylation and hypermethylation. Differentially methylated regions exhibit enhanced chromatin accessibility, indicating biological relevance. Hypomethylated regions are enriched for genes associated with developmental processes, reflecting changes in gene expression and highlighting their functional relevance in kidney development. The study also reveals that supplementing methionine, an essential amino acid, restores disrupted DNA methylation patterns, particularly in enhancer regions, emphasizing methionine's critical role in regulating nephron progenitor cell epigenetics and ensuring proper kidney development. The intricate relationship between maternal nutrition, dynamic DNA methylation, and kidney development is highlighted, emphasizing the enduring impact of early-life nutritional challenges on kidney function. This research elucidates epigenetic mechanisms as mediators for the lasting effects of maternal caloric restriction on kidney health. The study contributes valuable insights into the origins of chronic kidney diseases during early developmental stages, offering potential interventions to mitigate adverse outcomes. NEW & NOTEWORTHY: Our study establishes a direct link between maternal caloric restriction, DNA methylation patterns in nephron progenitor cells, and kidney development. We reveal consistent alterations in methylation patterns, coupled with corresponding shifts in the expression of genes related to kidney development and cell proliferation. Methionine supplementation emerges as a promising intervention, effectively restoring disrupted DNA methylation patterns. These findings pave the way for potential therapeutics, optimizing kidney development and mitigating the burden of chronic kidney disease in adulthood. [ABSTRACT FROM AUTHOR]

The safety of 18650 lithium-ion batteries is critical for the reliability and durability of electric vehicles, especially as interest in sustainable transportation grows. Battery failures, such as fires or explosions, pose significant risks to both users and manufacturers, highlighting the need for advanced power systems. This study used finite element method (FEM) simulations and crash tests to evaluate battery safety in accident scenarios. The results showed that mechanical damage, especially from collisions, can cause internal short circuits, increasing the risk of thermal runaway, especially when combined with high temperatures during normal operation or charging. This can be caused by mechanical damage to the battery causing a change in the distance inside the battery, causing it to short circuit. The results highlight the importance of designing battery systems that prevent internal short circuits, especially under extreme conditions, and the need for continuous monitoring of battery parameters to detect early signs of failure. In the context of improving battery safety, the battery not only saves lives, but also extends vehicle life, reduces electronic waste, and increases energy efficiency, which is consistent with global efforts to minimize the environmental impact of technology and promote safer transportation. [ABSTRACT FROM AUTHOR]

Introduction: Mitophagy, the selective degradation of damaged mitochondria, is essential for maintaining cellular health and function, particularly in high-energy demanding post-mitotic cells like neurons and in microglial cells. Aging results in impaired mitophagy, leading to mitochondrial dysfunction, oxidative stress, the release of damage-associated proteins (DAMPs), and neuroinflammation, which contribute to neurodegenerative diseases such as Alzheimer's and Parkinson's. Mitochondrial dysfunction also contributes to the pathophysiology of depression by affecting synaptic plasticity, increasing neuroinflammation, and heightening oxidative stress. Aim: In this review, we summarize the recent developments on mechanisms of mitophagy, its therapeutic role in neuroprotection, and its implications in aging and neuroinflammation, complemented by future research requirements and implications. Result/Discussion: Therapeutic strategies that promote mitochondrial health, including enhancing mitophagy and mitochondrial biogenesis, show promise in treating neurodegenerative diseases and depression. Recent findings have emphasized therapeutic strategies to modulate mitophagy, such as pharmacological agents like urolithin A and rapamycin, genetic interventions such as PINK1/Parkin gene therapy, mitochondrial transplantation, and lifestyle and dietary interventions such as caloric restriction, exercise, and dietary supplements such as resveratrol and CoQ10. Key regulators of mitophagy, including the PINK1/Parkin pathway and various proteins like BNIP3, NIX, and FUNDC1, which facilitate the removal of damaged mitochondria, play a crucial role. Conclusions: These results highlight the importance of understanding the interplay between mitophagy and neuroinflammation and show that modulation of mitophagy can reduce oxidative stress and improve neuroinflammatory outcomes and depression in age-related neurodegenerative diseases. However, despite significant progress, challenges remain in understanding the underlying molecular mechanisms of mitophagy and its therapeutic regulation in aging disorders. [ABSTRACT FROM AUTHOR]

Ketone bodies are molecules produced from fatty acids in the liver that act as energy carriers to peripheral tissues when glucose levels are low. Carbohydrate- and calorie-restricted diets, known to increase the levels of circulating ketone bodies, have attracted significant attention in recent years due to their potential health benefits in several diseases. Specifically, increasing ketones through dietary modulation has been reported to be beneficial for cardiovascular health and to improve glucose homeostasis and insulin resistance. Interestingly, although excessive production of ketones may lead to life-threatening ketoacidosis in diabetic patients, mounting evidence suggests that modest levels of ketones play adaptive and beneficial roles in pancreatic beta cells, although the exact mechanisms are still unknown. Of note, Sodium-Glucose Transporter 2 (SGLT2) inhibitors have been shown to increase the levels of beta-hydroxybutyrate (BHB), the most abundant ketone circulating in the human body, which may play a pivotal role in mediating some of their protective effects in cardiovascular health and diabetes. This systematic review provides a comprehensive overview of the scientific literature and presents an analysis of the effects of ketone bodies on cardiovascular pathophysiology and pancreatic beta cell function. The evidence from both preclinical and clinical studies indicates that exogenous ketones may have significant beneficial effects on both cardiomyocytes and pancreatic beta cells, making them intriguing candidates for potential cardioprotective therapies and to preserve beta cell function in patients with diabetes. [ABSTRACT FROM AUTHOR]

Meta-analysis is a beneficial approach to reevaluating the outcomes of independent previous studies in the same scope. Saccharomyces cerevisiae, or the baker's yeast, is a commonly used unicellular and eukaryotic model organism. In this study, 12 evolved S. cerevisiae strains that became resistant to diverse stress conditions (boron, caffeine, caloric restriction, cobalt, coniferyl aldehyde, ethanol, iron, nickel, oxidative stress, 2-phenylethanol, and silver stress) by adaptive laboratory evolution were reassessed to reveal the correlated stress/stressor clusters based on their transcriptomic and stress–cross-resistance data. Principal Component Analysis (PCA) with k-means clustering was performed. Five clusters for the transcriptomic data of strains and six clusters for cross-resistance stressors were identified. Through statistical evaluations, critical genes pertinent to each cluster were elucidated. The pathways associated with these genes were investigated using the KEGG database. The findings demonstrated that caffeine and coniferyl aldehyde stressors exhibit clear distinctions from other stressors in terms of both physiological stress-cross-resistance responses and transcriptomic profiles. Pathway analysis showed that ribosome biogenesis was downregulated, and starch and sucrose metabolism was upregulated across all clusters. Gene and pathway analyses have shown that stressors lead to distinct changes in yeast gene expression, and these alterations have been systematically documented for each cluster. Several of the highlighted genes are pivotal for further exploration and could potentially clarify new aspects of stress response mechanisms and multiple stress resistance in yeast. [ABSTRACT FROM AUTHOR]

Background: The beneficial effects of n‐3 polyunsaturated fatty acids (PUFA) in reducing high blood triglyceride (TG) levels have been well demonstrated. This study aimed to investigate the effect of chia seeds on blood TG and its associated cardiometabolic factors in hypertriglyceridaemic individuals. Methods: This three‐group randomised controlled trial compared the effects of a low‐calorie diet (n = 22), a low‐calorie diet with chia seeds (30 g/day, n = 22) or a low‐calorie diet with concentrated fish oil (1.8 g/day of n‐3 long‐chain PUFAs, n = 22) in patients with hypertriglyceridaemia. Anthropometrics, fasting blood lipids, proprotein convertase subtilisin/kexin type 9, insulin, adiponectin, leptin and interleukin‐6 levels were measured. Results: After 8 weeks, the mean reduction in weight exhibited by the three groups was not statistically different (2.0, 2.7 and 2.8 kg, respectively, for the control, fish oil and chia seed groups). The plasma TG decreased in both the chia seed and fish oil groups in comparison to the control group (p = 0.001). However, no significant difference was observed between the chia seed and fish oil groups (change from baseline mean: 145.2 and 136.7 mg/dL for the chia seed and fish oil groups, respectively). The consumption of chia seeds was associated with a reduction in diastolic blood pressure (change from baseline mean: 8.4 mmHg) compared to the other two groups. No significant alterations were observed in the other blood biochemical factors between the three groups. Conclusions: In people with moderate hypertriglyceridaemia, a low‐calorie diet with 30 g of chia seeds compared to fish oil supplements containing 1.8 g of long‐chain PUFAs has a similar effect on reducing plasma TG levels, whereas it has a higher blood pressure–lowering effect. Key points: It is recommended that individuals with hypertriglyceridaemia implement dietary and lifestyle modifications, including weight loss and an increase in n‐3 polyunsaturated fatty acids, to reduce blood triglyceride (TG) levels.The incorporation of chia seeds into a low‐calorie diet is comparable to the administration of a moderate dose of fish oil in terms of its impact on plasma TG levels. However, it is more effective in reducing blood pressure in individuals with moderate hypertriglyceridaemia. [ABSTRACT FROM AUTHOR]

This work investigated the biochemical disturbances and histological alteration in Psammomys obesus animal model fed different high calorie diets (HCDs) during three months. Four diets were used: a low-calorie natural diet, Chenopodiaceae halophyte plant used as control (LCD), a high standard carbohydrate diet rich in protein, HCD 0, a high carbohydrate diet rich in two concentrations of fat, HCD 1 and HCD 2. All animals having received HCDs developed dyslipidemia after one month of experiment with distinction of different sub-groups developing or not obesity and diabetes. HCDs induced a remarkable increasing in blood cholesterol, LDL-cholesterol and triglyceride levels indicating a fast induction of dyslipidemia and a significant increase of aminotransaminases activities revealing a pronounced hepatotoxicity. Animal developing diabetes showed a severe hepatic injury, a degeneration of the adipose tissue and a significant reduction of retinal thickness. P. obesus seems to be an excellent animal model to investigate nutritional metabolic diseases. [ABSTRACT FROM AUTHOR]

Context: Intermittent fasting, a new-age dietary concept derived from an age-old tradition, involves repetitive cycles of fasting/calorie restriction and eating. Objective: We aim to take a deep dive into the biological responses to intermittent fasting, delineate the disease-modifying and cognitive effects of intermittent fasting, and also shed light on the possible side effects. Methods: Numerous in vitro and in vivo studies were reviewed, followed by an in-depth analysis, and compilation of their implications in health and disease. Results: Intermittent fasting improves the body's stress tolerance, which is further amplified with exercise. It impacts various pathological conditions like cancer, obesity, diabetes, cardiovascular disease, and neurodegenerative diseases. Conclusion: During dietary restriction, the human body experiences a metabolic switch due to the depletion of liver glycogen, which promotes a shift towards utilising fatty acids and ketones in the system, thereby significantly impacting adiposity, ageing and the immune response to various diseases. KEY POINTS: Intermittent fasting (IF) comprises repetitive fasting and feeding cycles. There are many variations of IF schedules. Individuals practicing an appropriate IF pattern reap numerous health benefits. The possible side effects should be considered before commencing a new IF regimen. [ABSTRACT FROM AUTHOR]

Resource scarcity, the effects of climate change, food insecurity, and health issues related to dietary choices have prompted policymakers to develop new strategies to encourage populations to opt for healthy and sustainable (HS) diets. In this context, nudging strategies are promising tools to promote healthy and sustainable dietary behaviors. However, nudges are context-dependent as a specific nudging intervention should be employed in a specific context. This research aims at determining the effects of different nudges on students' food choices in the context of a hypothetical online pre-ordering system of the college canteen. An experimental study was conducted in the USA with 1400 American college students (18–24 years old). We used a between-subject design with one control and three treatment groups—i.e., a HS logo to identify HS dishes, dish placement (the order in which dishes are displayed on the menu), and a combination of the two nudges. Our main results showed that the logo and logo plus placement led to a significantly increased selection of HS dishes among students who already had strong HS eating behaviors. In addition, individual characteristics (e.g., being flexitarian or vegetarian, being on a low-calorie diet, being a graduate student, and living in dormitories on college campuses) also affected their HS food choices; thus, the population traits, living conditions, and eating habits should be taken into consideration in order to establish successful nudging techniques. [ABSTRACT FROM AUTHOR]

Background: Nowadays, obesity has become a major health issue. In addition to negatively affecting body composition and metabolic health, recent evidence shows unfavorable shifts in gut microbiota in individuals with obesity. However, the effects of weight loss on gut microbes and metabolites remain controversial. Therefore, the purpose of this study was to investigate the effects of a 12-week program on gut microbiota and metabolic health in patients with obesity. Methods: We conducted a controlled trial in 23 male and female patients with obesity. Twelve participants completed a 12-week program of caloric restriction combined with strength and HIIT training (INT, pre-BMI 37.33 ± 6.57 kg/m2), and eleven participants were designated as non-intervention controls (pre-BMI 38.65 ± 8.07 kg/m2). Metagenomic sequencing of the V3-V4 region of the 16S rDNA gene from fecal samples allowed for gut microbiota classification. Nuclear magnetic resonance spectroscopy characterized selected serum and fecal metabolite concentrations. Results: Within INT, we observed a significant improvement in body composition; a significant decrease in liver enzymes (AST, ALT, and GMT); a significant increase in the relative abundance of the commensal bacteria (e.g., Akkermansia muciniphila, Parabacteroides merdae, and Phocaeicola vulgatus); and a significant decrease in the relative abundance of SCFA-producing bacteria (e.g., the genera Butyrivibrio, Coprococcus, and Blautia). In addition, significant correlations were found between gut microbes, body composition, metabolic health biomarkers, and SCFAs. Notably, the Random Forest Machine Learning analysis identified predictors (Butyrivibrio fibrisolvens, Blautia caecimuris, Coprococcus comes, and waist circumference) with a moderate ability to discriminate between INT subjects pre- and post-intervention. Conclusions: Our results indicate that a 12-week caloric restriction combined with strength and HIIT training positively influences body composition, metabolic health biomarkers, gut microbiota, and microbial metabolites, demonstrating significant correlations among these variables. We observed a significant increase in the relative abundance of bacteria linked to obesity, e.g., Akkermansia muciniphila. Additionally, our study contributes to the ongoing debate about the role of SCFAs in obesity, as we observed a significant decrease in SCFA producers after a 12-week program. Trial registration: The trial was registered on [05/12/2014] with ClinicalTrials.gov (No: NCT02325804). [ABSTRACT FROM AUTHOR]

Background In 8 females, 1 will be diagnosed with breast cancer in their lifetime. Although medical advances have increased the likelihood of survival, up to 90% of females will gain weight during and after treatment increasing the risk of breast cancer recurrence and obesity-related comorbidities in survivorship. Behavioral lifestyle interventions focused on diet with or without physical activity can provide breast cancer survivors nonpharmacological options to decrease weight gain and cardiometabolic risk. Method A PubMed search was conducted to identify all behavioral lifestyle interventions focused on diet or diet combined with physical activity longer than 4 weeks of duration in breast cancer survivors that included body weight as an outcome. This review aims to summarize the effects on body weight, body composition, and cardiometabolic risk markers. Results The review shows there is high heterogeneity in type and duration of the intervention to affect weight and cardiometabolic risk in survivorship. Calorie restriction with and without physical activity appears to promote weight loss among breast cancer survivors. However, the effects on cardiometabolic factors are less clear. Conclusions Future studies should be powered for body weight and cardiometabolic effects. Researchers should also consider interventions that (1) are less complex, (2) recruit a more racially and ethnically diverse sample, (3) integrate resistance training, (4) implement the intervention in closer proximity to diagnosis, (5) target weight management in this population before it occurs, and (6) analyze body composition in addition to body weight measurements. [ABSTRACT FROM AUTHOR]

Objective: Caloric restriction (CR) is known to enhance insulin sensitivity and reduce the risk of metabolic disorders; however, its molecular mechanisms are not fully understood. This study aims to elucidate specific proteins and pathways responsible for these benefits. Methods: We examined adipose tissue from participants in the Comprehensive Assessment of Long‐term Effects of Reducing Intake of Energy Phase 2 (CALERIE 2) study, comparing proteomic profiles from individuals after 12 and 24 months of CR with baseline and an ad libitum group. Biochemical and cell‐specific physiological approaches complemented these analyses. Results: Our data revealed that CR upregulates prostacyclin synthase (PTGIS) in adipose tissue, an enzyme crucial for producing prostacyclin (PGI2). PGI2 improves the ability of insulin to stimulate the tether‐containing UBX domain for GLUT4 (TUG) cleavage pathway, which is essential for glucose uptake regulation. Additionally, iloprost, a PGI2 analog, was shown to increase insulin receptor density on cell membranes, increasing glucose uptake in human adipocytes. CR also reduces carbonylation of GLUT4, a modification that is detrimental to GLUT4 function. Conclusions: CR enhances insulin sensitivity by promoting PTGIS expression and stimulating the TUG cleavage pathway, leading to increased GLUT4 translocation to the cell surface and decreased GLUT4 carbonylation. These findings shed light on the complex molecular mechanisms through which CR favorably impacts insulin sensitivity and metabolic health. [ABSTRACT FROM AUTHOR]