
Obesity Pillars, Год журнала: 2025, Номер unknown, С. 100175 - 100175
Опубликована: Апрель 1, 2025
Язык: Английский
Obesity Pillars, Год журнала: 2025, Номер unknown, С. 100175 - 100175
Опубликована: Апрель 1, 2025
Язык: Английский
Diabetes Obesity and Metabolism, Год журнала: 2025, Номер unknown
Опубликована: Март 11, 2025
Abstract Obesity is a highly prevalent chronic multisystem disease associated with shortened life expectancy due to number of adverse health outcomes. Epidemiological data link body weight and parameters central fat distribution an increasing risk for type 2 diabetes, hypertension, fatty liver diseases, cardiovascular diseases including myocardial infarction, heart failure, atrial fibrillation, stroke, obstructive sleep apnoea, osteoarthritis, mental disorders some types cancer. However, the individual develop cardiometabolic other obesity‐related cannot entirely be explained by increased mass. Rather than excess accumulation, dysfunction adipose tissue may represent mechanistic between obesity There are people living who seem protected against premature development diseases. On hand, normal typical upon predominantly visceral distribution. The mechanisms linking impaired function in include adipocyte hypertrophy, altered cellular composition, limited expandability safe subcutaneous stores, ectopic deposition depots, organs, hypoxia, variety stresses, inflammatory processes, release pro‐inflammatory, diabetogenic atherogenic signals. Genetic environmental factors might contribute either alone or via interaction intrinsic biological variation function. still many open questions regarding how causes whether these pathologies could reversed. Evidence‐based loss interventions using behaviour change, pharmacological surgical approaches have clarified beneficial effects realistic sustained on complications as hard This review focusses recent advances understanding epidemiological trends Plain Language Summary complex progressive characterized excessive that impair quality life. Worldwide, adults has more doubled since 1990. lead reduced expectancy, because it increases (e.g., high blood pressure, stroke), musculoskeletal respiratory depression certain not every person develops For better prevention treatment, important understand mass related It become clear explain higher complications. People can low developing Compared those abdominal region, average bigger cells, immune cells signals released from directly affect brain, liver, vasculature organs. Both inherited environment cause abnormalities through changes lower calorie intake, physical activity), medications surgery improve health, reduce
Язык: Английский
Процитировано
2Cureus, Год журнала: 2025, Номер unknown
Опубликована: Янв. 14, 2025
Obesity is a complex and non-communicable disease with pandemic entity. Currently, multiple causes can lead to obesity, it not always easy create direct relationship between physical inactivity, poor quality of nutrients consumed, calculation excess calories. Among the associated comorbidities, obesity creates dysfunctional environment respiratory rhythms at central peripheral levels, functional, morphological, phenotypic alteration diaphragm muscle. This pathological adaptation breathing one most important dysregulation autonomic system, which will negatively affect progression comorbidities chronic non-physiological adaptations in obese persons. Introducing activity program involving training could be very valid strategy restore systemic response, delaying or avoiding onset pathologies fat. brief narrative review focuses on importance subjects.
Язык: Английский
Процитировано
1BioEssays, Год журнала: 2025, Номер unknown
Опубликована: Янв. 19, 2025
ABSTRACT Adipose tissue (AT) inflammation, a hallmark of the metabolic syndrome, is triggered by overburdened adipocytes sending out immune cell recruitment signals during obesity development. An AT landscape persistent throughout weight loss and regain constitutes an immune‐obesogenic memory that hinders long‐term management. Lipid‐associated macrophages (LAMs) are emerging as major players in diseased, inflamed tissues may be key contributors to obesogenic AT. Our previous study found LAM abundance increases with via intermittent fasting (IF) obese mice, which driven adipocyte p53 signalling. However, specific causing accumulation under IF remain unknown. In this piece, we hypothesise on range adipocyte‐secreted can harbor immune‐attractive features upon fasting/refeeding cycles. We highlight possible mechanisms including death signalling, matrikines, other damage‐associated molecular patterns (DAMPs), well adipo(‐cyto)kines, lipid mediators, metabolites, extracellular vesicles, epigenetic rewiring. Finally, consider how advances gleaned from preclinical models might translatable management humans. Thus, provide vantage points driving monocyte recruitment, polarisation towards LAMs, retention, harness therapeutic potential modulating levels impacting disease.
Язык: Английский
Процитировано
1Clinical and Translational Medicine, Год журнала: 2025, Номер 15(3)
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
1Nature Biotechnology, Год журнала: 2025, Номер 43(4), С. 516 - 533
Опубликована: Апрель 1, 2025
Язык: Английский
Процитировано
1Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)
Опубликована: Янв. 4, 2025
Abstract Background Obese subjects undergoing weight loss often fear the Yoyo dieting effect, which involves regaining or even surpassing their initial weight. To date, our understanding of such long-term obesity and cycling effects is still limited based on only short-term murine gain studies. This study aimed to investigate impacts glycemic control metabolic health, focusing adipose tissue, liver, hypothalamus. Methods Chow-fed mice subjected prolonged high-fat diet (HFD) consumption for 20 weeks, followed by 24 weeks dietary interventions either induce gain, loss, were monitored perturbations in feeding efficiency glucose homeostasis. Post-mortem analyses included qPCR, Western Blotting, biochemical microscopical assessments hepatic steatosis insulin resistance, hypothalamic tissue inflammation, circulating lipid, leptin IL-6 levels. Results Weight led hyperphagia rapid regain, matching weights continuously HFD. Despite inflammation persisted with elevated pro-inflammatory markers, macrophage infiltration, impaired Glut4 expression. HFD-induced dysregulation expression orexigenic peptides synaptic plasticity markers also after normalization suggesting long-lasting neural alterations. Weight-cycled exhibited higher levels, increased lipid storage, dysregulated metabolism compared those consistent diets, indicating worsened dieting. Conclusion In sum, highlights significant risks associated cycling, particularly following obesity. Persistent perturbed peptide tolerance emphasize need effective sustainable strategies mitigate adverse outcomes regain improve health.
Язык: Английский
Процитировано
0Nature Reviews Endocrinology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 6, 2025
Язык: Английский
Процитировано
0Journal of Hepatology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0Médecine des Maladies Métaboliques, Год журнала: 2025, Номер unknown
Опубликована: Янв. 1, 2025
Процитировано
0bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown
Опубликована: Янв. 10, 2025
ABSTRACT Obesity affects more than 15% of the world population and is associated with development glucose intolerance type 2 diabetes. In recent years, incretin analogs are prescribed at a high rate for treatment obesity diabetes due to their potent effects on lowering bodyweight improving homeostasis. However, studies suggest that many patients do not stay analog therapy thereby rapidly regain bodyweight. The non-compliance only drug shortage but also insufficient knowledge long-term therapy. To address this gap provide strategy obesity, we examined withdrawal adipose tissue functions in diet-induced obese mice. Our transcriptome data restored most obesity-mediated deregulated gene expression tissue. genes encoding lipogenic enzymes, downregulated by were treatment. Upon withdrawal, mice displayed rapid regain, impaired function, intolerance. contrast, dietary intervention following tissue, maintained homeostasis, increased lean mass minimized body weight regain. findings revealed highlight importance therapy, which may contribute guidelines obesity.
Язык: Английский
Процитировано
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