The Interplay between Obesity and Inflammation

Life, Journal Year: 2024, Volume and Issue: 14(7), P. 856 - 856

Published: July 8, 2024

Obesity is an important condition affecting the quality of life numerous patients and increasing their associated risk for multiple diseases, including tumors immune-mediated disorders. Inflammation appears to play a major role in development obesity represents central point activity cellular humoral components adipose tissue. Macrophages key as main component tissue regulating chronic inflammation modulating secretion differentiation various pro- anti-inflammatory cytokines. also involves series signaling pathways that might represent focus new therapies interventions. Weight loss essential decreasing cardiometabolic risks degree inflammation; however, latter can persist long after excess weight lost, involve changes macrophage phenotypes ensure metabolic adjustment. A clear understanding pathophysiological processes interplay between lead better comorbidities may future targets treatment obesity.

Language: Английский

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Obesity‐induced tissue alterations resist weight loss: A mechanistic review

Diabetes Obesity and Metabolism, Journal Year: 2024, Volume and Issue: 26(8), P. 3045 - 3057

Published: May 8, 2024

Abstract Interventions aimed at weight control often have limited effectiveness in combating obesity. This review explores how obesity‐induced dysfunction white (WAT) and brown adipose tissue (BAT), skeletal muscle, the brain blunt loss, leading to retention of stored fat. In obesity, increased adrenergic stimulation inflammation downregulate β‐adrenoreceptors impair catecholaminergic signalling adipocytes. disrupts adrenergic‐mediated lipolysis, diminishing lipid oxidation both adipocytes, lowering thermogenesis blunting fat loss. Emerging evidence suggests that WAT fibrosis is associated with worse loss outcomes; indeed, limiting collagen laminin‐α4 deposition mitigates accumulation, enhances browning, protects against high‐fat‐diet‐induced Obesity compromises mitochondrial oxidative capacity impairing its ability switch between glucose metabolism response varying nutrient levels exercise. dysfunctional phenotype muscle exacerbated presence obesity‐associated sarcopenia. Additionally, obesity suppresses sarcolipin‐induced sarcoplasmic reticulum calcium ATPase (SERCA) activation, resulting reduced capacity, diminished energy expenditure, adiposity. hypothalamus, overnutrition insulin leptin signalling. blunts central satiety signals, favouring a shift balance toward conservation body retention. Moreover, obese animals humans demonstrate impaired dopaminergic responses intake striatum, which tend persist after may result enduring inclinations overeating sedentary lifestyle. Collectively, adaptations described pose significant challenges effectively achieving sustaining

Language: Английский

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Inter-organ metabolic interaction networks in non-alcoholic fatty liver disease

Frontiers in Endocrinology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 9, 2025

Non-alcoholic fatty liver disease (NAFLD) is a multisystem metabolic disorder, marked by abnormal lipid accumulation and intricate inter-organ interactions, which contribute to systemic imbalances. NAFLD may progress through several stages, including simple steatosis (NAFL), non-alcoholic steatohepatitis (NASH), cirrhosis, potentially cancer. This closely associated with disorders driven overnutrition, key pathological processes dysregulation, impaired autophagy, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, local inflammation. While hepatic metabolism in well-documented, further research into communication mechanisms crucial for deeper understanding of progression. review delves intrahepatic networks tissue-specific signaling mediators involved pathogenesis, emphasizing their impact on distal organs.

Language: Английский

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Crosstalk Between Antioxidants and Adipogenesis: Mechanistic Pathways and Their Roles in Metabolic Health

Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 203 - 203

Published: Feb. 10, 2025

The interplay between oxidative stress and adipogenesis is a critical factor in the development of obesity its associated metabolic disorders. Excessive reactive oxygen species (ROS) disrupt key transcription factors such as peroxisome proliferator-activated receptor gamma (PPARγ) CCAAT/enhancer-binding protein alpha (C/EBPα), impairing lipid metabolism, promoting adipocyte dysfunction, exacerbating inflammation insulin resistance. Antioxidants, classified endogenous (e.g., glutathione, superoxide dismutase, catalase) exogenous polyphenols, flavonoids, vitamins C E), are pivotal mitigating these effects by restoring redox balance preserving functionality. Endogenous antioxidants neutralize ROS safeguard cellular structures; however, under heightened stress, defenses often insufficient, necessitating dietary supplementation. Exogenous derived from plant-based sources, polyphenols vitamins, act through direct scavenging, upregulation antioxidant enzymes, modulation signaling pathways like nuclear kappa B (NF-κB) PPARγ, reducing peroxidation, inflammation, dysfunction. Furthermore, they influence epigenetic regulation transcriptional networks to restore differentiation limit accumulation. Antioxidant-rich diets, including Mediterranean diet, strongly with improved health, reduced rates, enhanced sensitivity. Advances personalized therapies, guided biomarkers supported novel delivery systems, present promising avenues for optimizing therapeutic interventions. This review, "Crosstalk Between Antioxidants Adipogenesis: Mechanistic Pathways Their Role Metabolic Health", highlights mechanistic which regulate enhance health.

Language: Английский

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Modifiable risk factors and inflammation-related proteins in polymyalgia rheumatica: genome-wide meta-analysis and Mendelian randomisation

medRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: April 22, 2024

Abstract Objective Polymyalgia rheumatica (PMR) is an age-related inflammatory disease of unknown cause. We aimed to identify potentially modifiable risk factors and therapeutic targets for preventing or treating PMR. Methods meta-analysed genetic association data from 8,156 cases PMR (defined using diagnostic codes self-report) 416,495 controls European ancestry the UK Biobank FinnGen. then performed Mendelian randomization analyses estimate between eight (using up 1.2 million individuals) 65 inflammation-related circulating proteins (up 55,792 individuals), inverse variance weighted pleiotropy robust methods. Results identified three novel genome-wide significant loci in IL1R1, NEK6 CCDC88B genes confirmation previously described associations with HLA-DRB1 ANKRD55 . Genetically predicted smoking intensity (OR 1.32; 95%CI 1.08-1.60; p=0.006) visceral adiposity 1.22; 1.10-1.37; p=3.10x10 −4 ) were associated susceptibility. Multiple related IL-1 family signaling receptor-like 2, also known as IL-36 receptor 1.25; p=1.89x10 −32 ), serum amyloid A2 1.06, 9.91x10 −10 CXCL6 1.09, p=4.85x10 −7 retained significance after correction multiple testing. Conclusion Reducing at a population level might reduce incidence that may play causal roles PMR, suggesting new opportunities. Further research needed before these findings are applied clinical practice. Key messages Three Several proteins, notably those involved signalling, Visceral cigarette causally

Language: Английский

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Modifiable risk factors and inflammation-related proteins in polymyalgia rheumatica: genome-wide meta-analysis and Mendelian randomization

Lara D. Veeken, Journal Year: 2024, Volume and Issue: unknown

Published: May 23, 2024

Abstract Objective PMR is an age-related inflammatory disease of unknown cause. We aimed to identify potentially modifiable risk factors and therapeutic targets for preventing or treating PMR. Methods meta-analysed genetic association data from 8156 cases (defined using diagnostic codes self-report) 416 495 controls European ancestry the UK Biobank FinnGen. then performed Mendelian randomization analyses estimate between eight (using up 1.2 million individuals) 65 inflammation-related circulating proteins (up 55 792 individuals), inverse variance weighted pleiotropy robust methods. Results identified three novel genome-wide significant loci in IL1R1, NEK6 CCDC88B genes confirmation previously described associations with HLA-DRB1 ANKRD55. Genetically predicted smoking intensity (OR 1.32; 95%CI 1.08–1.60; P = 0.006) visceral adiposity 1.22; 1.10–1.37; 3.10 × 10−4) were associated susceptibility. Multiple related IL-1 family signalling receptor-like 2, also known as IL-36 receptor 1.25; 1.89 10−32), serum amyloid A2 1.06, 9.91 10−10) CXCL6 1.09, 4.85 10−7) retained significance after correction multiple testing. Conclusion Reducing at a population level might reduce incidence that may play causal roles PMR, suggesting new opportunities. Further research needed before these findings are applied clinical practice.

Language: Английский

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Balancing Act: Exploring the Gut Microbiota-Brown Adipose Tissue Axis in PCOS Pathogenesis and Therapeutic Frontiers

Frontiers in Bioscience-Landmark, Journal Year: 2024, Volume and Issue: 29(6)

Published: May 30, 2024

Polycystic ovary syndrome (PCOS) is a prevalent reproductive, endocrine, and metabolic disease that affects 5–18% of women worldwide, with rising incidence. Hyperandrogenemia insulin resistance are two key pathophysiological factors contribute to PCOS, both which variety health issues such as menstrual irregularities, obesity, dysfunctional glucose lipid homeostasis, infertility, mental disorders, cardiovascular cerebrovascular diseases. Despite ongoing studies, the origin pathogenesis PCOS remain elusive; there also clinical need for simpler, more effective, longer lasting, comprehensive treatments PCOS. The gut–fat axis, critical regulatory route metabolism, endocrine function, immune response, has received considerable interest in recent years research etiology treatment illnesses type 2 diabetes mellitus non-alcoholic fatty liver disease. latest revealed significant alterations homogeneity phylogenetic diversity gut microbiota. Animal using fecal microbiota transplantation confirmed importance regulating sensitivity sex hormone balance Furthermore, studies have shown decrease volume and/or activity brown adipose tissue (BAT) patients, change alters adipokine release, leading hyperandrogenemia, aggravating progression. Given function BAT increasing energy expenditure alleviating parameters, efforts activate or induce browning white emerged possible Recent suggested can influence creation via metabolites short-chain acids bile acids, well gut–brain axis. Cold exposure, healthy dieting, metformin, bariatric surgery, glucagon-like peptide 1 receptor agonists melatonin all been basic modulate by influencing microbiota, demonstrating potential. However, into regulation mechanisms gut–BAT axis required produce comfortable, safe tailored therapeutics

Language: Английский

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Visceral adipose tissue-derived extracellular vesicles promote stress susceptibility in obese mice via miR-140-5p

Acta Pharmacologica Sinica, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 10, 2025

Language: Английский

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Deciphering Significances of Autophagy in the Development and Metabolism of Adipose Tissue

Experimental Cell Research, Journal Year: 2025, Volume and Issue: unknown, P. 114478 - 114478

Published: Feb. 1, 2025

Language: Английский

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Role of genetic variants and DNA methylation of lipid metabolism-related genes in metabolic dysfunction-associated steatotic liver disease

Frontiers in Physiology, Journal Year: 2025, Volume and Issue: 16

Published: March 17, 2025

Metabolic dysfunction-associated steatotic liver disease (MASLD), is one of the most common chronic diseases, which encompasses a spectrum from metabolic (MASL) to steatohepatitis (MASH), and may ultimately progress MASH-related cirrhosis hepatocellular carcinoma (HCC). MASLD complex that influenced by genetic environmental factors. Dysregulation hepatic lipid metabolism plays crucial role in development progression MASLD. Therefore, focus this review discuss links between variants DNA methylation metabolism-related genes pathogenesis. We first summarize interplay disturbance metabolism. Next, we on reviewing related gene loci onset existing literature around single nucleotide polymorphisms (SNPs) associated with identified genome-wide association studies (GWAS) candidate analyses. Moreover, based recent evidence human animal studies, further discussed regulatory function mechanisms changes levels occurrence MASLD, particular emphasis its MASH. Furthermore, alterations blood MASH patients. Finally, introduce potential value profiles developing novel prognostic biomarkers therapeutic targets for intending provide references future

Language: Английский

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