RESUMEN
Background: Deposition of adipose tissue may have a promoting role in the development of diabetic complications. This study is aimed at investigating the relationship between adipose tissue thickness and risk of contrast-induced nephropathy (CIN) in patients with Type 2 diabetes mellitus (T2DM). Methods: A total of 603 T2DM patients undergoing percutaneous coronary angiography or angioplasty with suspicious or confirmed stable coronary artery disease were enrolled in this study. The thicknesses of perirenal fat (PRF), subcutaneous fat (SCF), intraperitoneal fat (IPF), and epicardial fat (ECF) were measured by color Doppler ultrasound, respectively. The association of various adipose tissues with CIN was analyzed. Results: Seventy-seven patients (12.8%) developed CIN in this cohort. Patients who developed CIN had significantly thicker PRF (13.7 ± 4.0 mm vs. 8.9 ± 3.6 mm, p < 0.001), slightly thicker IPF (p = 0.046), and similar thicknesses of SCF (p = 0.782) and ECF (p = 0.749) compared to those who did not develop CIN. Correlation analysis showed that only PRF was positively associated with postoperation maximal serum creatinine (sCr) (r = 0.18, p = 0.012), maximal absolute change in sCr (r = 0.33, p < 0.001), and maximal percentage of change in sCr (r = 0.36, p < 0.001). In receiver operating characteristic (ROC) analysis, the area under the curve (AUC) of PRF (0.809) for CIN was significantly higher than those of SCF (0.490), IPF (0.594), and ECF (0.512). Multivariate logistic regression analysis further confirmed that thickness of PRF, rather than other adipose tissues, was independently associated with the development of CIN after adjusted for confounding factors (odds ratio (OR) = 1.53, 95% CI: 1.38-1.71, p < 0.001). Conclusions: PRF is independently associated with the development of CIN in T2DM patients undergoing coronary catheterization.
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Medios de Contraste , Angiografía Coronaria , Diabetes Mellitus Tipo 2 , Nefropatías Diabéticas , Humanos , Diabetes Mellitus Tipo 2/complicaciones , Femenino , Masculino , Medios de Contraste/efectos adversos , Persona de Mediana Edad , Anciano , Angiografía Coronaria/efectos adversos , Factores de Riesgo , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Tejido Adiposo/diagnóstico por imagen , Tejido Adiposo/patología , Enfermedades Renales/inducido químicamente , Grasa Intraabdominal/diagnóstico por imagen , Cateterismo Cardíaco/efectos adversos , Creatinina/sangreRESUMEN
This retrospective study investigates perivascular adipose tissue (PVAT) alterations in CT as a marker of inflammation in patients with abdominal aortic aneurysms (AAA). 100 abdominal CT scans of patients with abdominal aortic aneurysms and 100 age and sex matched controls without underlying aortic disease were included. Artificial Intelligence (AI) assisted segmentation of the aorta and the surrounding adipose tissue was performed. Adipose tissue density was measured in Hounsfield units (HU) close (2-5mm, HUclose) and distant (10-12mm, HUdistant) to the aortic wall. To investigate alterations in adipose tissue density close to the aorta (HUclose) as a potential marker of inflammation, we calculated the difference HUΔ = HUclose-HUdistant and the fat attenuation ratio HUratio = HUclose/HUdistant as normalized attenuation measures. These two markers were compared i) inter-individually between AAA patients and controls and ii) intra-individually between the aneurysmal and non-aneurysmal segments in AAA patients. Since most AAAs are generally observed infrarenal, the aneurysmal section of the AAA patients was compared with the infrarenal section of the aorta of the control patients. In inter-individual comparisons, higher HUΔ and a lower HUratio were observed (aneurysmal: 8.9 ± 5.1 HU vs. control: 6.9 ± 4.8 HU, p-value = 0.006; aneurysmal: 89.8 ± 5.7% vs. control: 92.1 ± 5.5% p-value = 0.004). In intra-individual comparisons, higher HUΔ and lower HUratio were observed (aneurysmal: 8.9 ± 5.1 HU vs. non-aneurysmal: 5.5 ± 4.1 HU, p-value < 0.001; aneurysmal: 89.8 ± 5.7% vs. non-aneurysmal 93.3 ± 4.9%, p-value < 0.001). The results indicate PVAT density alterations in AAA patients. This motivates further research to establish non-invasive imaging markers for vascular and perivascular inflammation in AAA.
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Tejido Adiposo , Aneurisma de la Aorta Abdominal , Tomografía Computarizada por Rayos X , Humanos , Aneurisma de la Aorta Abdominal/diagnóstico por imagen , Aneurisma de la Aorta Abdominal/patología , Masculino , Femenino , Anciano , Tejido Adiposo/diagnóstico por imagen , Tejido Adiposo/patología , Tomografía Computarizada por Rayos X/métodos , Estudios Retrospectivos , Persona de Mediana Edad , Anciano de 80 o más Años , Estudios de Casos y Controles , Aorta Abdominal/diagnóstico por imagen , Aorta Abdominal/patologíaRESUMEN
BACKGROUND: The effect of fat infiltration in the paraspinal muscles on cervical degenerative disease has been confirmed by multiple studies. However, little is known about fat infiltration in the paraspinal extensors in patients with acute cervical spinal cord injury (SCI). This study aimed to investigate the difference in paraspinal extensor fatty infiltration between patients with acute cervical SCI and healthy controls, and to further explore the protective role of the paravertebral extensor muscles in patients with cervical SCI. METHODS: A total of 50 patients with acute cervical SCI admitted to the emergency department from January 2019 to November 2023 were retrospectively analyzed, including 26 males and 24 females, with an average age of 59.60 ± 10.81 years. A control group of 50 healthy middle-aged and elderly individuals was also included, comprising 28 males and 22 females, with an average age of 55.00 ± 8.21 years. Cervical spine magnetic resonance imaging (MRI) was used to measure the cross-sectional areas of the superficial and deep cervical extensor muscles, the corresponding vertebral body cross-sectional areas, and the fat area within the superficial and deep extensor muscle groups using Image J software. Differences between the two groups were compared, and the cervical SCI patients were further analyzed based on the severity of the spinal cord injury and gender differences. RESULTS: The deep fatty infiltration ratio (DFIR) and superficial fatty infiltration ratio (SFIR) at C4-C7 in the cervical SCI group were significantly higher than those in the control group (P < 0.001). The cross-sectional area of the functional deep extensor area (FDEA) relative to the vertebral body area (VBA) and the cross-sectional area of the functional superficial extensor area (FSEA) relative to the VBA at the C5 and C6 levels in the cervical SCI group were significantly lower than those in the control group (P < 0.001, P < 0.001, P = 0.034, P = 0.004 respectively). Among the cervical SCI patients, the cross-sectional areas of the deep extensor area (DEA) and the superficial extensor area (SEA) in males were significantly higher than those in females (P < 0.001). At the C6 and C7 levels, the FDEA/VBA and FSEA/VBA ratios in the male group were higher than those in the female group (P = 0.009, P = 0.022, P = 0.019, P = 0.005, respectively). CONCLUSION: Patients with acute cervical SCI exhibit significantly higher fatty infiltration and a greater degree of paravertebral extensor muscle degeneration compared to healthy controls. This finding underscores the importance of the paravertebral extensor muscles in the context of cervical SCI and may guide future therapeutic strategies.
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Tejido Adiposo , Vértebras Cervicales , Imagen por Resonancia Magnética , Músculos Paraespinales , Traumatismos de la Médula Espinal , Humanos , Masculino , Femenino , Traumatismos de la Médula Espinal/diagnóstico por imagen , Traumatismos de la Médula Espinal/patología , Estudios Retrospectivos , Persona de Mediana Edad , Músculos Paraespinales/diagnóstico por imagen , Músculos Paraespinales/patología , Vértebras Cervicales/diagnóstico por imagen , Vértebras Cervicales/patología , Anciano , Tejido Adiposo/diagnóstico por imagen , Tejido Adiposo/patología , Adulto , Estudios de Casos y ControlesRESUMEN
Atrial fibrillation (AF) is the most common sustained arrhythmia and carries an increased risk of stroke and heart failure. Here we investigated how the immune infiltrate of human epicardial adipose tissue (EAT), which directly overlies the myocardium, contributes to AF. Flow cytometry analysis revealed an enrichment of tissue-resident memory T (TRM) cells in patients with AF. Cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) and single-cell T cell receptor (TCR) sequencing identified two transcriptionally distinct CD8+ TRM cells that are modulated in AF. Spatial transcriptomic analysis of EAT and atrial tissue identified the border region between the tissues to be a region of intense inflammatory and fibrotic activity, and the addition of TRM populations to atrial cardiomyocytes demonstrated their ability to differentially alter calcium flux as well as activate inflammatory and apoptotic signaling pathways. This study identified EAT as a reservoir of TRM cells that can directly modulate vulnerability to cardiac arrhythmia.
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Tejido Adiposo , Fibrilación Atrial , Células T de Memoria , Pericardio , Fibrilación Atrial/inmunología , Fibrilación Atrial/genética , Fibrilación Atrial/patología , Fibrilación Atrial/metabolismo , Humanos , Pericardio/metabolismo , Pericardio/patología , Pericardio/inmunología , Tejido Adiposo/metabolismo , Tejido Adiposo/inmunología , Tejido Adiposo/patología , Células T de Memoria/inmunología , Células T de Memoria/metabolismo , Masculino , Linfocitos T CD8-positivos/inmunología , Linfocitos T CD8-positivos/metabolismo , Transcriptoma , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Miocitos Cardíacos/inmunología , Femenino , Persona de Mediana Edad , Perfilación de la Expresión Génica , Anciano , Fenotipo , Señalización del Calcio , Apoptosis , Memoria Inmunológica , Transcripción Genética , Estudios de Casos y Controles , Atrios Cardíacos/patología , Atrios Cardíacos/inmunología , Atrios Cardíacos/metabolismo , Fibrosis/patología , Tejido Adiposo EpicárdicoRESUMEN
BACKGROUND: Obesity poses a significant global health challenge, given its association with the excessive accumulation of adipose tissue (AT) and various systemic disruptions. Within the adipose microenvironment, expansion and enrichment with immune cells trigger the release of inflammatory mediators and growth factors, which can disrupt tissues, including bones. While obesity's contribution to bone loss is well established, the direct impact of obese AT on osteoblast maturation remains uncertain. This study aimed to explore the influence of the secretomes from obese and lean AT on osteoblast differentiation and activity. METHODS: SAOS-2 cells were exposed to the secretomes obtained by culturing human subcutaneous AT from individuals with obesity (OATS) or lean patients, and their effects on osteoblasts were evaluated. RESULTS: In the presence of the OATS, mature osteoblasts underwent dedifferentiation, showing an increased proliferation accompanied by a morphological shift towards a mesenchymal phenotype, with detrimental effects on osteogenic markers and the calcification capacity. Concurrently, the OATS promoted the expression of mesenchymal and adipogenic markers, inducing the formation of cytoplasmic lipid droplets in SAOS-2 cells exposed to an adipogenic differentiation medium. Additionally, TGF-ß1 emerged as a key mediator of these effects, as the OATS was enriched with this growth factor. CONCLUSIONS: Our findings demonstrate that obese subcutaneous AT promotes the dedifferentiation of osteoblasts and increases the adipogenic profile in these cells.
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Adipogénesis , Tejido Adiposo , Desdiferenciación Celular , Obesidad , Osteoblastos , Fenotipo , Transducción de Señal , Factor de Crecimiento Transformador beta1 , Humanos , Osteoblastos/metabolismo , Osteoblastos/patología , Obesidad/patología , Obesidad/metabolismo , Factor de Crecimiento Transformador beta1/metabolismo , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Secretoma/metabolismo , Diferenciación Celular , Proliferación Celular , Osteogénesis , MasculinoRESUMEN
Lipodystrophic laminopathies are a group of ultra-rare disorders characterised by the presence of pathogenic variants in the same gene (LMNA) and other related genes, along with an impaired adipose tissue pattern and other features that are specific of each of these disorders. The most fascinating traits include their complex genotype-phenotype associations and clinical heterogeneity, ranging from Dunnigan disease, in which the most relevant feature is precisely adipose tissue dysfunction and lipodystrophy, to the other laminopathies affecting adipose tissue, which are also characterised by the presence of signs of premature ageing (Hutchinson Gilford-progeria syndrome, LMNA-atypical progeroid syndrome, mandibuloacral dysplasia types A and B, Nestor-Guillermo progeria syndrome, LMNA-associated cardiocutaneous progeria). This raises several questions when it comes to understanding how variants in the same gene can lead to similar adipose tissue disturbances and, at the same time, to such heterogeneous phenotypes and variable degrees of metabolic abnormalities. The present review aims to gather the molecular basis of adipose tissue impairment in lipodystrophic laminopathies, their main clinical aspects and recent therapeutic strategies. In addition, it also summarises the key aspects for their differential diagnosis.
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Lamina Tipo A , Laminopatías , Lipodistrofia , Progeria , Humanos , Progeria/genética , Progeria/patología , Lamina Tipo A/genética , Lamina Tipo A/metabolismo , Lipodistrofia/genética , Lipodistrofia/metabolismo , Lipodistrofia/patología , Laminopatías/genética , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Fenotipo , MutaciónRESUMEN
Diabetic cardiomyopathy (DCM) represents one of the typical complications associated with diabetes. It has been described as anomalies in heart function and structure, with consequent high morbidity and mortality. DCM development can be described by two stages; the first is characterized by left ventricular hypertrophy and diastolic dysfunction, and the second by heart failure (HF) with systolic dysfunction. The proposed mechanisms involve cardiac inflammation, advanced glycation end products (AGEs) and angiotensin II. Furthermore, different studies have focused their attention on cardiomyocyte death through the different mechanisms of programmed cell death, such as apoptosis, autophagy, necrosis, pyroptosis and ferroptosis. Exosome release, adipose epicardial tissue and aquaporins affect DCM development. This review will focus on the description of the mechanisms involved in DCM progression and development.
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Tejido Adiposo , Cardiomiopatías Diabéticas , Exosomas , Fibrosis , Pericardio , Humanos , Exosomas/metabolismo , Cardiomiopatías Diabéticas/metabolismo , Cardiomiopatías Diabéticas/patología , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Animales , Pericardio/metabolismo , Pericardio/patología , Muerte Celular , Miocitos Cardíacos/metabolismo , Miocitos Cardíacos/patología , Tejido Adiposo EpicárdicoRESUMEN
The onset and progression mechanisms of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are being studied. We developed and analyzed a new mouse model of obesity by combining maternal Id-like molecule (Maid) and melanocortin-4 receptor (Mc4r) gene deletions. Four mice, each at 12 and 28 weeks of age, were analyzed for each genotype: Maid gene knockout, Mc4r gene knockout, combined Mc4r and Maid gene knockout, and Mc4r gene knockout with a high-fat diet. Mice with a combined deficiency of Mc4r and Maid gene showed significantly more severe obesity compared to all other genotypes, but no liver fibrosis or a decline in metabolic status were observed. In visceral white adipose tissue, Maid and Mc4r gene knockout mice had fewer CD11c-positive cells and lower mRNA expression of both inflammatory and anti-inflammatory cytokines. Furthermore, Maid and Mc4r gene knockout mice showed lower expression of adipocytokines in visceral white adipose tissue and uncoupling protein-1 in scapular brown adipose tissue. The expression of adipocytokines and uncoupling protein-1 is regulated by sympathetic nerve signaling that contribute severe obesity in Maid and Mc4r gene knockout mice. These mechanisms contribute hyperobesity in Maid and Mc4r gene knockout mice.
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Inflamación , Ratones Noqueados , Obesidad , Receptor de Melanocortina Tipo 4 , Animales , Receptor de Melanocortina Tipo 4/genética , Receptor de Melanocortina Tipo 4/deficiencia , Receptor de Melanocortina Tipo 4/metabolismo , Obesidad/genética , Obesidad/metabolismo , Ratones , Inflamación/genética , Inflamación/metabolismo , Inflamación/patología , Dieta Alta en Grasa/efectos adversos , Modelos Animales de Enfermedad , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Masculino , Tejido Adiposo Pardo/metabolismo , Tejido Adiposo Pardo/patología , Proteína Desacopladora 1/genética , Proteína Desacopladora 1/metabolismo , Hígado Graso/genética , Hígado Graso/patología , Hígado Graso/metabolismo , Adipoquinas/metabolismo , Adipoquinas/genética , Tejido Adiposo Blanco/metabolismo , Tejido Adiposo Blanco/patologíaRESUMEN
Failure rate after chronic rotator cuff repair is considerably high. Moreover, diabetes mellitus is known as a compromising factor of rotator cuff tear. The effect of Polydeoxyribonucleotide (PDRN) and polynucleotide (PN) on tendon healing and fatty infiltration is unclear as tissue regeneration activator in diabetic state. Therefore, a diabetic rat model with chronic rotator cuff tear was made for mechanical, histologic and blood tests. In the animal study using a diabetic rat cuff repair model, the administration of PDRN and PN increased the load to failure of repaired cuffs and improved tendon healing and decreased fatty infiltration. Also, the plasma levels of vascular endothelial growth factor and fibroblast growth factor were elevated in PDRN and PN administrated groups. We concluded that PDRN and PN appear to boost tendon recovery and reduce the presence of fatty infiltration following cuff repair in diabetic state. Also, PN showed a later onset and a longer duration than PDRN associated with the mean plasma growth factors.
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Diabetes Mellitus Experimental , Polidesoxirribonucleótidos , Polinucleótidos , Lesiones del Manguito de los Rotadores , Cicatrización de Heridas , Animales , Polidesoxirribonucleótidos/farmacología , Polidesoxirribonucleótidos/uso terapéutico , Diabetes Mellitus Experimental/tratamiento farmacológico , Ratas , Cicatrización de Heridas/efectos de los fármacos , Lesiones del Manguito de los Rotadores/tratamiento farmacológico , Lesiones del Manguito de los Rotadores/patología , Lesiones del Manguito de los Rotadores/metabolismo , Masculino , Polinucleótidos/farmacología , Manguito de los Rotadores/patología , Manguito de los Rotadores/efectos de los fármacos , Modelos Animales de Enfermedad , Factor A de Crecimiento Endotelial Vascular/metabolismo , Factor A de Crecimiento Endotelial Vascular/sangre , Ratas Sprague-Dawley , Tejido Adiposo/efectos de los fármacos , Tejido Adiposo/metabolismo , Tejido Adiposo/patologíaRESUMEN
Dysregulated lipid metabolism in obesity leads to adipose tissue expansion, a major contributor to metabolic dysfunction and chronic disease. Lipid metabolism and fatty acid changes play vital roles in the progression of obesity. In this proof-of-concept study, Raman techniques combined with histochemical imaging methods were utilized to analyze the impact of a high-fat diet (HFD) on different types of adipose tissue in mice, using a small sample size (n = 3 per group). After six weeks of high-fat diet (HFD) feeding, our findings showed hypertrophy, elevated collagen levels, and increased macrophage presence in the adipose tissues of the HFD group compared to the low-fat diet (LFD) group. Statistical analysis of Raman spectra revealed significantly lower unsaturated lipid levels and higher lipid to protein content in different fat pads (brown adipose tissue (BAT), subcutaneous white adipose tissue (SWAT), and visceral white adipose tissue (VWAT)) with HFD. Raman images of adipose tissues were analyzed using Empty modeling and DCLS methods to spatially profile unsaturated and saturated lipid species in the tissues. It revealed elevated levels of ω-3, ω-6, cholesterol, and triacylglycerols in BAT adipose tissues of HFD compared to LFD tissues. These findings indicated that while cholesterol, ω-6/ω-3 ratio, and triacylglycerol levels have risen in the SWAT and VWAT adipose tissues of the HFD group, the levels of ω-3 and ω-6 have decreased following the HFD. The study showed that Raman spectroscopy provided invaluable information at the molecular level for investigating lipid species remodeling and spatial mapping of adipose tissues during HFD.
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Tejido Adiposo , Dieta Alta en Grasa , Metabolismo de los Lípidos , Espectrometría Raman , Animales , Espectrometría Raman/métodos , Ratones , Dieta Alta en Grasa/efectos adversos , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Masculino , Obesidad/metabolismo , Obesidad/patología , Ratones Endogámicos C57BL , Lípidos/análisisRESUMEN
Biochemical recurrence is a process that progresses to castration-resistant prostate cancer (CRPC) and prediction of biochemical recurrence is useful in determining early therapeutic intervention and disease treatment. Prostate cancer is surrounded by adipose tissue, which secretes adipokines, affecting cancer progression. This study aimed to investigate the correlation between blood adipokines and CRPC biochemical recurrence. We retrospectively analyzed the clinical data, including preoperative serum adipokine levels, of 99 patients with pT3a pN0 prostate cancer who underwent proctectomy between 2011 and 2019. The primary outcome was biochemical recurrence (prostate-specific antigen: PSA > 0.2). We identified 65 non-recurrences and 34 biochemical recurrences (one progressed to CRPC). The initial PSA level was significantly higher (p = 0.006), but serum adiponectin (p = 0.328) and leptin (p = 0.647) levels and their ratio (p = 0.323) were not significantly different in the biochemical recurrence group compared with the non-recurrence group. In contrast, significantly more biochemical recurrences were observed in the group with adiponectin < 6 µg/mL and Leptin < 4 ng/mL (p = 0.046), initial PSA > 15 ng/mL, clinical Gleason pattern ≥ 4, and positive resection margin. A significant difference was also observed in the multivariate analysis (hazard ratio: 4.04, 95% confidence interval: 1.21-13.5, p = 0.0232). Thus, low preoperative serum adiponectin and high leptin levels were significantly associated with biochemical recurrence in adipose tissue-invasive prostate cancer, suggesting that they may be useful predictors of biochemical recurrence. Further studies with larger cases are needed to increase the validity of this study.
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Adiponectina , Tejido Adiposo , Leptina , Recurrencia Local de Neoplasia , Antígeno Prostático Específico , Neoplasias de la Próstata , Humanos , Masculino , Adiponectina/sangre , Leptina/sangre , Anciano , Recurrencia Local de Neoplasia/sangre , Recurrencia Local de Neoplasia/patología , Persona de Mediana Edad , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Antígeno Prostático Específico/sangre , Estudios Retrospectivos , Neoplasias de la Próstata/sangre , Neoplasias de la Próstata/patología , Neoplasias de la Próstata/cirugía , Biomarcadores de Tumor/sangre , Pronóstico , Neoplasias de la Próstata Resistentes a la Castración/sangre , Neoplasias de la Próstata Resistentes a la Castración/patologíaRESUMEN
Perivascular adipose tissue (PVAT) is a special deposit of fat tissue surrounding the vasculature. Previous studies suggest that PVAT modulates the vasculature function in physiological conditions and is implicated in the pathogenesis of vascular diseases. Understanding how PVAT influences vasculature function and vascular disease progression is important. Extracellular vesicles (EVs) are novel mediators of intercellular communication. EVs encapsulate molecular cargo such as proteins, lipids, and nucleic acids. EVs can influence cellular functions by transferring the carried bioactive molecules. Emerging evidence indicates that PVAT-derived EVs play an important role in vascular functions under health and disease conditions. This review will focus on the roles of PVAT and PVAT-EVs in obesity, diabetic, and metabolic syndrome-related vascular diseases, offering novel insights into therapeutic targets for vascular diseases.
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Tejido Adiposo , Vesículas Extracelulares , Enfermedades Vasculares , Humanos , Vesículas Extracelulares/metabolismo , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Enfermedades Vasculares/metabolismo , Enfermedades Vasculares/patología , Animales , Obesidad/metabolismo , Obesidad/patologíaRESUMEN
BACKGROUND: Changes in the fatty infiltration and/or muscle volume of neck muscles can alter cervical spine alignment and cranial load distribution, which may cause pain in the orofacial region. OBJECTIVES: The aim of the study was to examine the muscle volume and fatty infiltration of neck muscles in patients with temporomandibular disorders (TMD). MATERIAL AND METHODS: This case-control study included 18 patients with TMD and 18 ageand sex-matched controls. The muscle volume and fatty infiltration of the neck muscles of the participants were measured using magnetic resonance imaging (MRI) and ITK-SNAP software. The 3D models of the sternocleidomastoid (SCM), splenius capitis (SPLC), semispinalis cervicis (SC)-semispinalis capitis (SCP), and multifidus (M) muscles within the C3-C7 range were created using ITK-SNAP, a semi-automatic segmentation software. The models were used to determine the volumes and fatty infiltration levels. The Neck Disability Index (NDI) was used to assess neck pain-related disability. The severity of TMD was determined using the Fonseca Anamnestic Index (FAI), while jaw-related disability was measured with the Jaw Functional Limitation Scale-20 (JFLS-20). Pain levels were recorded at rest and during chewing using the numeric rating scale (NRS). RESULTS: There were no statistically significant differences in total muscle volume, fatty infiltration volume and fatty infiltration percentage of the SCM, SPLC, SCP, SC, and M muscles between the 2 groups (p > 0.05). The patient group had higher NDI scores compared to the controls (p < 0.001). The NDI scores correlated positively with the JFLS-20 (r = 0.831, p < 0.001), FAI (r = 0.815, p < 0.001) and NRS scores at rest (r = 0.753, p < 0.001) and during chewing (r = 0.686, p < 0.001). CONCLUSIONS: The present study did not identify any significant differences in the neck muscle volume or fatty infiltration between the TMD patients and controls. However, the severity of neck disability was found to correlate with jaw function, pain and TMD levels.
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Imagen por Resonancia Magnética , Músculos del Cuello , Trastornos de la Articulación Temporomandibular , Humanos , Estudios de Casos y Controles , Femenino , Masculino , Músculos del Cuello/patología , Músculos del Cuello/diagnóstico por imagen , Trastornos de la Articulación Temporomandibular/diagnóstico por imagen , Trastornos de la Articulación Temporomandibular/patología , Adulto , Tejido Adiposo/diagnóstico por imagen , Tejido Adiposo/patología , Adulto Joven , Dolor de Cuello/diagnóstico por imagen , Dolor de Cuello/patología , Imagenología Tridimensional , Persona de Mediana EdadRESUMEN
Recent research into laminopathic lipodystrophies-rare genetic disorders caused by mutations in the LMNA gene-has greatly expanded our knowledge of their complex pathology and metabolic implications. These disorders, including Hutchinson-Gilford progeria syndrome (HGPS), Mandibuloacral Dysplasia (MAD), and Familial Partial Lipodystrophy (FPLD), serve as crucial models for studying accelerated aging and metabolic dysfunction, enhancing our understanding of the cellular and molecular mechanisms involved. Research on laminopathies has highlighted how LMNA mutations disrupt adipose tissue function and metabolic regulation, leading to altered fat distribution and metabolic pathway dysfunctions. Such insights improve our understanding of the pathophysiological interactions between genetic anomalies and metabolic processes. This review merges current knowledge on the phenotypic classifications of these diseases and their associated metabolic complications, such as insulin resistance, hypertriglyceridemia, hepatic steatosis, and metabolic syndrome, all of which elevate the risk of cardiovascular disease, stroke, and diabetes. Additionally, a range of published therapeutic strategies, including gene editing, antisense oligonucleotides, and novel pharmacological interventions aimed at addressing defective adipocyte differentiation and lipid metabolism, will be explored. These therapies target the core dysfunctional lamin A protein, aiming to mitigate symptoms and provide a foundation for addressing similar metabolic and genetic disorders.
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Lamina Tipo A , Lipodistrofia , Humanos , Lamina Tipo A/genética , Lamina Tipo A/metabolismo , Lipodistrofia/genética , Lipodistrofia/metabolismo , Lipodistrofia/terapia , Animales , Laminopatías/genética , Laminopatías/metabolismo , Progeria/genética , Progeria/metabolismo , Progeria/patología , Mutación , Lipodistrofia Parcial Familiar/genética , Lipodistrofia Parcial Familiar/metabolismo , Lipodistrofia Parcial Familiar/terapia , Metabolismo de los Lípidos/genética , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Resistencia a la Insulina/genética , Edición GénicaRESUMEN
Adipose tissue dysfunction, which is associated with an increased risk of colorectal cancer (CRC), is a significant factor in the pathophysiology of obesity. Obesity-related inflammation and extracellular matrix (ECM) remodeling promote colorectal cancer metastasis (CRCM) by shaping the tumor microenvironment (TME). When CRC occurs, the metabolic symbiosis of tumor cells recruits adjacent adipocytes into the TME to supply energy. Meanwhile, abundant immune cells, from adipose tissue and blood, are recruited into the TME, which is stimulated by pro-inflammatory factors and triggers a chronic local pro-inflammatory TME. Dysregulated ECM proteins and cell surface adhesion molecules enhance ECM remodeling and further increase contractibility between tumor and stromal cells, which promotes epithelial-mesenchymal transition (EMT). EMT increases tumor migration and invasion into surrounding tissues or vessels and accelerates CRCM. Colorectal symbiotic microbiota also plays an important role in the promotion of CRCM. In this review, we provide adipose tissue and its contributions to CRC, with a special emphasis on the role of adipocytes, macrophages, neutrophils, T cells, ECM, and symbiotic gut microbiota in the progression of CRC and their contributions to the CRC microenvironment. We highlight the interactions between adipocytes and tumor cells, and potential therapeutic approaches to target these interactions.
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Adipocitos , Neoplasias Colorrectales , Transición Epitelial-Mesenquimal , Microambiente Tumoral , Humanos , Neoplasias Colorrectales/patología , Neoplasias Colorrectales/metabolismo , Adipocitos/metabolismo , Adipocitos/patología , Animales , Metástasis de la Neoplasia , Matriz Extracelular/metabolismo , Tejido Adiposo/metabolismo , Tejido Adiposo/patología , Microbioma GastrointestinalRESUMEN
Relative fat mass (RFM) is a novel indicator for measuring body fat. This cross-section study aims to explore the association between RFM and periodontitis and to investigate possible effect modifiers in U.S. adults based on the National Health and Nutrition Examination Survey 2009-2014. The category of periodontitis was defined by the CDC/AAP. Mean clinical attachment loss and mean pocket probing depth (PPD) were calculated. The RFM formula is: 64 - (20 × height/WC) + (12 × sex), with sex coded as 1 for female and 0 for male. Natural cubic spline and weighted multivariable regression analyses were conducted to investigate the relationship between RFM and periodontal status. Subgroup and interaction analyses were also employed to assess the moderating roles of age, gender, and race. A total of 10,307 participants were included in our study. Compared to the lowest quartiles, individuals in the highest quartiles of RFM levels were more likely to have moderate/severe periodontitis (ORQ4vs1 = 1.64, 95% CI 1.30-2.06) and had a higher mean PPD (ßQ4vs1 = 0.15, 95% CI 0.09-0.22). This association was particularly stronger in populations under the age of 60, with significant interactions. Taken together, RFM is positively associated with periodontitis, particularly in those under 60 years old.
Asunto(s)
Encuestas Nutricionales , Periodontitis , Humanos , Masculino , Periodontitis/epidemiología , Femenino , Persona de Mediana Edad , Adulto , Estudios Transversales , Estados Unidos/epidemiología , Tejido Adiposo/patología , Anciano , Adulto Joven , Índice de Masa CorporalRESUMEN
Macrophages in obese adipose tissue have been shown to damage nerve fibers, however, the mechanism underlying how macrophages cause glial cell damage remains unknown. This study aimed to characterize the mechanism by which macrophages induce apoptosis in glial cell during obesity formation in mice by single-nucleus RNA sequencing (snRNA-seq). Cells obtained from paraepididymal adipose tissue in obese mice underwent snRNA-seq. Eighteen different clusters were identified, and 12 cell types were annotated, including glial cells, macrophages, and fibroblasts. There was a negative correlation between the number of glial cells and macrophages in mouse adipose tissue during the formation of obesity. The pro-apoptotic factor PHLPP1 was identified in GO Terms. The interaction between adipose tissue glial cells and macrophages was revealed via in-depth analysis, and the cell-cell communication mechanism between the TNF-α and NF-KB/PHLPP1 axes was perfected. Apoptosis of glial cell by upregulation of TNF-α via obesity-derived macrophages and activation of the NF-κB/PHLPP1 axis. We further revealed how macrophages induce apoptosis in glial cells during obesity formation, as well as different changes in the two cell populations. This study provides valuable resources and foundations for understanding the mechanistic effects of macrophages and glial cells during obesity formation, as well as diseases and potential interventions.
Asunto(s)
Apoptosis , Macrófagos , Ratones Endogámicos C57BL , FN-kappa B , Neuroglía , Obesidad , Factor de Necrosis Tumoral alfa , Regulación hacia Arriba , Animales , Obesidad/metabolismo , Obesidad/inmunología , Macrófagos/inmunología , Macrófagos/metabolismo , Ratones , Factor de Necrosis Tumoral alfa/metabolismo , Neuroglía/metabolismo , Neuroglía/inmunología , FN-kappa B/metabolismo , Masculino , Fosfoproteínas Fosfatasas/metabolismo , Fosfoproteínas Fosfatasas/genética , Transducción de Señal , Proteínas Nucleares/metabolismo , Proteínas Nucleares/genética , Tejido Adiposo/metabolismo , Tejido Adiposo/patologíaRESUMEN
BACKGROUND: Chitinase-3 like-protein-1 (CHI3L1) is a member of the mammalian chitinase-like proteins and elevated serum CHI3L1 level has been proved to be associated with poor prognosis in hepatocellular carcinoma (HCC). This study aimed to investigate the relationship between serum CHI3L1 levels and body composition parameters in patients with HCC after liver transplantation (LT). METHODS: This retrospective study enrolled 200 patients after LT for HCC. Blood samples were collected and serum concentrations of CHI3L1 were measured by enzyme-linked immunosorbent assay. Computer tomography (CT) were used to estimate skeletal muscle and adipose tissue mass. Spearman's rank correlation test was performed to assess associations between serum CHI3L1 levels and these body composition parameters. A Cox proportional-hazards regression model was performed to identify independent prognostic factors. Overall survival (OS) and recurrence-free survival (RFS) curves were constructed using the Kaplan-Meier method and compared by the log-rank test. RESULTS: Total 71 patients (35.5%) were diagnosed with myosteatosis according to skeletal muscle radiation attenuation (SMRA). The 5-year OS rates were 66.9% in non-myosteatosis group, significantly higher than 49.5% in myosteatosis group (p = 0.025), while the RFS of myosteatosis group (5-year RFS: 52.6%) or non-myosteatosis group (5-year RFS: 42.0%) shown no significant difference (p = 0.068). The serum CHI3L1 level were significantly negative correlated with SMRA (r = -0.3, p < 0.001). Interestingly, in patients with myosteatosis, Kaplan-Meier analysis revealed that elevated serum CHI3L1 levels were associated with worse OS (p < 0.001) and RFS (p = 0.047). However, in patients without myosteatosis, Kaplan-Meier analysis found elevated serum CHI3L1 levels were not associated with OS (p = 0.070) or RFS (p = 0.104). CONCLUSIONS: Elevated CHI3L1 was negatively correlated with SMRA, and predicted poorer prognosis in Chinese population after LT for HCC, especially in those patients with concomitant myosteatosis. Monitoring serum CHI3L1 can predict prognosis and effectively guide individual nutrition intervention.