Non-alcoholic fatty liver disease (NAFLD) is associated with overweight/obesity, metabolic syndrome and type 2 diabetes (T2D) due to chronic caloric excess and physical inactivity. Previous meta-analyses have confirmed associations between ultra-processed food (UPF) intake and obesity and T2D. We aim to ascertain the contribution of UPF consumption to the risk of developing NAFLD. We performed a systematic review and meta-analysis (PROSPERO (CRD42022368763)). All records registered on Ovid Medline and Web of Science were searched from inception until December 2022. Studies that assessed UPF consumption in adults, determined according to the NOVA food classification system, and that reported NAFLD determined by surrogate (steatosis) scores, imaging or liver biopsy were included. The association between UPF consumption and NAFLD was assessed using random-effects meta-analysis methods. Study quality was assessed, and evidence credibility evaluated, using the Newcastle Ottawa Scale and NutriGrade systems, respectively. A total of 5454 records were screened, and 112 records underwent full text review. From these, 9 studies (3 cross-sectional, 3 case-control and 3 cohort), analysing 60,961 individuals, were included in the current review. Both moderate (vs. low) (pooled relative risk 1.03 (1.00–1.07) (p = 0.04) (I2 = 0%)) and high (vs. low) (1.42 (1.16–1.75) (<0.01) (I2 = 89%)) intake of UPF significantly increased the risk of NAFLD. Funnel plots demonstrate low risk of publication bias. Consumption of UPF is associated with NAFLD with a dose–response effect. Public health measures to reduce overconsumption of UPF are imperative to reduce the burden of NAFLD, and the related conditions, obesity and T2D.
The liver is the central detoxifying organ, continuously removing xenobiotics from the vascular system. Given its role in drug metabolism, a functional understanding of liver physiology is crucial to optimizing drug efficacy and patient safety. The Virtual Liver Network (VLN), a German national flagship research program, focuses on producing validated computer models of human liver physiology. These models are used to analyze patient-derived data and thereby gain mechanistic insights in the processes underlying drug pharmacokinetics (PK).
Medical Research Society 19rin affected sibling pairs provided evidence for linkage with 12 markers in 5 distinct regions of chromosomes 2, 3, 7, 12 and 15 (p
Funding Acknowledgements Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Canadian Institute of Health Research Michael Smith Foreign Study Supplement Background Image and performance enhancing drugs (IPED) cause cardiac enlargement and dysfunction. Previous work has not assessed impact of user status (current [CU] vs. past [PU]) or allometric scaling cardiac dimensions for individual differences in fat-free mass (FFM). Purpose To investigate CU and PU of IPED and allometric scaling on LV and RV remodeling in strength-trained athletes. Methods Thirty-four (29 ± 6 years; 82% male) strength-trained athletes were recruited. Fourteen were CU, 9 PU and 11 non-users (NU) of IPEDs. Participants underwent bioelectric impedance body composition analysis, IPED and training questionnaire and 2D echocardiography with strain imaging. All structural data was allometrically scaled to FFM according to the laws of geometric similarity. Results CU and PU had significantly higher FFM compared to NU (82.4 ± 10.1 kg vs. 72.0 ± 6.3 kg vs. 58.2 ± 14.0 kg). Absolute values of all RV and LV size were larger between CU and NU. LV mean wall thickness (MWT) was larger in CU compared to PU but there were no differences between PU and NU. Allometric scaling eliminated all differences with exception of LV mass and LVMWT. LVEF was significantly lower in CU and PU compared to NU (55 ± 3 vs. 57 ± 4 vs. 61 ± 4) whilst LV GLS was lower in CU compared to PU and NU and LV GCS was lower in CU compared to NU but not PU. There was no significant difference between groups for RV functional indices. Conclusion Strength-trained athletes currently using IPEDs have bi-ventricular enlargement as well as reduced LV function. Allometric scaling highlights that increased size is partially associated with a larger FFM, with exception of LVMWT which is independently increased through IPED use. PUs demonstrate reverse structural remodeling whilst functional differences partially remain. CU PU NU RVD1 (mm) 45 ± 5* 43 ± 6 37 ± 6 Scaled RVD1 (mm/kg^0.33) 10.5 ± 0.9 10.4 ± 1.5 9.7 ± 1.0 LVd (mm) 58 ± 7* 55 ± 4 50 ± 4 Scaled LVd (mm/kg^0.33) 13.4 ± 1.2 13.3 ± 0.7 13.1 ± 0.6 MWT (mm) 10 ± 1*” 8 ± 1 8 ± 1 Scaled MWT (mm/kg^0.33) 2.3 ± 0.2*” 2.0 ± 0.1 2.0 ± 0.2 LVEDV (ml) 169 ± 42* 135 ± 28 116 ± 28 Scaled LVEDV (ml/kg) 2.0 ± 0.4 1.9 ± 0.3 2.0 ± 0.2 LV Mass (g) 255 ± 85*” 179 ± 30 137 ± 40 LV mass index (g/kg) 3.1 ± 0.8* 2.5 ± 0.3 2.4 ± 0.4 * CU and NU “ CU and PU ^ PU and NU Abstract Figure. Myocardial strain imaging
Extracellular matrix breakdown is essential for the migration and proliferation of vascular smooth muscle cells (VSMC) in balloon angioplasty restenosis. Tissue inhitor of metalloproteinases-1 (TIMP-I) potently inbibits the matrix metalloproteinase enzynes and may m o w this process. The effects of overexpression of TIMP-1 were investigated and the gene delivered to the rat carotid artery. A replication deficient recombinant adenoviral vector AvI.TIMP-I containing the cDNA for human TIMP-I was constructed. Its ability to express TIMP-I in rat primary VSMC was compared with cells infected a PGalactosidase expressing adenovirus Avl.pGal and control cells. Westem blottmg showed a dose dependent protem expression in response to AvI.TIMP-I (n=3). Reverse zymography showed biologically active protein with an increase proportional to the multiiplicky of infection (MOI) of Av1.TIMF' -1 (n=3). TIMP-I is a mitogen in some cell types but no change in H3 thymidine incorporation was seen versus control cells (n=6). Studies of migration of VSMC infected with Av1.TIMP-1, Avl.pGal, and control cells across an 8 CM pore sizs membrane showed inhiition of migration by viral infection alone (68% reduction in migration by Avl.pGal p<0.05, n=9) but a 90% reduction by AvI.TIMP-I indicating a significant additional effect ofthe TIMP-I versus f3 Galactosidase (p<0.05, n=9). In contrast VSMC invasion through an artificial basement membrane bamer was not affected by infection with Avl.~GaI but showed 30% inbibition by infection of the cells with AvI.TIMp-I @<0.05, n=12). Balloon injured rat carotid arteries exposed to Avl.PGal and AvI.TIMP-I in vivo showed transgene expression 2 and 14 days later. Immunohistochemistry and western blotting demonstrated human =-I. Conclusion: We have generated an adenoviral vector overexpressing biologically active TIMP-1. This vector inhibits migration and invasion of VSMC and successll protem expression follows in vivo administration after vascular injury. This vector nlaybe of interest for gene therapy.Glucocorticoids such as cortisol are immunoregulatory and promote reactivation of TB. Cortisol activity is regulated in each tissue by its inactivation to cortisone. It has previously been shown that the mtio of cortisol to cortisone is elevated in patients with active pulmonary TB .This study aimed to establish whether altered cortisol metabolism is a constitutive abnormality in TB. We studied 5 patients with active pulmonary TB (ATB). 7 with cured pulmonary TB (CTB). 7 healthy controls (CON) and 3 disease controls (pneumonia, DC). Ratios of urinary metabolites of cortisol and cortisone. measured by gas chromatography and mass spectrometry in 24 h urine, showed that a high ratio is exclusive to ATB (1.52 +I-0.17; vs 0.93 +/-0.06 in CTB, p4.05: 0.77 +I-0.02 CON, p4.01 and 0.76 DC, ~4 . 0 1 ) . This is attributable, at least in part, to enhanced conversion of cortisone to cortisol, since serum cortisol was higher after an oral dose of cortisone in ATB (peak 992+/-107nmol/l vs582+/-M nmolll in CON; P4.01 and...
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