61 research outputs found
Exercise as a mean to reverse the detrimental effect of high-fat diet on bone’s fracture characteristics
The aim of this study is to investigate whether exercise can
reverse some of the adverse effects of high-fat-diet-induced obesity on lipid
metabolism and bone biomechanical properties. A total of 26 adult male
C57bl/6J mice were randomly assigned into three groups: (A) Control group
(n=6), (B) High-fat diet group (n=10), (C) High-fat diet and exercise group
(n=10). Body mass and relevant biochemical parameters were measured for
the duration of the experimental protocol (37 weeks). Mechanical strength of
both femurs of each animal was assessed in-vitro based on three point bending
tests. It was revealed that exposure to high-fat diet led to significant increase
of body mass and cholesterol levels and also to substantial changes in bone
morphology and strength. Ultimate stress for the animals exposed to high-fat
diet and those exposed to high-fat-diet and exercise was 25% and 24% lower
compared to control, respectively. Exercise increased bone thickness by 15%
compared to animals that were not exposed to exercise. It was concluded that
high-fat-diet appears to have a detrimental effect on bone biomechanics and
strength. Exercise reversed the reduction in bone thickness that appears to be
induced by high-fat diet. However no statistically significant increase in bone
strength was observed
Exercise as a mean to reverse the detrimental effect of high-fat diet on bone’s fracture characteristics
The aim of this study is to investigate whether exercise can reverse some of the adverse effects of high-fat-diet-induced obesity on lipid metabolism and bone biomechanical properties. A total of 26 adult male C57bl/6J mice were randomly assigned into three groups: (A) Control group (n=6), (B) High-fat diet group (n=10), (C) High-fat diet and exercise group (n=10). Body mass and relevant biochemical parameters were measured for the duration of the experimental protocol (37 weeks). Mechanical strength of both femurs of each animal was assessed in-vitro based on three point bending tests. It was revealed that exposure to high-fat diet led to significant increase of body mass and cholesterol levels and also to substantial changes in bone morphology and strength. Ultimate stress for the animals exposed to high-fat diet and those exposed to high-fat-diet and exercise was 25% and 24% lower compared to control, respectively. Exercise increased bone thickness by 15% compared to animals that were not exposed to exercise. It was concluded that high-fat-diet appears to have a detrimental effect on bone biomechanics and strength. Exercise reversed the reduction in bone thickness that appears to be induced by high-fat diet. However no statistically significant increase in bone strength was observed
Correlation between mesenteric fat thickness and serum apolipoproteins in patients with peripheral arterial occlusive disease
BACKGROUND: Visceral fat possesses the most detrimental potential for cardiovascular morbidity through the release of adipokines, as well as metabolic and proinflammatory mediators, which adversely affect metabolic and vascular homeostasis. Among the different types of visceral adipose tissue, mesenteric fat is considered particularly detrimental, due to its close proximity to the portal circulation, affecting directly the liver, which is the main regulator of body metabolic homeostasis. Mesenteric fat can be reliably estimated using abdominal ultrasonography, the only available imaging method able to depict individual mesenteric leaves. Aim of the present study was to investigate the correlation of mesenteric fat thickness (MFT) with serum apolipoprotein levels in patients undergoing digital subtraction angiography in a single center. METHODS: 35 male patients with peripheral arterial disease were examined. After careful examination of the periumbilical area, the mesenteric leaves were identified. The maximal distance between each pair of sequential leaves was measured, and the mean value of the three thickest leaves was determined as the mesenteric fat thickness. Six apolipoprotein fasting serum concentrations were measured using a Luminex proteomics platform (xMAP Multiplex immunoassay): apolipoprotein A-I (apoAI), apolipoprotein A-II (apoAII), apolipoprotein B (apoB), apolipoprotein C-II (apoCII), apolipoprotein C-III (apoCIII) and apolipoprotein E (apoE). RESULTS: MFT correlated with apoAII and apoB serum concentrations. The correlations with apoAII and apoB remained significant following correction for BMI. No correlations were noted between MFT and serum apoAI, apoCII, apoCIII or apoE levels before or after adjustment for BMI. CONCLUSIONS: Our study indicates that MFT is significantly correlated with the concentration of atherogenic low density lipoproteins particles, as well as with apoAII, a determinant of free fatty acids levels. No correlation was observed between mesenteric fat thickness and very low density lipoprotein or chylomicron particles concentration
Correlation between mesenteric fat thickness and serum apolipoproteins in patients with peripheral arterial occlusive disease
Pacemaker Implantation following Heart Transplantation: Analysis of a Nation-Wide Database
Background: The 2018 United-Network-for-Organ-Sharing (UNOS) allocation-system changes resulted in greater recognition of mechanical circulatory support (MCS), leading to more heart transplantations (HTx) in patients with MCS. We aimed to investigate the effect of the new UNOS allocation system on the need for a permanent pacemaker and associated complications following HTx. Methods: The UNOS Registry was questioned, to identify patients that received HTx in the US between 2000 and 2021. The primary objectives were to identify risk factors for the need for a pacemaker implantation following HTx. Results: 49,529 HTx patients were identified, 1421 (2.9%) requiring a pacemaker post-HTx. Patients who required a pacemaker were older (53.9 ± 11.5 vs. 52.6 ± 12.8 years, p < 0.001), more frequently white (73% vs. 67%; p < 0.001) and less frequently black (18% vs. 20%; p < 0.001). In the pacemaker group, UNOS status 1A (46% vs. 41%; p < 0.001) and 1B (31% vs. 27%; p < 0.001) were more prevalent, and donor age was higher (34.4 ± 12.4 vs. 31.8 ± 11.5 years; p < 0.001). One-year survival was no different between the groups (HR: 1.08; 95% CI: 0.85, 1.37; p = 0.515). An era effect was observed (per year: OR: 0.97; 95% CI: 0.96, 0.98; p = 0.003), while ECMO pre-transplant was associated with lower risk of a pacemaker (OR: 0.41; 95% CI: 0.19, 0.86; p < 0.001). Conclusions: While associated with various patient and transplant characteristics, pacemaker implantation does not seem to impact one-year survival after HTx. The need for pacemaker implantation was lower in the more recent era and in patients who required ECMO pre-transplant, a finding explained by recent advances in perioperative care
Investigation of the effect of metabolic health on the proteome of serum and white adipose tissue of patients undergoing bariatric surgery
Aim: Metabolically healthy obesity is characterized as a comorbidity-free obesity status, however the exact pathogenetic mechanisms implicated in its transition to unhealthy obesity have not yet been unveiled. Our aim was to investigate the effect of metabolic health on the proteomic profile both in serum and visceral fat of morbidly obese subjects. Methods: 28 patients undergoing bariatric surgery and 10 healthy normal-weight blood donors were prospectively enrolled. The obese patients were divided into two groups: metabolically healthy (MHO, n=18) and unhealthy (MUO, n=10) obese patients. 31 biomarkers were measured in serum and visceral adipose tissue with the use of targeted proteomic analysis (Luminex assays). Results: Regarding the comparisons between normal weight and obese subjects, significant differences were observed in the majority of the measured proteomic markers. TNF weak inducer of apoptosis (TWEAK) (p=0.043), TNF related apoptosis inducing ligand (TRAIL) (p=0.037), Growth differentiation factor-15 (GDF-15) (p=0.04), Resistin (RETN) (p=0.047), Matrix metalloproteinase-9 (MMP-9) (p=0.011) and C-terminal telopeptide (ICTP) (p=0.022) were up-regulated in the MUO group in the visceral white adipose tissue. Moreover, C-C motif ligand-3 (CCL-3) (p=0.056), Interleukin-20 (IL-20) (p=0.04), Prokineticin-1 (PROK-1) (p=0.028) and TWEAK (p=0.016) were found to be suppressed in the serum of MHO group. Significant correlations between serum and adipose tissue levels of certain cytokines were also observed, while 16 biomarkers were associated with BMI. Our results indicate metabolic health substantially attenuates the expression of TWEAK, TRAIL, GDF-15, RETN, MMP-9 and ICTP expression locally, in the visceral white adipose tissue, and the expression of CCL-3, IL-20, PROK-1 and TWEAK in the peripheral blood. Intriguingly, different cytokines –except for TWEAK- are up-regulated in each site, suggesting that obesity is not a homogenous but a multi-dimensional disease.Σκοπός: Η μεταβολικά υγιής παχυσαρκία ορίζεται ως μία κατάσταση παχυσαρκίας που δεν συνοδεύεται από την παρουσία συννοσηροτήτων, ωστόσο οι ακριβείς παθογενετικοί μηχανισμοί που εμπλέκονται στη μετάβαση από τη μεταβολικά υγιή στη μη υγιή παχυσαρκία δεν έχουν διαλευκανθεί πλήρως. Στόχος της παρούσας μελέτης ήταν η διερεύνηση του ρόλου της μεταβολικής υγείας στο πρωτεομικό προφίλ του περιφερικού αίματος και του σπλαχνικού λιπώδους ιστού σε ασθενείς με νοσογόνο παχυσαρκία. Μεθοδολογία: Συνολικά συμμετείχαν 28 ασθενείς που επρόκειτο να υποβληθούν σε βαριατρικό χειρουργείο (επιμήκης γαστρεκτομή, γαστρική παράκαμψη κατά Roux En Y και χολοπαγκρεατική εκτροπή) και 10 νορμοβαρείς εθελοντές αιμοδότες. Οι παχύσαρκοι ασθενείς χωρίστηκαν σε 2 ομάδες: Μεταβολικά υγιείς (n=18) και μεταβολικά μη υγιείς (n=10) παχύσαρκοι ασθενείς. 31 βιοδείκτες μετρήθηκαν στον ορό και στο σπλαχνικό λίπος με την χρήση πρωτεομικών μεθόδων. Αποτελέσματα: Όσον αφορά τις συγκρίσεις μεταξύ παχύσαρκων και νορμοβαρών ατόμων, παρατηρήθηκαν σημαντικές διαφορές στην πλειοψηφία των συγκρίσεων. Οι TNF weak inducer of apoptosis (TWEAK) (p=0.043), TNF related apoptosis inducing ligand (TRAIL) (p=0.037), Growth differentiation factor-15 (GDF-15) (p=0.04), Resistin (RETN) (p=0.047), Matrix metalloproteinase-9 (MMP-9) (p=0.011) και το C-terminal telopeptide (ICTP) (p=0.022) ήταν αυξημένα στους μεταβολικά μη υγιείς παχύσαρκους ασθενείς
Διερεύνηση της επίδρασης της μεταβολικής υγείας στο πρωτέομα του ορού και του λευκού λιπώδους ιστού ασθενών που υποβάλλονται σε βαριατρικό χειρουργείο
Σκοπός: Η μεταβολικά υγιής παχυσαρκία ορίζεται ως μία κατάσταση παχυσαρκίας που δεν συνοδεύεται από την παρουσία συννοσηροτήτων, ωστόσο οι ακριβείς παθογενετικοί μηχανισμοί που εμπλέκονται στη μετάβαση από τη μεταβολικά υγιή στη μη υγιή παχυσαρκία δεν έχουν διαλευκανθεί πλήρως. Στόχος της παρούσας μελέτης ήταν η διερεύνηση του ρόλου της μεταβολικής υγείας στο πρωτεομικό προφίλ του περιφερικού αίματος και του σπλαχνικού λιπώδους ιστού σε ασθενείς με νοσογόνο παχυσαρκία.
Μεθοδολογία: Συνολικά συμμετείχαν 28 ασθενείς που επρόκειτο να υποβληθούν σε βαριατρικό χειρουργείο (επιμήκης γαστρεκτομή, γαστρική παράκαμψη κατά Roux En Y και χολοπαγκρεατική εκτροπή) και 10 νορμοβαρείς εθελοντές αιμοδότες. Οι παχύσαρκοι ασθενείς χωρίστηκαν σε 2 ομάδες: Μεταβολικά υγιείς (n=18) και μεταβολικά μη υγιείς (n=10) παχύσαρκοι ασθενείς. 31 βιοδείκτες μετρήθηκαν στον ορό και στο σπλαχνικό λίπος με την χρήση πρωτεομικών μεθόδων.
Αποτελέσματα: Όσον αφορά τις συγκρίσεις μεταξύ παχύσαρκων και νορμοβαρών ατόμων, παρατηρήθηκαν σημαντικές διαφορές στην πλειοψηφία των συγκρίσεων. Οι TNFweakinducerofapoptosis (TWEAK) (p=0.043), TNFrelatedapoptosisinducingligand (TRAIL) (p=0.037), Growthdifferentiationfactor-15 (GDF-15) (p=0.04), Resistin (RETN) (p=0.047), Matrixmetalloproteinase-9 (MMP-9) (p=0.011) και το Cterminaltelopeptide (ICTP) (p=0.022) ήταν αυξημένα στους μεταβολικά μη υγιείς παχύσαρκους ασθενείς.Aim: Metabolically healthy obesity is characterized as a comorbidity-free obesity status, however the exact pathogenetic mechanisms implicated in its transition to unhealthy obesity have not yet been unveiled. Our aim was to investigate the effect of metabolic health on the proteomic profile both in serum and visceral fat of morbidly obese subjects.
Methods: 28 patients undergoing bariatric surgery and 10 healthy normalweight blood donors were prospectively enrolled. The obese patients were divided into two groups: metabolically healthy (MHO, n=18) and unhealthy (MUO, n=10) obese patients. 31 biomarkers were measured in serum and visceral adipose tissue with the use of targeted proteomic analysis (Luminex assays).
Results: Regarding the comparisons between normal weight and obese subjects, significant differences were observed in the majority of the measured proteomic markers.TNF weak inducer of apoptosis (TWEAK) (p=0.043), TNF related apoptosis inducing ligand (TRAIL) (p=0.037), Growth differentiation factor-15 (GDF-15) (p=0.04), Resistin (RETN) (p=0.047), Matrix metalloproteinase-9 (MMP-9) (p=0.011) and C-terminal telopeptide (ICTP) (p=0.022) were up-regulated in the MUO group in the visceral white adipose tissue. Moreover, C-C motif ligand-3 (CCL-3) (p=0.056), Interleukin-20 (IL-20) (p=0.04), Prokineticin-1 (PROK-1) (p=0.028) and TWEAK (p=0.016) were found to be suppressed in the serum of MHO group. Significant correlations between serum and adipose tissue levels of certain cytokines were also observed, while 16 biomarkers were associated with BMI. Our results indicate metabolic health substantially attenuates the expression of TWEAK, TRAIL, GDF-15, RETN, MMP-9 and ICTP expression locally, in the visceral white adipose tissue, and the expression of CCL-3, IL-20, PROK-1 and TWEAK in the peripheral blood. Intriguingly, different cytokines –except for TWEAK- are up-regulated in each site, suggesting that obesity is not a homogenous but a multi-dimensional disease
Reply: Right ventricle-to-pulmonary artery conduits for truncus arteriosus repair: Let's shift the focus
- …