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How to Lose Body Fat With Breathing Respiratory Research Energy conservation during long events 22Article number: Calorie tracking app Cite this article. Metrics details. The effects of fzt adiposity Viscearl decreased lung function have drawn much attention. Recently, the visceral adiposity index VAI has been proposed as a visceral fat distribution and dysfunction marker. However, the relationship between the VAI and lung function has not been investigated.Visceral fat and respiratory problems -
E LM: resin embedded, toluidine-blue stained tissue. Large free lipid droplets yellow are evident in the capillaries lumen in alveolar septa arrows.
F Transmission electron microscopy TEM : showing lipid droplet LD into an alveolar septum mixed with erythrocytes. G TEM: alveolar macrophage M in a COVID subject. Note: diffuse dilated rough endoplasmic reticulum RER denoting cellular stress arrows H TEM: enlargement of the squared area in G showing two virions at stages 1—2 and 5 of the reproductive cycle into the dilated RER similar to what observed in I TEM: 1 to 5 stages of the reproductive cycle of SARS-CoV-2 virions in VeroE6 infected cells.
Reference in the main text. Consistently, all subjects with type 2 diabetes had fat embolism. Of note, electron microscopy observations revealed several structures with size and morphology compatible with those of SARS-CoV-2 viruses [ 6 ] in pneumocytes, endothelial cells and macrophages, the last of which displayed disseminated, dilated endoplasmic reticulum denoting cellular stress [ 26 , 32 ] and signs of virus presence only in subjects with COVID Fig.
Several Weibel-Palade bodies, signs of activated coagulative phenomena [ 31 ], were also observed in most of the capillary endothelial cells of subjects with COVID data not shown. Unexpectedly, the used lipid-specific histochemistry technique evidenced that all alveolar structures reminiscent of HM were ORO-positive Fig.
Interestingly, this last subject displayed a fainted HM positivity for ORO staining, suggesting a lower lipidic presence. This finding is consistent with other reports describing HM in the lungs of patients with non-COVIDrelated pneumonia [ 7 ].
Several aspects suggesting a direct role of embolic fat in HM formation were observed. Specifically, free lipid droplets occupying the alveolar space and lining and spreading on the alveolar surface were observed Fig. A Light microscopy LM : hyaline membranes lining alveolar surfaces arrows at low magnification.
Lipid-rich macrophages free in the alveolar space red arrows and inside hyaline membranes red arrow. D LM: enlargement of the squared area in C. Arrows indicate lipid vacuoles. F TEM: free lipid droplets lining the alveolar surface composed by pneumocytes type II PT2 with classic surfactant granules arrow.
Lastly, since the embolic material from abdominal visceral tissues should necessarily pass through the liver parenchyma to reach the lung, we exploited the ORO staining technique to study liver samples belonging to 9 individuals with COVID and 8 control subjects.
Liver autoptic samples showed focal, macrovesicular steatosis with lipid droplets of very variable size Supplementary Fig. In particular, signs consistent with fat embolism, i. This is the first study investigating the ultrastructural features of VAT among individuals with COVID and assessing lipid distribution in lungs and liver samples by histomorphology.
Our data support the presence of higher local VAT inflammation and higher prevalence of fat embolism and lipidic HM formations in the lungs of subjects dead due to COVID compared to control individuals dead for different reasons. In addition, our data support SARS-CoV-2 ability to infect human adipocytes in vitro.
Considering the strong association between COVIDrelated complications and obesity, especially with visceral adipose content excess [ 10 , 11 , 13 , 14 , 15 , 16 ], the comprehension of the biological phenomenon at the basis of such association holds critical clinical implications in the era of the COVID pandemic.
Our study provides the first evidence of higher local VAT inflammation among subjects with COVID, independently of obesity status and support an exacerbation of obesity-related inflammation by SARS-CoV-2 infection, a novel finding consistent with studies reporting higher systemic inflammation among infected patients [ 18 ].
Adipocyte inflammation is associated with cell stress, death, and lipid release in the extracellular space [ 19 , 20 , 25 , 26 ]. We hence studied adipocyte features by TEM and revealed the presence of the typical signs of cellular stress, together with prominent features of lipids spill-over from suffering adipocytes.
Of note, these data are supported by a recent work showing an increased number of autoimmune antibodies against the malondialdehyde and the adipocyte-derived protein antigen markers of lipid peroxidation and adipocytes death, respectively [ 35 ] among subjects with COVID and obesity as compared to individuals suffering from each condition independently [ 36 ].
In addition, hyperglycemia among subjects with COVID was demonstrated to be strongly associated with insulin resistance and low plasma adiponectin levels [ 29 ].
The authors from the same study also demonstrated that SARS-CoV-2 could infect hamster adipose tissue, leading to reduced adiponectin production and speculated that SARS-CoV-2 infection might result in adipocyte dysfunction driving insulin resistance.
Importantly, we detected lipids in the extracellular space, inside endothelial cells, inside the capillary lumen, and extruding from endothelial cells into the capillary lumen, all features indicative of fat embolism.
Although virus-like structures were evidenced by TEM in the same VAT depots, the lack of SARS-CoV-2 detection by qPCR did not allow us to conclude that such inflammation, cellular stress, and death were all related to the presence of the virus.
It is, in fact, possible that the described VAT features were secondary to the systemic inflammation induced by COVID or due to the presence of different viruses within the depot.
On the other side, we demonstrated that SARS-CoV-2 could infect human adipocytes even though neither adipocytes nor adipocyte progenitors gathered all of the known molecular requirements for the virus entry e. This set of data is in part consistent with other findings and suggests that additional, not yet characterized, receptors and proteases may be exploited for this purpose [ 16 , 37 ].
Puray-Chavez et al. in fact indicated that human H lung adenocarcinoma cells are permissive to SARS-CoV-2 infection despite complete ACE2 absence and that virus entry is dependent on heparan sulfate in this cell line [ 37 ].
Importantly, despite being the first SARS-CoV-2 targets, olfactory and respiratory epithelial cells express low ACE2 protein levels [ 38 ]. For these reasons, additional co-factors facilitating the virus-host cell interaction e. In our study, BASIGIN receptor and FURIN protease were highly expressed in differentiated hMADS and could be exploited for SARS-CoV-2 infection.
However, it should be noted that, although FURIN critical role in mediating SARS-CoV-2 infection is widely accepted and seem to be of relevance in patients with type 2 diabetes where the protease is highly expressed [ 41 ], the role of BASIGIN has been recently questioned [ 42 ].
Given the widespread presence of lipid droplets in the capillary lumen of VAT and our preliminary data [ 23 ], we studied lipid distribution in lung and liver samples and confirmed the presence of fat embolism.
Fat embolism in the lungs was not exclusive to, but more prevalent among subjects with COVID; it was in fact also detected among subjects with obesity independently of SARS-CoV-2 infection. These data are not surprising given that adipocyte death and release of lipids are both phenomena occurring in obesity [ 19 , 25 , 26 ].
This finding provides the first evidence pointing out fat embolism as a complication of obesity and obesity plus type 2 diabetes , determined by adipocyte death and possibly exacerbated by the COVIDinduced inflammatory status. HM were present in all patients with COVID and in only one control who died for pneumonia, a finding consistent with other reports describing HM presence in this latter disease [ 7 ].
Our histomorphologic assessment revealed several aspects indicative of a direct role of embolic fat in HM formation. Consistently, the presence of lung HM of lipidic nature in the lungs was associated with VAT inflammation.
Our findings on intestinal and liver fat embolism strongly support the embolic nature of lipid droplets in the lungs. As the portal system drains venous blood from most abdominal fat depots to the liver, the embolic fat originated in the VAT necessarily pass through the liver to reach other organs.
The unequivocal presence of lipid droplets into sinusoids and liver veins supports the fat embolic production by abdominal fat. In summary, in our case series, although fat embolism may be present in obesity and type 2 diabetes independently of COVID, the embolic lipidic material could contribute to the formation of HM only in the case of COVIDrelated pneumonia.
This novel finding holds critical clinical implications and deserves further investigation. Furthermore, these data provide insights into HM nature, as their formation process has not been characterized yet [ 44 ].
Additional studies investigating the HM nature of non-COVIDrelated pneumonia are required to detail such histopathological features. Collectively our data reveal higher local VAT inflammation in subjects with COVID and SARS-CoV-2 ability to infect human adipocytes.
In addition, we provide the first evidence that supports the fat embolism as a complication of obesity, likely determined by adipocyte death and exacerbated by the COVIDinduced inflammatory status.
Consistently, fat embolism displays similar signs and symptoms as observed in COVID, in line with a recently published case report [ 45 ].
When fat embolism and COVID are suspected, differential diagnosis is critical for proper patient care. Based on our findings, the assessment of fat embolism symptoms is mandatory in the context of the COVID pandemic, especially among patients with pulmonary symptoms, obesity, and high waist circumference, last two of which are recognized as signs of high visceral adipose accumulation.
Such complex clinical status should be therefore adequately assessed and properly addressed. Our data hold critical clinical implications in the context of obesity and COVID pandemics and need to be confirmed by additional studies with larger sample size.
Our study did not entail any physical risk for the subjects. In Italy, the evaluation of non-pharmacological observational studies is not governed by the same normative references provided for the evaluation of clinical trials and observational studies concerning drugs.
Furthermore, as reported in the above report [ 46 ] in the section dedicated to our type of study in conditions of pandemic and therefore of high risk for the communities, some administrative steps may be abolished.
Therefore, our Institutional Review Board does not require ethical approval for studies conducted on autoptic specimens and not collecting personal or sensitive data. Autoptic lung, liver, and VAT samples of 49 subjects were collected at the Department of Legal Medicine of the Ospedali Riuniti of Ancona between March and May Twenty-four subjects were affected by COVID, while the remaining 25 were not and died for different reasons.
SARS-CoV-2 infection was assessed in all subjects by RT-PCR tests on a nasopharyngeal swab. Among the studied subjects, 15 had documented respiratory conditions, i. VAT was sampled from the omentum and mesentery region. Lungs were extensively sampled across central and peripheral regions of each lobe bilaterally.
A median of seven tissue blocks range five to nine were taken from each lung. Liver samples were collected from the right and left lobes. Samples were sliced into different pieces to be studied by LM and transmission electron microscopy TEM.
A comprehensive methodological description for such methodologies has been described elsewhere [ 47 ]. Samples were then embedded in paraffin to be studied by LM and to perform immunohistochemistry and morphometric analyses.
A comprehensive description of the protocol has been described elsewhere [ 47 ]. To study SARS-CoV-2 presence in VAT, we used the SARS-CoV-2 nucleocapsid Invitrogen MA and spike protein Sino Biological T62 antibodies at different dilutions. The same antibodies were used to detect the virus on infected VeroE6 at dilution: for nucleocapsid protein and for the spike protein.
Negative control in which primary antibody was omitted were always included in each set of reactions to assess antibody specificity. Tissue sections were observed with a Nikon Eclipse E light microscope. For morphometric purposes, for each paraffin section, ten digital images were acquired at ×20 magnification with a Nikon DXM camera.
Tissue slices were then counterstained with hematoxylin and covered with a cover-slip using Vectashield mounting medium Vector Laboratories. The day before infection, a confluent monolayer was trypsinized, and 1. Confluent monolayers were infected with SARS-CoV-2 isolates, accession no.
MT [ 49 ] at a multiplicity of infection of 3. Uninfected cell monolayer controls were treated as infected ones.
Aliquots of infected supernatants, collected as above, were analyzed using RT-qPCR assay as described elsewhere [ 49 ]. Human adipocytes progenitors -Aps- hMADS cells were isolated from adipose tissue, as surgical scraps from a surgical specimen of various surgeries of young donors, with the informed consent of the parents.
All methods were approved and performed following the guidelines and regulations of the Centre Hospitalier Universitaire de Nice Review Board. hMADS cells were maintained and differentiated as previously described [ 50 ]. They will be further referred to as hMADS adipocytes. They were routinely tested for the absence of mycoplasma.
Treatments and biological assays were carried out in duplicates on control or differentiated hMADS cells from days 4 to Total RNA was extracted using the TRI-Reagent kit Euromedex, Soufflweyersheim, France and reverse transcription RT was performed using MMLV reverse transcriptase Promega, Charbonnieres, France , as recommended by the manufacturers.
All primer sequences are described in the Supplementary section. Real-time PCR assays were run on an ABI Prism One-step real-time PCR machine Applied Biosystems, Courtaboeuf, France. Normalization was performed using 36B4 as a reference gene. Quantification was performed using the comparative Ct method.
Statistical significance was determined by t- tests BiostaTGV INSERM and Sorbonne University, PARIS, France. HP Eschborn, Germany. Following incubation, the medium containing the inoculum was removed, the cells were washed twice, and the medium was supplemented with different specific compounds.
Uninfected cell monolayer controls were treated as the infected ones. Louis, MO, USA. Following the incubation with the virus, cells were placed in supplemented medium. Results were expressed as percentages of viable cells relative to uninfected controls.
Alterations in nuclear morphology were determined by assessment of nuclear staining using fluorescent stains and fluorescent microscopy [ 51 ]. For these experiments, hMADS adipocytes were differentiated in 2-well Lab-Tek Chamber Slides Nalge Nunc International, Naperville, IL, USA , washed with PBS pH 7.
After washing with PBS, nuclear staining was performed with Hoechst. Finally, cells were airdried and cover-slipped using Vectashield mounting medium Vector Laboratories, Burlingame, CA, USA and analyzed by fluorescent microscopy.
The number of altered nuclei were counted in the field displaying nuclear fragmentation and nuclear condensation and divided by the total number of nuclei multiplied by Observations were carried out by Lucia IMAGE 4. Lipid droplet size μm 2 was measured in SARS-CoVinfected hMADS adipocytes and untreated controls.
For this purpose, we used a drawing tablet and a morphometric program Nikon LUCIA IMAGE, Laboratory Imaging, version 4. hMADS adipocytes were examined with a Nikon Eclipse Ti-S inverted light microscope Nikon Instruments S.
A, Calenzano, Italy , and digital images were captured at ×20 with a Nikon DS-L2 camera Nikon Instruments S. A, Calenzano, Italy. Five random fields were analyzed, at least lipid droplets were measured for each sample, and the difference between infected and non-infected cells was assessed by unpaired t -test.
Similarly, the quantitative assessment of the material extruded from the hMADS was calculated using the same microscope and software and expressed as the number of vacuoles extruded from the cells on the total cell amount.
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All authors approve the manuscript for publication and declare that the work described was an original research that has not been published previously, in whole or in part. All the authors listed have approved the manuscript that is enclosed. This study was supported by Guangxi colleges and Universities Key Laboratory of Human Development and Disease Research NO: C , Guangxi Medical University innovation and entrepreneurship training program NO: 、 Effects of physical activity on body composition and bone mineral density of Guangxi multi-ethnic college students C.
Department of Anatomy, Guangxi Medical University, No. Guangxi Medical University, Nanning, , Guangxi, China. You can also search for this author in PubMed Google Scholar. LH and CK wrote the first draft of the manuscript, helped interpret the results, and critically revised the manuscript.
ZY and JL supervised the data processing and helped interpret the statistical results. QZ, BH, ZW, and JG helped collect the data and interpret the results. LX, QD, and PL helped develop the questionnaire and interpret the results and critically revised the manuscript.
All authors read and approved the final manuscript. Correspondence to Peng Liu. Participants of this study signed an informed consent form, and the study was approved by the Medical Ethics Committee of Guangxi Medical University. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Open Access This article is distributed under the terms of the Creative Commons Attribution 4. Reprints and permissions. Huang, L. et al. Effects of fat distribution on lung function in young adults.
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Skip to main content. Fat tissue is also known to increase inflammation in the body, which may be playing a role, they said. Although the reasons may not be clear, Dr. Paul Enright of the University of Arizona said in a commentary there is now enough evidence to include waist measurements as part of routine assessments of lung function.
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Beyond Antifungal properties common Viscersl related to obesity, such as type 2 ane and cardiovascular diseases, impaired Visceral fat and nutrient partitioning function is reepiratory known, Muscular strength progression workouts, whether the fat distribution sub-cutaneous, abdominal, aft affects Calorie tracking app lung Visferal and pulmonary immune response are poorly known. Visceral fat is associated with insulin resistance and low-grade inflammation and reduced lung function. In the present study, the body composition and fat distribution was evaluated by multi-frequency octopolar bioimpedance. Thus, increased visceral fat directly influences impairment of lung function and of systemic and pulmonary immune response of obese women. e-learning resources. Virtual Login Search all ERS.
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