• Adipose tissue
• Inflammation
• Insulin resistance
• Metabolic diseases
• Obesity

• R01 DK040484 NIDDK NIH HHS
• R01 DK045343 NIDDK NIH HHS
• R37 DK040484 NIDDK NIH HHS

• Abdominal
• Adipose
• Obesity
• Physiological oxygen concentration
• Superficial and deep layers

• Humans
• Body Mass Index
• Female
• Male
• Adult
• Middle Aged
• Abdominal Fat/metabolism
• Abdominal Fat/surgery
• Oxygen/metabolism
• Oxygen Consumption/physiology
• Obesity/metabolism
• Overweight/metabolism

• 2021-I2M-1-052 Chinese Academy of Medical Sciences Innovation Funds for Medical Sciences

• BMI
• Emergency surgery
• Laparotomy
• Obesity
• Obesity paradox
• Outcomes

• Humans
• Male
• Female
• Obesity/complications
• Obesity/epidemiology
• Middle Aged
• Postoperative Complications/epidemiology
• Postoperative Complications/etiology
• Aged
• Body Mass Index
• Adult
• Length of Stay/statistics & numerical data
• Reoperation/statistics & numerical data
• Retrospective Studies
• Operative Time
• Emergencies
• Risk Factors
• United States/epidemiology
• Surgical Procedures, Operative/adverse effects
• Surgical Procedures, Operative/statistics & numerical data
• Acute Care Surgery

• Adipokines
• Diabetes
• Hypertrophic skin scarring
• Metabolic syndrome
• Obesity
• Preclinical animal models
• Tissue fibrosis
• Wound healing
• Wound tension

• O2
• PO2
• adipose tissue
• hypoxic
• obesity

The ever-increasing burden of obesity demands a better pathophysiological understanding, especially regarding adipose tissue pathophysiology. Animal models of obesity are of great importance in investigating potential mechanisms and implications of obesity. Many issues should be considered while interpreting the preclinical results as anatomical and pathophysiological differences exist among species. Importantly, the natural history of obesity development differs considerably. An important example of conflicting results among preclinical models and human physiological studies is that of adipose tissue oxygenation, where rodent models almost unanimously have shown the presence of hypoxia in the adipose tissue of obese animals while human studies have yielded conflicting results to date. Other issues which require further clarification before generalizing preclinical data in humans include adipose tissue browning, endocrine function and fibrosis. The aim of this mini-review is to synopsize similarities and differences between rodent models and humans, which should be taken into consideration in obesity studies.

• Diabesity
• Obesity
• Osteoarthritis
• Patient-reported outcomes
• Total hip replacement
• Type 2 diabetes mellitus

It is increasingly recognized that hypoxia may develop in adipose tissue as its mass expands. Adipose tissue is also the main reservoir of lipophilic pollutants, including polychlorinated biphenyls (PCBs). Both hypoxia and PCBs have been shown to alter adipose tissue functions. The signaling pathways induced by hypoxia and pollutants may crosstalk, as they share a common transcription factor: aryl hydrocarbon receptor nuclear translocator (ARNT). Whether hypoxia and PCBs crosstalk and affect adipokine secretion in human adipocytes remains to be explored. Using primary human adipocytes acutely co-exposed to different levels of hypoxia (24 h) and PCB126 (48 h), we observed that hypoxia significantly inhibits the PCB126 induction of cytochrome P450 (CYP1A1) transcription in a dose-response manner, and that Acriflavine (ACF)—an HIF1α inhibitor—partially restores the PCB126 induction of CYP1A1 under hypoxia. On the other hand, exposure to PCB126 did not affect the transcription of the vascular endothelial growth factor-A (VEGFA) under hypoxia. Exposure to hypoxia increased leptin and interleukin-6 (IL-6), and decreased adiponectin levels dose-dependently, while PCB126 increased IL-6 and IL-8 secretion in a dose-dependent manner. Co-exposure to PCB126 and hypoxia did not alter the adipokine secretion pattern observed under hypoxia and PCB126 exposure alone. In conclusion, our results indicate that (1) hypoxia inhibits PCB126-induced CYP1A1 expression at least partly through ARNT-dependent means, suggesting that hypoxia could affect PCB metabolism and toxicity in adipose tissue, and (2) hypoxia and PCB126 affect leptin, adiponectin, IL-6 and IL-8 secretion differently, with no apparent crosstalk between the two factors.

• Adipocytes/metabolism
• Adipokines/metabolism
• Adiponectin/metabolism
• Aryl Hydrocarbon Receptor Nuclear Translocator
• Cytochrome P-450 CYP1A1/genetics
• Cytochrome P-450 CYP1A1/metabolism
• Environmental Pollutants/toxicity
• Humans
• Hypoxia
• Interleukin-6/metabolism
• Interleukin-8/metabolism
• Leptin/metabolism
• Polychlorinated Biphenyls/toxicity
• Vascular Endothelial Growth Factor A/metabolism

• COVID-19
• Cardio Metabolic Risk Factors
• Diabetes mellitus
• Dyslipidemia
• Hypertension
• Obesity

Recent studies have shown that obesity is associated with the severity of coronavirus disease (COVID-19). We reviewed clinical studies to clarify the obesity relationship with COVID-19 severity, comorbidities, and discussing possible mechanisms.

The electronic databases, including Web of Science, PubMed, Scopus, and Google Scholar, were searched and all studies conducted on COVID-19 and obesity were reviewed. All studies were independently screened by reviewers based on their titles and abstracts.

Forty relevant articles were selected, and their full texts were reviewed. Obesity affects the respiratory and immune systems through various mechanisms. Cytokine and adipokine secretion from adipose tissue leads to a pro-inflammatory state in obese patients, predisposing them to thrombosis, incoordination of innate and adaptive immune responses, inadequate antibody response, and cytokine storm. Obese patients had a longer virus shedding. Obesity is associated with other comorbidities such as hypertension, cardiovascular diseases, diabetes mellitus, and vitamin D deficiency. Hospitalization, intensive care unit admission, mechanical ventilation, and even mortality in obese patients were higher than normal-weight patients. Obesity could alter the direction of severe COVID-19 symptoms to younger individuals. Reduced physical activity, unhealthy eating habits and, more stress and fear experienced during the COVID-19 pandemic may result in more weight gain and obesity.

Obesity should be considered as an independent risk factor for the severity of COVID-19. Paying more attention to preventing weight gain in obese patients with COVID-19 infection in early levels of disease is crucial during this pandemic.

Perioperative subcutaneous tissue oxygen tension (PsqO₂) is substantially reduced in obese surgical patients. Goal-directed fluid therapy optimizes cardiac performance and thus tissue perfusion and oxygen delivery. We therefore tested the hypothesis that intra- and postoperative PsqO₂ is significantly reduced in obese patients undergoing standard fluid management compared to goal-directed fluid administration.

We randomly assigned 60 obese patients (BMI ≥ 30 kg/m²) undergoing laparoscopic bariatric surgery to receive either esophageal Doppler-guided goal-directed fluid management or conventional fluid treatment. Our primary outcome parameter was intra- and postoperative PsqO₂ measured with a polarographic electrode in the subcutaneous tissue of the upper arm. A random effects linear regression model was used to analyze the effect of intervention.

Overall, mean (± SD) PsqO₂ was significantly higher in obese patients receiving goal-directed therapy compared to conventional fluid therapy (65.8 ± 28.0 mmHg vs. 53.7 ± 21.7, respectively; repeated measures design adjusted difference: 13.0 mmHg [95% CI 2.3 to 23.7; p = 0.017]). No effect was seen intraoperatively (69.6 ± 27.9 mmHg vs. 61.4 ± 28.8, difference: 9.7 mmHg [95% CI -3.8 to 23.2; p = 0.160]); however, goal-directed fluid management improved PsqO₂ in the early postoperative phase (63.1 ± 27.9 mmHg vs. 48.4 ± 12.5, difference: 14.5 mmHg [95% CI 4.1 to 24.9; p = 0.006]). Intraoperative fluid requirements did not differ between the two groups.

Goal-directed fluid therapy improved subcutaneous tissue oxygenation in obese patients. This effect was more pronounced in the early postoperative period.

The study was registered at ClinicalTrials.gov (NCT 01052519).

• Goal-directed fluid therapy
• Laparoscopic surgery
• Obesity
• Tissue oxygen tension

We experienced a case of early stage lung cancer involving a morbidly obese patient. Obesity is associated with a higher incidence of surgical complications. We examined the effectiveness of laparoscopic sleeve gastrectomy as a primary weight loss procedure in a morbidly obese patient who required oncological surgery.

A 64-year-old morbidly obese female with a body mass index of 43.5 kg/m² was referred to our hospital to undergo weight loss. A right-sided lung mass was found incidentally on computed tomography conducted in preparation for laparoscopic sleeve gastrectomy, which was performed prior to tumor surgery. As a result, weight loss was achieved within 2.5 months after the laparoscopic sleeve gastrectomy, and the patient’s type-2 diabetes, hypertension, and dyslipidemia, which are linked to obesity, were markedly ameliorated. After a quick intraoperative pathological inspection revealed that the tumor was malignant, thoracoscopic right lung superior lobe resection was performed safely.

Laparoscopic sleeve gastrectomy proved to be a powerful approach in a case in which a morbidly obese patient with early stage cancer needed to lose weight rapidly.

• Bariatric surgery
• Laparoscopic sleeve gastrectomy
• Lung cancer
• Morbid obesity
• Weight reduction before surgery

The oxygen levels organ and tissue microenvironments vary depending on the distance of their vasculature from the left ventricle of the heart. For instance, the oxygen levels of lymph nodes and the spleen are significantly lower than that in atmospheric air. Cellular detection of oxygen and their response to low oxygen levels can exert a significant impact on virus infection. Generally, viruses that naturally infect well-oxygenated organs are less able to infect cells under hypoxic conditions. Conversely, viruses that infect organs under lower oxygen tensions thrive under hypoxic conditions. This suggests that in vitro experiments performed exclusively under atmospheric conditions ignores oxygen-induced modifications in both host and viral responses. Here, we review the mechanisms of how cells adapt to low oxygen tensions and its impact on viral infections. With growing evidence supporting the role of oxygen microenvironments in viral infections, this review highlights the importance of factoring oxygen concentrations into in vitro assay conditions. Bridging the gap between in vitro and in vivo oxygen tensions would allow for more physiologically representative insights into viral pathogenesis.

• Hypoxia
• Viruses

Obesity is a complex disorder of excessive adiposity, and is associated with adverse health effects such as cardiometabolic complications, which are to a large extent attributable to dysfunctional white adipose tissue. Adipose tissue dysfunction is characterized by adipocyte hypertrophy, impaired adipokine secretion, a chronic low‐grade inflammatory status, hormonal resistance and altered metabolic responses, together contributing to insulin resistance and related chronic diseases. Adipose tissue hypoxia, defined as a relative oxygen deficit, in obesity has been proposed as a potential contributor to adipose tissue dysfunction, but studies in humans have yielded conflicting results. Here, we will review the role of adipose tissue oxygenation in the pathophysiology of obesity‐related complications, with a specific focus on human studies. We will provide an overview of the determinants of adipose tissue oxygenation, as well as the role of adipose tissue oxygenation in glucose homeostasis, lipid metabolism and inflammation. Finally, we will discuss the putative effects of physiological and experimental hypoxia on adipose tissue biology and whole‐body metabolism in humans. We conclude that several lines of evidence suggest that alteration of adipose tissue oxygenation may impact metabolic homeostasis, thereby providing a novel strategy to combat chronic metabolic diseases in obese humans.

• adipose tissue
• hypoxia
• inflammation
• metabolism
• obesity
• oxygen

• Goal-directed fluid therapy
• cardiac index
• colorectal surgery
• tissue oxygen saturation

• Body mass index
• Cervical fusion
• Cervical spine surgery
• Posterior cervical
• Surgical site infection
• Trauma

• Infection prevention
• Patient comorbidities
• Prophylactic antibiotics
• Skin preparation and risk stratification
• Surgical site infection

• Adipose tissue
• Cell cultures
• SGBS adipocytes
• Volatile organic compounds

The aim of the present review is to evaluate effects of intermittent hypoxia and exercise therapy in cardiometabolic parameters on adult obese people.

Three well-known databases were selected: EMBASE, MEDLINE and Web of Science. Studies selection: Inclusion criteria were: (a) human healthy overweight or obese adults, (b) study randomized controlled trial, (c) original experimental study, (d) English languages and (e) therapy with intermittent hypoxia and exercise.

The assessment of the methodological quality of each study was based upon the risk of bias (PEDro scale) and level of evidence (CBO Guidelines). Data extraction: five articles clearly met inclusion criteria and were reviewed to data extraction.

In the hypoxia groups, weight, body mass index, waist circumference, waist–hip ratio, fat mass and lean mass improved in at least two studies in comparison with the baseline. Systolic blood pressure improved in one study. The lipid profile and the aerobic capacity were not reduced significantly.

Results suggest that combined hypoxia with exercise may help to improve cardiometabolic parameters in obese people.

• Ejercicio
• Environmental physiology
• Exercise
• Fisiología
• Hipoxia y mujer
• Hypoxia and women
• Obesidad
• Obesity

• ARIC (Atherosclerosis Risk in Communities)
• critical limb ischemia
• obesity
• peripheral artery disease
• peripheral vascular disease

• Body Mass Index
• Cohort Studies
• Extremities/blood supply
• Female
• Hospitalization/statistics & numerical data
• Humans
• Incidence
• Ischemia/epidemiology
• Male
• Middle Aged
• Obesity/epidemiology
• Overweight/epidemiology
• Peripheral Arterial Disease/epidemiology
• Proportional Hazards Models
• Prospective Studies
• Thinness/epidemiology
• United States/epidemiology

• HHSN268201700002I NHLBI NIH HHS
• K24 DK106414 NIDDK NIH HHS
• R01 DK089174 NIDDK NIH HHS
• R21 HL133694 NHLBI NIH HHS

• Blood glucose
• Inflammation
• Phytochemical
• Polyphenol
• Type 2 diabetes

• bariatric surgery
• dietary supplements
• gastric bypass
• obesity
• vertical sleeve gastrectomy
• vitamin deficiency
• vitamins

• ACS-NSQIP
• Cervical spine surgery
• Obesity
• Posterior cervical
• Surgical site infection

• Exercise
• Lactate
• Monocarboxylate transporter
• Training
• Type 2 diabetes

• Diabetes Mellitus, Type 2/blood
• Diabetes Mellitus, Type 2/complications
• Diabetes Mellitus, Type 2/rehabilitation
• Exercise Therapy/methods
• Female
• Humans
• Hyperlactatemia/etiology
• Hyperlactatemia/prevention & control
• Insulin Resistance/physiology
• Lactates/metabolism
• Male
• Physical Fitness/physiology
• Prognosis
• Severity of Illness Index
• Treatment Outcome

• Adipocytes
• Gene expression profiling
• Gene ontology
• HIF-1
• Hypoxia
• SGBS

• Adipocytes/metabolism
• Adipocytes/pathology
• Adipogenesis
• Arrhythmias, Cardiac/genetics
• Arrhythmias, Cardiac/metabolism
• Arrhythmias, Cardiac/pathology
• Biomarkers/metabolism
• Cell Hypoxia/genetics
• Gene Expression Profiling
• Gene Expression Regulation
• Genetic Diseases, X-Linked/genetics
• Genetic Diseases, X-Linked/metabolism
• Genetic Diseases, X-Linked/pathology
• Gigantism/genetics
• Gigantism/metabolism
• Gigantism/pathology
• Glutathione/biosynthesis
• Glycogen/biosynthesis
• Glycolysis
• Heart Defects, Congenital/genetics
• Heart Defects, Congenital/metabolism
• Heart Defects, Congenital/pathology
• Humans
• Hypoxia-Inducible Factor 1, alpha Subunit/genetics
• Hypoxia-Inducible Factor 1, alpha Subunit/metabolism
• Insulin Resistance
• Intellectual Disability/genetics
• Intellectual Disability/metabolism
• Intellectual Disability/pathology
• Oligonucleotide Array Sequence Analysis
• Protein Interaction Mapping
• Signal Transduction/genetics
• Transcription Factor AP-1/genetics
• Transcription Factor AP-1/metabolism
• Transcription, Genetic

Hypoxia-inducible factor 1 (HIF-1), a master regulator of oxygen homeostasis, is a heterodimer consisting of HIF-1α and HIF-1β subunits, and is implicated in calcification of cartilage and vasculature. The goal of this study was to determine the relationship between serum HIF-1α with coronary artery calcification (CAC) in patients with type 2 diabetes.

The subjects were 405 (262 males, 143 females, age 51.3 ± 6.4 years) asymptomatic patients with type 2 diabetes mellitus. Serum HIF-1α and interleukin-6 (IL-6) levels were measured by ELISA. CAC scores were assessed by a 320-slice CT scanner. The subjects were divided into 4 quartiles depending on serum HIF-1α levels.

Average serum HIF-1α was 184.4 ± 66.7 pg/ml. Among patients with higher CAC scores, HIF-1α levels were also significantly increased (p <0.001). HIF-1α levels positively correlated with CRP, IL-6, UKPDS risk score, HbA1c, FBG, and CACS, but did not correlate with diabetes duration, age, and LDL. According to the multivariate analysis, HIF-1α levels significantly and independently predict the presence of CAC. ROC curve analysis showed that the serum HIF-1α level can predict the extent of CAC, but the specificity was lower than the traditional risk factors UKPDS and HbA1c.

As a marker of hypoxia, serum HIF-1α level may be an independent risk factor for the presence of CAC. These findings indicate that elevated serum HIF-1α may be involved in vascular calcification in patients with type 2 diabetes mellitus.

• Preadipocyte
• SePP1
• hypoxia
• interleukin 6
• monocyte chemoattractant protein-1
• type I collagen
• vascular fibroblasts

• adipose tissue
• human
• hypoxia
• metabolic signatures
• metabolism
• oxygen tension

• Adult
• Body Mass Index
• Cell Hypoxia
• Fasting
• Female
• Forearm
• Glucose/metabolism
• Glycolysis
• Humans
• Lactic Acid/blood
• Lactic Acid/metabolism
• Male
• Middle Aged
• Muscle, Skeletal/blood supply
• Muscle, Skeletal/metabolism
• Obesity/blood
• Obesity/metabolism
• Overweight/blood
• Overweight/metabolism
• Oxygen Consumption
• Postprandial Period
• Pyruvic Acid/blood
• Pyruvic Acid/metabolism
• Subcutaneous Fat/blood supply
• Subcutaneous Fat/metabolism
• Young Adult

• FS/11/18/28633 British Heart Foundation
• Wellcome Trust

To review the current best surgical practice and detail a multi-disciplinary approach that could further reduce joint replacement infection.

Review of relevant literature indexed in PubMed.

Surgical site infection is a major complication following arthroplasty. Despite its rarity in contemporary orthopaedic practice, it remains difficult to treat and is costly in terms of both patient morbidity and long-term health care resources.

Emphasis on education of patients and all members of the health-care team and raising awareness in how to participate in preventative efforts is imperative.

• Hip
• Knee arthroplasty
• Multidisciplinary approach
• Prevention
• Surgical site infection

• Obesity
• anesthesia
• laparoscopy
• surgery

Obesity is associated with tissue hypoxia and the up-regulation of hypoxia inducible factor 1 alpha (HIF-1α). Prior studies in transgenic mice have shown that HIF-1α plays a role in the metabolic dysfunction associated with obesity. Therefore, we hypothesized that, after the development of diet-induced obesity (DIO), metabolic function could be improved by administration of HIF-1α antisense oligonucleotides (ASO). DIO mice were treated with HIF-1α ASO or with control ASO for 8 weeks and compared with an untreated group. We found that HIF-1α ASO markedly suppressed Hif-1α gene expression in adipose tissue and the liver. HIF-1α ASO administration induced weight loss. Final body weight was 41.6±1.4 g in the HIF-1α ASO group vs 46.7±0.9 g in the control ASO group and 47.9±0.8 g in untreated mice (p<0.001). HIF-1α ASO increased energy expenditure (13.3±0.6 vs 12±0.1 and 11.9±0.4 kcal/kg/hr, respectively, p<0.001) and decreased the respiratory exchange ratio (0.71±0.01 vs 0.75±0.01 and 0.76±0.01, respectively, p<0.001), which suggested switching metabolism to fat oxidation. In contrast, HIF-1a ASO had no effect on food intake or activity. HIF-1α ASO treatment decreased fasting blood glucose (195.5±8.4 mg/dl vs 239±7.8 mg/dl in the control ASO group and 222±8.2 mg/dl in untreated mice, p<0.01), plasma insulin, hepatic glucose output, and liver fat content. These findings demonstrate that the metabolic consequences of DIO are attenuated by HIF-1α ASO treatment.

• Adipose Tissue/metabolism
• Animals
• Blood Glucose/drug effects
• Blotting, Western
• Body Weight/drug effects
• Diet, High-Fat/adverse effects
• Energy Metabolism/drug effects
• Gene Expression Regulation/drug effects
• Histological Techniques
• Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors
• Insulin/blood
• Liver/metabolism
• Male
• Mice
• Mice, Inbred C57BL
• Mice, Obese
• Obesity/etiology
• Obesity/physiopathology
• Oligonucleotides, Antisense/genetics
• Oligonucleotides, Antisense/pharmacology
• Real-Time Polymerase Chain Reaction

• P50 HL084945 NHLBI NIH HHS
• R01 HL080105 NHLBI NIH HHS

• Adipose Tissue/drug effects
• Adipose Tissue/pathology
• Animals
• Anti-Inflammatory Agents/pharmacology
• Anti-Inflammatory Agents/therapeutic use
• Biological Products/pharmacology
• Biological Products/therapeutic use
• Diabetes Mellitus, Type 2/drug therapy
• Diabetes Mellitus, Type 2/etiology
• Diabetes Mellitus, Type 2/physiopathology
• Humans
• Inflammation/drug therapy
• Inflammation/pathology
• Phytotherapy/methods
• Plant Extracts/pharmacology
• Plant Extracts/therapeutic use

• Adipose Tissue/blood supply
• Adipose Tissue/metabolism
• Humans
• Inflammation/metabolism
• Insulin Resistance/physiology
• Male
• Obesity/metabolism
• Oxygen/metabolism
• Thinness/metabolism

Hypoxia in adipose tissue is suggested to be involved in the development of a chronic mild inflammation, which in obesity can further lead to insulin resistance. The effect of hypoxia on gene expression in adipocytes appears to play a central role in this inflammatory response observed in obesity. However, the global impact of hypoxia on transcriptional changes in human adipocytes is unclear. Therefore, we compared gene expression profiles of human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes under normoxic or hypoxic conditions to detect hypoxia-responsive genes in adipocytes by using whole human genome microarrays. Microarray analysis showed more than 500 significantly differentially regulated mRNAs after incubation of the cells under low oxygen levels. To gain further insight into the biological processes, hypoxia-regulated genes after 16 hours of hypoxia were classified according to their function. We identified an enrichment of genes involved in important biological processes such as glycolysis, response to hypoxia, regulation of cellular component movement, response to nutrient levels, regulation of cell migration, and transcription regulator activity. Real-time PCR confirmed eight genes to be consistently upregulated in response to 3, 6 and 16 hours of hypoxia. For adipocytes the hypoxia-induced regulation of these genes is shown here for the first time. Moreover in six of these eight genes we identified HIF response elements in the proximal promoters, specific for the HIF transcription factor family members HIF1A and HIF2A. In the present study, we demonstrated that hypoxia has an extensive effect on gene expression of SGBS adipocytes. In addition, the identified hypoxia-regulated genes are likely involved in the regulation of obesity, the incidence of type 2 diabetes, and the metabolic syndrome.

• Adipocytes/metabolism
• Base Sequence
• Cell Hypoxia/genetics
• Cells, Cultured
• DNA Primers
• Gene Expression Regulation
• Humans
• Oligonucleotide Array Sequence Analysis
• Oxygen/metabolism
• Real-Time Polymerase Chain Reaction