scholarly journals Increased Gustatory Response Score in Obesity and Association Levels with IL-6 and Leptin

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Nesrine Remla ◽  
Zeyneb Hadjidj ◽  
Kamel Ghezzaz ◽  
Soraya Moulessehoul ◽  
Mourad Aribi

Background. The aim of this study was to investigate the relationship between the circulating IL-6 and leptin levels with taste alteration in young obese patients.Methods. A retrospective case-control study was conducted in thirty obese patients and thirty age- and sex-matched healthy controls.Results. Circulating levels of IL-6 and leptin were significantly increased in obese patients than in controls. However, catalase and ORAC levels were significantly decreased in obese patients compared to controls. Additionally, obese participants had high scores for the detection of fats (gustatory response scores [GRS];p<0.001). Moreover, IL-6 and leptin were strongly associated with GRS alteration among patients with GRS 4 (resp., OR =17.5 [95% CI, 1.56–193.32;p=0.007]; OR = 16 [95% CI, 1.69–151.11;p=0.006]). For the Mantel-Haenszel common odds ratio estimate (MH OR), IL-6 and leptin were strongly associated with obesity, in patients with either GRS 4 or GRS > 4 (resp., MH OR = 8.77 [95% CI, 2.06–37.44;p=0.003]; MH OR = 5.76 [95% CI, 1.64–20.24;p=0.006]).Conclusions. In a low grade inflammation linked to obesity, taste alteration is associated with high levels of IL-6 and leptin.

2021 ◽  
Vol 12 (47) ◽  
pp. 138-142
Author(s):  
Giordana Gregório Fritsch ◽  
Michael Wesley Schmidt ◽  
Antônio Carlos Gargioni Filho ◽  
Hussein Nasser Fares

The worldwide population is facing a double burden of epidemic, the COVID-19and obesity. This is even more alarming as obesity increases the COVID-19 severity. However, the relationship between obesity and COVID-19 severity is more complex than a simple association with BMI. In particular, obesity has been associated with low death rates in patients with acute respiratory distress syndrome, a fatal comorbidity to COVID-19, possibly due to the obesity paradox. Also, visceral adiposity could be a major risk factor for COVID- -19severity, due to its immune activation component, release of ACE2 and involvement in the cytokine storm, It is also known to correlate with metabolic disorders, low-grade inflammation and higher mortality rates.


Endocrinology ◽  
2007 ◽  
Vol 149 (3) ◽  
pp. 1350-1357 ◽  
Author(s):  
Florian W. Kiefer ◽  
Maximilian Zeyda ◽  
Jelena Todoric ◽  
Joakim Huber ◽  
René Geyeregger ◽  
...  

Obesity is associated with a chronic low-grade inflammation characterized by macrophage infiltration of adipose tissue (AT) that may underlie the development of insulin resistance and type 2 diabetes. Osteopontin (OPN) is a multifunctional protein involved in various inflammatory processes, cell migration, and tissue remodeling. Because these processes occur in the AT of obese patients, we studied in detail the regulation of OPN expression in human and murine obesity. The study included 20 morbidly obese patients and 20 age- and sex-matched control subjects, as well as two models (diet-induced and genetic) of murine obesity. In high-fat diet-induced and genetically obese mice, OPN expression was drastically up-regulated in AT (40 and 80-fold, respectively) but remained largely unaltered in liver (&lt;2-fold). Moreover, OPN plasma concentrations remained unchanged in both murine models of obesity, suggesting a particular local but not systemic importance for OPN. OPN expression was strongly elevated also in the AT of obese patients compared with lean subjects in both omental and sc AT. In addition, we detected three OPN isoforms to be expressed in human AT and, strikingly, an obesity induced alteration of the OPN isoform expression pattern. Analysis of AT cellular fractions revealed that OPN is exceptionally highly expressed in AT macrophages in humans and mice. Moreover, OPN expression in AT macrophages was strongly up-regulated by obesity. In conclusion, our data point toward a specific local role of OPN in obese AT. Therefore, OPN could be a critical regulator in obesity induced AT inflammation and insulin resistance.


2019 ◽  
Vol 20 (4) ◽  
pp. 839 ◽  
Author(s):  
Erika Di Zazzo ◽  
Rita Polito ◽  
Silvia Bartollino ◽  
Ersilia Nigro ◽  
Carola Porcile ◽  
...  

Adipose tissue is a key regulator of energy balance playing an active role in lipid storage as well as in synthesizing several hormones directly involved in the pathogenesis of obesity. Obesity represents a peculiar risk factor for a growing list of cancers and is frequently associated to poor clinical outcome. The mechanism linking obesity and cancer is not completely understood, but, amongst the major players, there are both chronic low-grade inflammation and deregulation of adipokines secretion. In obesity, the adipose tissue is pervaded by an abnormal number of immune cells that create an inflammatory environment supporting tumor cell proliferation and invasion. Adiponectin (APN), the most abundant adipokine, shows anti-inflammatory, anti-proliferative and pro-apoptotic properties. Circulating levels of APN are drastically decreased in obesity, suggesting that APN may represent the link factor between obesity and cancer risk. The present review describes the recent advances on the involvement of APN and its receptors in the etiology of different types of cancer.


2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Jian Zhu ◽  
Lu Yuan ◽  
Wen-ji Ni ◽  
Yong Luo ◽  
Jian-hua Ma

Insulin antibody (IA) may potentially affect a patient’s glycemic control due to its variability in both binding and/or releasing insulin. However, the association between IA titer and daily glycemic variability (GV) is still unknown. We thus performed this cross-sectional, retrospective case-control study to assess the relationship between IA titer and mean amplitude glycemic excursion (MAGE) in type 2 diabetes mellitus (T2DM) patients using a continuous glucose monitoring (CGM) system. We recruited 100 eligible patients (IA>5%, IA positive) and divided them into two groups—a low (L) group and a high (H) group—based on their IA titer. The control (C) group consisted of 47 patients (IA≤5%, IA negative) matched for age, BMI, gender, and glycosylated hemoglobin A1c (HbA1c). The CGM determined the GV of enrolled patients. The primary outcome was the relationship between the IA titer and the MAGE, and the secondary outcome was the differences of GV among the three groups. We found that patients in the H group had higher levels of blood glucose fluctuation parameters than those in the L and C groups. The Ln(IA) was positively correlated with Ln(MAGE) even after adjusting for age, gender, BMI, HbA1c, and fasting and postprandial C-peptide(r=0.423, p<0.001). Multiple linear stepwise regression analysis revealed that Ln(IA) was an independent factor of Ln(MAGE) (beta=0.405, p<0.001). In conclusion, the higher circulating IA titer was associated with increased MAGE in T2DM patients, indicating that those patients with elevated IA titer should receive GV assessment and individualized treatment.


2019 ◽  
Vol 47 (6) ◽  
pp. 917-923 ◽  
Author(s):  
Jaelim Cho ◽  
Nicola Dalbeth ◽  
Maxim S. Petrov

Objective.After acute pancreatitis, individuals often have low-grade inflammation, and subsequently develop metabolic sequelae such as post-pancreatitis diabetes mellitus (PPDM). Although numerous studies have investigated the relationship between gout and type 2 diabetes, little is known about the relationship between gout and PPDM. The aim was to investigate the associations between gout and PPDM.Methods.Using nationwide pharmaceutical dispensing data linked to hospital discharge data in New Zealand, gout and PPDM were identified among individuals after first episode of acute pancreatitis between January 1, 2007, and December 31, 2015. Multivariable Cox regression analyses were conducted, adjusting for age, sex, ethnicity, social deprivation index, alcohol consumption, tobacco smoking, comorbidities, medications (glucocorticoids, statins, and estrogens), and characteristics of acute pancreatitis.Results.A total of 10,117 individuals were included in the analysis of risk for gout and 9471 in the analysis of risk for PPDM. PPDM was significantly associated with a higher risk of gout in the overall cohort (adjusted HR 1.88, 95% CI 1.15–3.06) and women (2.72, 95% CI 1.31–5.65), but not in men (1.42, 95% CI 0.73–2.78). Preexisting gout was significantly associated with a higher risk of PPDM in the overall cohort (adjusted HR 1.58, 95% CI 1.04–2.41) and women (2.66, 95% CI 1.29–5.49), but not in men (1.31, 95% CI 0.78–2.20).Conclusion.The relationship between gout and PPDM is bidirectional in the post-pancreatitis setting. A history of gout is a risk factor of PPDM, particularly in women.


Diabetologia ◽  
2019 ◽  
Vol 63 (2) ◽  
pp. 253-260 ◽  
Author(s):  
Martijn C. G. J. Brouwers ◽  
Nynke Simons ◽  
Coen D. A. Stehouwer ◽  
Aaron Isaacs

Abstract Non-alcoholic fatty liver disease (NAFLD) is highly prevalent among individuals with type 2 diabetes. Although epidemiological studies have shown that NAFLD is associated with cardiovascular disease (CVD), it remains unknown whether NAFLD is an active contributor or an innocent bystander. Plasma lipids, low-grade inflammation, impaired fibrinolysis and hepatokines are potential mediators of the relationship between NAFLD and CVD. The Mendelian randomisation approach can help to make causal inferences. Studies that used common variants in PNPLA3, TM6SF2 and GCKR as instruments to investigate the relationship between NAFLD and coronary artery disease (CAD) have reported contrasting results. Variants in PNPLA3 and TM6SF2 were found to protect against CAD, whereas variants in GCKR were positively associated with CAD. Since all three genes have been associated with non-alcoholic steatohepatitis, the second stage of NAFLD, the question of whether low-grade inflammation is an important mediator of the relationship between NAFLD and CAD arises. In contrast, the differential effects of these genes on plasma lipids (i.e. lipid-lowering for PNPLA3 and TM6SF2, and lipid-raising for GCKR) strongly suggest that plasma lipids account for their differential effects on CAD risk. This concept has recently been confirmed in an extended set of 12 NAFLD susceptibility genes. From these studies it appears that plasma lipids are an important mediator between NAFLD and CVD risk. These findings have important clinical implications, particularly for the design of anti-NAFLD drugs that also affect lipid metabolism.


2009 ◽  
Vol 46 (3) ◽  
pp. 314-318 ◽  
Author(s):  
Arja Heliövaara ◽  
Jorma Rautio

Objective: To evaluate cephalometrically the craniofacial and pharyngeal morphology in 7-year-old boys with unoperated submucous cleft palate and to compare the findings with the morphology of 7-year-old boys without clefts. Setting and Patients: Thirty-two boys with unoperated submucous cleft palate and 49 boys without a cleft were compared retrospectively from lateral cephalograms taken at the mean age of 7 years (range, 5.5 to 8.6 years). Design: A retrospective case-control study. Outcome Measure: Linear and angular measurements were obtained from lateral cephalograms. A Student's t test was used in the statistical analysis. Results: The maxilla of the boys with submucous cleft palate was shorter and slightly more retrusive in relation to the cranial base than that of boys without clefts. Also, the mandible of the boys with submucous cleft palate was smaller, with a steeper mandibular plane. The relationship between the jaws was similar in both groups; although, those without clefts showed higher values for soft tissue maxillary prominence. In the pharyngeal area, the boys with submucous cleft palate had larger nasopharyngeal depths, smaller hypopharyngeal depths, and shorter soft palates than the boys without a cleft. Conclusions: This small study suggests that the boys with unoperated submucous cleft palate have minor distinctive morphological features in the maxillary, mandibular, and pharyngeal areas.


2019 ◽  
Author(s):  
A Gialluisi ◽  
M Bonaccio ◽  
A Di Castelnuovo ◽  
S Costanzo ◽  
A De Curtis ◽  
...  

AbstractMental health modulates the risk of common chronic conditions like cardiovascular disease, cancer and diabetes. Although inflammation is thought to partly explain this link, its relation with mental health is still unclear and largely unexplored.We investigated three scales assessing psychological resilience (CD-RISC), depression symptoms (PHQ8) and mental wellbeing (SF36-MCS) in an Italian adult population cohort (Nmax=16,952). We performed stepwise generalized linear models to test the association between each scale and INFLA-score, a composite blood-based inflammation index. At each step, a class of potential mediators was included in the model, namely health conditions, lifestyle factors, or both (full model). Full model analysis was also conducted on single blood markers involved in the inflammatory process.In the baseline model, we observed significant associations of PHQ8 (standardized β=0.024, p=8.9×10−3) and SF36-MCS (β = −0.021, p=7×10−3) with INFLA-score. These associations survived adjustment for health conditions but not for lifestyle factors, which explained 81% and 17% of the association with PHQ8 and SF36-MCS, respectively. Significant associations (p<4.2×10−3) after mediator adjustment were observed for single low-grade inflammation markers, including platelet distribution width (with PHQ8 and CD-RISC), granulocyte-and neutrophil-to-lymphocyte ratios, monocyte and lymphocyte fractions (with SF36-MCS).These findings suggest that the relationship between mental health and low-grade inflammation is largely influenced by lifestyle. However, the associations with specific biomarkers related to inflammation are partly independent and might be explained by biological factors. Interestingly, these associations are in line with recent blood transcriptomic analyses of depressed subjects, reporting up- and down-regulation of genes related to innate and adaptive immunity, respectively.


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