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Aims: The association between asthma and obesity has been shown but its accurate mechanism is unknown. In the current study, we sought to investigate the gene expression levels of IL-17/TRAF6/MAPK/USP25 axis and pro-inflammatory cytokine level (IL-6, IL-1β, and TNF-α) in obese Ovalbumin (OVA)-sensitized female and male Wistar rats lung tissue., Main Methods: Animals in both males and females were divided into eight groups (four groups in each sex) based on diet and OVA-sensitization: normal diet, a normal diet with OVA-sensitization, high-fat diet (HFD), and OVA-sensitization with an HFD., Key Findings: In both sexes, obese OVA-sensitized rats, the methacholine concentration-response curve shifted to the left and EC 50 methacholine decreased. Increased pro-inflammatory cytokines as well as elevated IL-17/TRAF6/MAPK axis genes and decreased USP25 gene expression were identified in obese OVA-sensitized groups., Significance: The results indicate that in obese OVA-sensitized rats, the IL-17 axis were involved in the pathogenesis of the disease and can be considered as a therapeutic target in subjects with obesity-related asthma., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Over the past decades, obesity and infertility in men increased in parallel, and the association between both phenomena have been examined by several researchers. despite the fact that there is no agreement, obesity appears to affect the reproductive potential of men through various mechanisms, such as changes in the hypothalamic-pituitary-testicular (HPT) axis, spermatogenesis, sperm quality and/or alteration of sexual health. Leptin is a hormone produced by the adipose tissue, and its production elevates with increasing body fat. Many studies have supported the relationship between raised leptin production and reproductive function regulation. In fact, Leptin acts on the HPT axis in men at all levels. However, most obese men are insensitive to increased production of endogenous leptin and functional leptin resistance development. Recently, it has been recommended that Kisspeptin neurons mediate the leptin's effects on the reproductive system. Kisspeptin binding to its receptor on gonadotropin-releasing hormone (GnRH) neurons, activates the mammal's reproductive axis and stimulates GnRH release. Increasing infertility associated with obesity is probably mediated by the Kisspeptin-GnRH pathway. In this review, the link between obesity, kisspeptin, leptin, and male fertility will be discussed., (© 2021 Walter de Gruyter GmbH, Berlin/Boston.)

Epidemiological and clinical studies have demonstrated a close association between obesity and asthma. The current study investigated the effect of high-fat diet on tracheal responsiveness to methacholine and insulin resistance in ovalbumin (OVA) sensitized male and female rats. The rats were divided into eight groups (n=6 per group): female with the normal diet (F+ND), male with the normal diet (M+ND), female OVA-sensitized with the normal diet (F+SND), male OVA-sensitized with the normal diet (M+SND), female with high-fat diet (F+HFD), male with high-fat diet (M+HFD), female OVA-sensitized with high-fat diet (F+SHFD), and male OVA-sensitized with high-fat diet (M+SHFD). All rats were fed for 8 weeks with high-fat diet or standard pelts, and for another 4 weeks, they were sensitized with OVA or saline. At the end of the study, the tracheal responsiveness to methacholine, serum insulin, and blood glucose levels was measured. Also, insulin resistance indexes were determined. OVA-sensitization and diet-induced obesity caused the curve of methacholine concentration response to shifting to the left. In addition, results indicated that the EC50 (the effective concentration of methacholine generating 50% of peak response) in F+SHFD rats was statistically lower than M+SHFD group (p<0.05). Moreover, insulin resistance was higher in the F+SHFD than the M+SHFD group (p<0.001). These results suggest that insulin resistance and metabolic syndrome may be involved in the pathogenesis of obesity associated with OVA-sensitized rats condition, especially in female animals.

The present study aimed to investigate the role of microRNA-146a and its adapter proteins [interleukin-1 receptor-associated kinase 1 (IRAK1) and tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6)] in the pathogenesis of ovalbumin (OVA)-sensitized rats in association with the diet-induced obesity condition. Twenty male Wistar rats were divided into four groups: control with normal diet (ND), OVA-sensitized with normal diet (S + ND), high-fat diet (HFD), and OVA-sensitized with high-fat diet (S + HFD). All the animals were fed for 8 weeks with standard pelts or high-fat diet, and were then sensitized and challenged with OVA or saline for another 4 weeks. The tracheal responsiveness to methacholine, serum protein levels, and lipid profile levels was measured by the ELISA method. Moreover, the gene expression level of microRNA-146a (miR-146a) was measured in the lung tissue of the rats using the real-time PCR method. Maximum response to methacholin increased in the S + HFD group in compared with ND, S + ND, and HFD groups (P < 0.05 to P < 0.001). Moreover, in the S + HFD group the mRNA expression levels of miRNA-146a increased in the lung tissue (P < 0.001). In addition, the protein analysis results showed that IRAK1, TRAF6, NF-kB, and IL-1β protein levels were high in the S + HFD group compared to the ND and HFD groups; however, in compared with the S + ND group, only the IL-1β protein level was higher in the S + HFD group (P < 0.05). These results suggest that a defect in the NF-kB-miR-146a negative feedback loop may be involved in the pathogenesis of obesity associated with OVA-sensitized condition. © 2018 BioFactors, 45(1):75-84, 2019., (© 2018 International Union of Biochemistry and Molecular Biology.)

Many studies have shown a close relationship between obesity and asthma severity. In the present study, the effects of diet-induced obesity were examined on airway responsiveness to methacholine in addition to visfatin level in female Wistar rats' tracheae after sensitization with ovalbumin. The rats were divided into four groups: control with normal diet (ND), ovalbumin (OVA)-sensitized with normal diet (S + ND), high-fat diet (HFD), and OVA-sensitized with a high-fat diet (S + HFD). The animals were fed for 8 weeks with standard pelts or high-fat diet and then sensitized and challenged with OVA or saline for another 4 weeks. At the end of the study, the tracheae were isolated and assessed for airway responsiveness and visfatin protein levels. Diet-induced obesity groups developed increased weight and obesity indices (p < 0.001). After sensitization with OVA and diet-induced obesity, there were marked leftward shifts in methacholine concentration-response curves in S + HFD group compared to other groups. Also, maximum response was the highest (p < 0.05 to p < 0.001), EC 50 was the lowest (p < 0.05 to p < 0.001), and visfatin protein level was the highest (p < 0.05 to p < 0.01) in S + HFD. According to results, diet-induced obesity caused airway hyperresponsiveness to methacholine and enhanced visfatin protein levels in the tracheae of ovalbumin-sensitized female rats. Our results suggested that, in obese ovalbumin-sensitized conditions in female rats, the local production of adipocytokines, such as visfatin, may be increased, resulting in the deterioration of inflammation in lungs. This finding shows a possible mechanism for the altered phenotype in obesity-ovalbumin sensitization conditions in female rats.

Objective: To investigate the effects of diet-induced obesity on the expression of nuclear factor-κB (NF-κB) and visfatin messenger RNA in male Wistar rats' tracheae after sensitization with ovalbumin (OVA)., Materials and Methods: Twenty male Wistar rats were divided into 4 groups (n = 5 for each group), which included a control group fed a normal diet (ND) and groups fed normal diet, OVA-sensitized (S+ND); high-fat diet (HFD) only (diet-induced obesity); and high-fat diet, OVA-sensitized (S+HFD). All animals were fed for 8 weeks with standard chow or a high-fat diet, and then were sensitized and challenged with OVA or saline for another 4 weeks as per the above groups. The rats were anesthetized, after which the necks were exposed and the tracheae isolated and examined for expression levels of NF-κB and visfatin mRNA with the real-time polymerase chain reaction method. Data were compared between the different groups using one-way analysis of variance., Results: The expression level of NF-κB mRNA in the S+HFD group was 2.67, which was statistically higher than the levels in the ND (0.96; p = 0.001), S+ND (1.86; p = 0.05), and HFD (1.26; p = 0.001) groups. Also, the visfatin mRNA expression level in the S+HFD group was 4.21, which was higher than the levels in the ND (0.92), S+ND (1.79), and HFD (2.20) (p = 0.001) groups., Conclusion: In this study, the expression levels of NF-κB and visfatin were markedly higher in the S+HFD group in comparison to the other groups. These findings indicate that alternative signaling pathways might be activated in diet-induced obesity associated with the OVA-sensitized animal model and could be responsible for possible altered sensitization phenotype., (© 2017 S. Karger AG, Basel.)

Epidemiological and clinical studies indicate a close relationship between obesity and asthma. Here, we determined the impact of diet-induced obesity on the expression levels of IL-1β, IRAK-1 and TRAF-6 mRNA as well as IL-1β protein level and pathological changes in male Wistar rat's lung after sensitization with ovalbumin (OVA). Twenty male Wistar rats divided into four groups, control with normal diet (C+ND), OVA-sensitized with normal diet (S+ND), control with high-fat diet (C+HFD), and OVA-sensitized with high-fat diet (S+HFD). All rats fed for 12 weeks with standard pellets or high-fat diet while sensitization and challenging with OVA or saline were done for groups in the last month. In the end of intervention, lung was isolated and tested for the expression levels of IL-1β, IRAK-1 and TRAF-6 mRNA with real time-PCR method, and pathological changes were determined. Diet-induced obesity groups showed increased weight, obesity indexes and lipid profiles The expression levels of IL-1β mRNA in OVA-sensitization groups (S+ND and S+HFD) showed a significant increase compared with other groups. Also in S+HFD group, expression level of IRAK-1 and TRAF-6 mRNA were markedly higher than other groups (p<0.001). The pathological changes were marked in sensitized groups compared to non-sensitized groups; with marked increase in obese sensitized rat. The results showed that high fat diet caused overexpression of IL-1β, IRAK-1 and TRAF-6 mRNA as well as IL-1β protein in an experimental model of asthma. Our results suggest that obese-asthmatic conditions may lead to the local production and activation of pro-inflammatory agents.