Musa acuminate seed extract attenuates the risk of obesity and associated inflammation in obese mice via suppression of PPARγ and MCP-1.

Obesity is a severe public health burden and a major component of metabolic syndrome. It is critical to identify treatment medicines for obesity and associated inflammation. We examined the anti-obesity and anti-inflammatory properties of Musa acuminate seeds methanol extract in high-fat diet-induced obesity. Changes in body weight, Lee index, fat mass accumulation, serum cholesterol, and serum triglyceride were monitored. Alteration in the expression of PPARγ, GLUT4, and MCP-1 at the transcript level in adipose tissue was also studied. After tabulation of our data, a significant reduction (p < 0.05) was recorded for body weight gain, and fat mass accumulation followed by significant changes (p < 0.05) in serum cholesterol, and serum triglyceride levels by the extract. In agreement with the biochemical data, the extract was capable enough (p < 0.05) to reduce the mRNA expression of PPARγ, and MCP-1, confirming the ability of the extract to ameliorate the risk of obesity and obesity-associated inflammation. Moreover, an in-silico study showed the high binding affinity of the reported compounds from M. acuminate like Delphinidin, Umbelliferon with COX-2, PPARγ, and MCP-1, supporting the notion of the risk-reducing potential of M.acuminate for obesity and obesity mediated inflammatory.

Aspirin attenuates the expression of adhesion molecules, risk of obesity, and adipose tissue inflammation in high-fat diet-induced obese mice.

The prevalence of obesity is increasing at an alarming rate and keeps on being one of the significant challenges of this century. Obesity promotes adipose tissue hypertrophy and causes the release of different pro-inflammatory cytokines, playing a significant role in the pathophysiology of metabolic syndrome. Aspirin is known as a potent anti-inflammatory drug, but its role in adipogenesis, adipocyte-specific inflammation, and metabolic syndrome is not well characterized. Thus, in this experiment, we aimed to determine the effect of low-dose aspirin on obesity, obesity-induced inflammation, and metabolic syndrome. High-fat diet-induced obese female mice (Swiss Albino) were used in our study. Mice were fed on a normal diet, a high-fat diet, and a low dose of aspirin (LDA) in the presence of a high-fat diet for 11 weeks. Body weight, lipid profile, adipose tissue size, and inflammatory status were analyzed after that period. The ∆∆CT method was used to calculate the relative mRNA expression of target genes. Treatment with a low dose of aspirin resulted in a significant reduction of body weight, visceral fat mass and serum total cholesterols, serum and adipose tissue triglycerides, and blood glucose levels in high-fat diet-induced obese mice compared to the untreated obese group. Consistent with these biochemical results, a significant reduction in mRNA expression of different genes like PPARγ, GLUT4, IL-6, TNFα, MCP-1, ICAM-I, and VCAM-I associated with adipogenesis and inflammation were noticed. Overall, current study findings indicate that low-dose aspirin reduces obesity, hyperlipidemia, adipocyte-specific inflammation, and metabolic syndrome in high-fat diet-induced obese mice.

Arachidonic acid supplementation attenuates adipocyte inflammation but not adiposity in high fat diet induced obese mice.

Obesity is associated with low-grade chronic inflammation and has a remarkable role in the pathophysiology of metabolic complications. In triggering these inflammatory responses, the arachidonic acid (AA) cascade plays a key role. However, there is a lack of data on how supplementary AA would affect obesity, adipose tissue inflammation, and the AA cascade in obesity. This study aims to investigate how AA supplementation affects obesity, adipocyte morphology, inflammation, and AA cascade signaling. Male Swiss Albino mice were used in our experiment. The mice were fed high-fat diets to induce obesity, and these obese mice were treated with two different doses of AA for 3 weeks. A normal diet non-obese group and an untreated obese group were kept as controls. Bodyweight and daily food intake data were recorded during that period. After the treatment period, blood serum and white adipose tissue of the experimental mice were collected for colorimetric lipid profile tests, histology, and mRNA extraction. The ΔΔCT method was employed for calculating the relative mRNA expression of target genes. The findings of our study suggest that AA has no significant effects on body weight, visceral adiposity, adipose tissue morphology, and serum lipid profile. However, AA treatment has resulted in a significant down-regulation of pro-inflammatory markers as well as the COX pathway. Besides, up-regulation of 12/15-LOX has been observed, indicating the metabolism pathway of supplementary AA through the LOX pathway. Our findings indicate that AA treatment may not provide significant benefits in terms of body weight, visceral fat mass, or serum lipid profile. However, it has effectively alleviated obesity-induced adipocyte inflammation in high-fat diet-induced obese mice.

Association of serum C-reactive protein (CRP) and D-dimer concentration on the severity of COVID-19 cases with or without diabetes: a systematic review and meta-analysis.

INTRODUCTION: Coronavirus disease (COVID-19) is a highly contagious disease that poses major public health risks. Fewer studies link high CRP and D-dimer levels to severe COVID-19 infection. Therefore, this study investigates the association of serum CRP and D-dimer concentration with COVID-19 severity in diabetic and non-diabetic patients. AREAS COVERED: Relevant published articles were identified using electronic search engines, such as Google Scholar, PubMed, Springer, Science Direct, and Researchgate. A total of 29 articles reporting on 15,282 patients (4,733 diabetes and 10,549 non-diabetes) were included in this systematic review and meta-analysis. RevMan V5.4, STATA V14 software, and SPSS V25 were used for the meta-analysis. Egger's regression and Begg-Mazumdar's test were used for assessing publication bias. The pooled result of all studies revealed that serum CRP (Standard mean difference (SMD) 0.41 mg/L; P < 0.0001; I2 93%) and D-dimer (SMD 0.32 mg/L; P < 0.0001; I2 83%) concentration was significantly higher in COVID-19 diabetic patients. The prevalence of COVID-19 infection was comparatively higher in male diabetic patients (OR 2.41; P < 0.00001; I2 88%). There was no publication bias. CRP and D-dimer rose with age in COVID-19 diabetic and non-diabetic patients. EXPERT OPINION: Overall, the serum CRP and D-dimer concentration in COVID-19 diabetic patients was significantly higher than non-diabetic patients indicating severe illness.

Assessment of Polyunsaturated Fatty Acids on COVID-19-Associated Risk Reduction.

Pooled evidence conveys the association between polyunsaturated fatty acids and infectious disease. SARS-CoV-2, an enveloped mRNA virus, was also reported to interact with polyunsaturated fatty acids. The present review explores the possible mode of action, immunology, and consequences of these polyunsaturated fatty acids during the viral infection. Polyunsaturated fatty acids control protein complex formation in lipid rafts associated with the function of two SARS-CoV-2 entry gateways: angiotensin-converting enzyme-2 and cellular protease transmembrane protease serine-2. Therefore, the viral entry can be mitigated by modulating polyunsaturated fatty acids contents in the body. α-Linolenic acid is the precursor of two clinically important eicosanoids eicosapentaenoic acid and docosahexaenoic acid, the members of ω-3 fats. Resolvins, protectins, and maresins derived from docosahexaenoic acid suppress inflammation and augment phagocytosis that lessens microbial loads. Prostaglandins of 3 series, leukotrienes of 5 series, and thromboxane A3 from eicosapentaenoic acid exhibit anti-inflammatory, vasodilatory, and platelet anti-aggregatory effects that may also contribute to the control of pre-existing pulmonary and cardiac diseases. In contrast, ω-6 linoleic acid-derived arachidonic acid increases the prostaglandin G2, lipoxins A4 and B4, and thromboxane A2. These cytokines are pro-inflammatory and enhance the immune response but aggravate the COVID-19 severity. Therefore, the rational intake of ω-3-enriched foods or supplements might lessen the complications in COVID-19 and might be a preventive measure.

Obesity, a major risk factor for immunity and severe outcomes of COVID-19.

An influenza-like virus named severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is responsible for COVID-19 disease and spread worldwide within a short time. COVID-19 has now become a significant concern for public health. Obesity is highly prevalent worldwide and is considered a risk factor for impairing the adaptive immune system. Although diabetes, hypertension, cardiovascular disease (CVD), and renal failure are considered the risk factors for COVID-19, obesity is not yet well-considered. The present study approaches establishing a systemic association between the prevalence of obesity and its impact on immunity concerning the severe outcomes of COVID-19 utilizing existing knowledge. Overall study outcomes documented the worldwide prevalence of obesity, its effects on immunity, and a possible underlying mechanism covering obesity-related risk pathways for the severe outcomes of COVID-19. Overall understanding from the present study is that being an immune system impairing factor, the role of obesity in the severe outcomes of COVID-19 is worthy.

Role of arachidonic cascade in COVID-19 infection: A review.

The World Health Organization has described the 2019 Coronavirus disease caused by an influenza-like virus called SARS-CoV-2 as a pandemic. Millions of people worldwide are already infected by this virus, and severe infection causes hyper inflammation, thus disrupting lung function, exacerbating breath difficulties, and death. Various inflammatory mediators bio-synthesized through the arachidonic acid pathway play roles in developing cytokine storms, injuring virus-infected cells. Since pro-inflammatory eicosanoids, including prostaglandins, and leukotrienes, are key brokers for physiological processes such as inflammation, fever, allergy, and pain but, their function in COVID-19 is not well defined. This study addresses eicosanoid's crucial role through the arachidonic pathway in inflammatory cascading and recommends using bioactive lipids, NSAIDs, steroids, cell phospholipase A2 (cPLA2) inhibitors, and specialized pro-resolving mediators (SPMs) to treat COVID-19 disease. The role of soluble epoxide hydrolase inhibitors (SEHIs) in promoting the activity of epoxyeicosatrienoic acids (EETs) and 17-hydroxide-docosahexaenoic acid (17-HDHA) is also discussed. Additional research that assesses the eicosanoid profile in COVID-19 patients or preclinical models generates novel insights into coronavirus-host interaction and inflammation regulation.