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The effectiveness of diet intervention in improving the metabolism of overweight and obese women: a systematic review and meta-analysis.
Chen, M, Chen, Q, Liu, W, Tong, H, Wu, Y
American journal of translational research. 2022;14(5):2926-2938
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At present, the treatment for obesity includes regular physical activity, diet intervention, medication and bariatric surgery. The aim of this study was to summarise the current literature and investigate whether different dietary interventions influence the metabolic indicators of overweight or obesity. This study is a systematic review and meta-analysis of twelve papers, eight of which were of medium quality. The duration of dietary therapy was usually an average of 19 weeks, from 4 weeks to 24 weeks. Dietary interventions included a calorie-restricted diet, a Mediterranean diet, a low-carb diet, a low-fat diet, and a ketogenic diet. Results show that dietary intervention had a significant effect on changes in fasting insulin, fasting glucose and insulin resistance changes in women. Additionally, dietary intervention also had a positive effect on triglycerides, total cholesterol, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol. Authors conclude that obese women should follow dietary interventions to improve their metabolic index. Furthermore, future large-scale randomised controlled trial experiments should be performed on specific diet therapies.
Abstract
OBJECTIVES Dietary therapy may improve glucose and lipid metabolism function in women. However, there is no systematic review to investigate the association between metabolic effects and different dietary interventions in obese women. The main purpose of this study is to summarize the current literature and investigate whether different dietary interventions have an effect on glucose and metabolic indicators of overweight or obese women. METHODS We conducted a scoping review of randomized controlled trial (RCT) studies from 1991 to 2022 by adopting a systematic review and meta-analysis. The database includes Google Scholar, PubMed, Embase and Web of Science. Literature screening, data extraction, and quality assessment were independently completed by 2 researchers. Meta-analysis was performed with RevMan. RESULTS Twelve articles were extracted and the meta-analysis results showed that the mean difference of metabolic indexes of obese women before and after dietary intervention, including fasting glucose, fasting insulin, HOMA-IR (Homeostasis model assessment-insulin resistance), TG (triglyceride), TC (total cholesterol), LDL-C (low-density lipoprotein cholesterol), HDL-C (high-density lipoprotein cholesterol) are -0.13 [-0.15, -0.10], -2.41 [-3.44, -1.38], -0.13 [-0.15, -0.10], -21.71 [-24.19, -19.22], -21.71 [-24.19, -19.22], -13.29 [-17.86, -8.72], 3.31 [2.22, 4.40], respectively. CONCLUSIONS Different dietary interventions benefit glucose and lipid metabolism of overweight or obese women. Further study is needed to determine which specific dietary effects have the greatest effect on improving metabolic indicators.
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Berberine reduces circulating inflammatory mediators in patients with severe COVID-19.
Zhang, BY, Chen, M, Chen, XC, Cao, K, You, Y, Qian, YJ, Yu, WK
The British journal of surgery. 2021;108(1):e9-e11
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Berberine has a long history in traditional Chinese medicine for the treatment of diarrhoea and gastroenteritis owing to its antimicrobial, antimotility and antisecretory properties. The aim of this study was to examine the effect of berberine on laboratory parameters in patients who have been hospitalised due to COVID-19. This study enrolled prospectively 39 patients with severe COVID-19 who were hospitalized, of which 18 patients were allocated to the berberine group and 17 to the control group. Patients in the berberine group were given berberine plus routine therapy within 14 days of admission, and those in the control group received only routine therapy. Results indicate that there wasn’t any significant difference between the two groups in relation to the laboratory parameters namely interleukin-6, tumour necrosis factor-alpha, C-reactive protein, procalcitonin and white blood cells levels within 14 days. In subgroup analyses of patients with diarrhoea, berberine significantly improved the changes in interleukin-6, tumour necrosis factor-alpha and C-reactive protein. Authors conclude that it is unclear whether berberine has any antiviral effect on SARS-CoV-2, and further experiments are needed to clarify this.
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Treatment With a Marine Oil Supplement Alters Lipid Mediators and Leukocyte Phenotype in Healthy Patients and Those With Peripheral Artery Disease.
Schaller, MS, Chen, M, Colas, RA, Sorrentino, TA, Lazar, AA, Grenon, SM, Dalli, J, Conte, MS
Journal of the American Heart Association. 2020;9(15):e016113
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Peripheral artery disease (PAD) is one of the most advanced forms of atherosclerosis. This disease state begins from an inflammatory lesion. The aim of this study was to investigate the impact of a short-course, oral, enriched marine oil supplement on circulating leukocytes and biochemical mediators in patients with symptomatic PAD and healthy controls. This study is a prospective, open-label, nonblinded study. Twenty participants completed the study: ten with PAD and 10 healthy individuals. Results show: - a shift in the leukocyte profiling towards a less inflammatory and more pro-resolving phenotype, most notably within the PAD cohort. - that supplementation led to an increase in phagocytic [a type of immune cell] activity of peripheral blood monocytes and neutrophils. - that circulating monocyte phenotyping demonstrated reduced expression of multiple proinflammatory markers. - that gene expression patterns in mono-derived macrophage from patients with PAD displayed a less inflammatory (type 1 macrophage) and greater reparative (type 2 macrophage) phenotype after supplementation. Authors conclude that their findings provide a foundation for characterising biochemical and cellular biomarkers of inflammation and resolution in PAD.
Abstract
Background Peripheral artery disease (PAD) is an advanced form of atherosclerosis characterized by chronic inflammation. Resolution of inflammation is a highly coordinated process driven by specialized pro-resolving lipid mediators endogenously derived from omega-3 fatty acids. We investigated the impact of a short-course, oral, enriched marine oil supplement on leukocyte phenotype and biochemical mediators in patients with symptomatic PAD and healthy volunteers. Methods and Results This was a prospective, open-label study of 5-day oral administration of an enriched marine oil supplement, assessing 3 escalating doses in 10 healthy volunteers and 10 patients with PAD. Over the course of the study, there was a significant increase in the plasma level of several lipid mediator families, total specialized pro-resolving lipid mediators, and specialized pro-resolving lipid mediator:prostaglandin ratio. Supplementation was associated with an increase in phagocytic activity of peripheral blood monocytes and neutrophils. Circulating monocyte phenotyping demonstrated reduced expression of multiple proinflammatory markers (cluster of differentiation 18, 163, 54, and 36, and chemokine receptor 2). Similarly, transcriptional profiling of monocyte-derived macrophages displayed polarization toward a reparative phenotype postsupplementation. The most notable cellular and biochemical changes over the study occurred in patients with PAD. There were strong correlations between integrated biochemical measures of lipid mediators (specialized pro-resolving lipid mediators:prostaglandin ratio) and phenotypic changes in circulating leukocytes in both healthy individuals and patients with PAD. Conclusions These data suggest that short-term enriched marine oil supplementation dramatically remodels downstream lipid mediator pathways and induces a less inflammatory and more pro-resolution phenotype in circulating leukocytes and monocyte-derived macrophages. Further studies are required to determine the potential clinical relevance of these findings in patients with PAD. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT02719665.