scholarly journals Perilla Seed Oil Alleviates Gut Dysbiosis, Intestinal Inflammation and Metabolic Disturbance in Obese-Insulin-Resistant Rats

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 3141
Author(s):  
Napapan Kangwan ◽  
Wasana Pratchayasakul ◽  
Aphisek Kongkaew ◽  
Komsak Pintha ◽  
Nipon Chattipakorn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Gut Microbiota ◽  
Seed Oil ◽  
Metabolic Disturbance ◽  
Metabolic Parameters ◽  
Gut Barrier ◽  
Gut Dysbiosis ◽  
Metabolic Endotoxemia ◽  
Perilla Seed

Background: High-fat diet (HFD) consumption induced gut dysbiosis, inflammation, obese-insulin resistance. Perilla seed oil (PSO) is a rich source of omega-3 polyunsaturated fatty acids with health promotional effects. However, the effects of PSO on gut microbiota/inflammation and metabolic disturbance in HFD-induced obesity have not been investigated. Therefore, we aimed to compare the effects of different doses of PSO and metformin on gut microbiota/inflammation, and metabolic parameters in HFD-fed rats. Methods: Thirty-six male Wistar rats were fed either a normal diet or an HFD for 24 weeks. At week 13, HFD-fed rats received either 50, 100, and 500 mg/kg/day of PSO or 300 mg/kg/day metformin for 12 weeks. After 24 weeks, the metabolic parameters, gut microbiota, gut barrier, inflammation, and oxidative stress were determined. Results: HFD-fed rats showed gut dysbiosis, gut barrier disruption with inflammation, increased oxidative stress, metabolic endotoxemia, and insulin resistance. Treatment with PSO and metformin not only effectively attenuated gut dysbiosis, but also improved gut barrier integrity and decreased gut inflammation. PSO also decreased oxidative stress, metabolic endotoxemia, and insulin resistance in HFD-fed rats. Metformin had greater benefits than PSO. Conclusion: PSO and metformin had the beneficial effect on attenuating gut inflammation and metabolic disturbance in obese-insulin resistance.

scholarly journals Fatty acids from diet and microbiota regulate energy metabolism

F1000Research ◽  
2015 ◽  
Vol 4 ◽  
pp. 738 ◽  
Author(s):  
Joe Alcock ◽  
Henry C. Lin
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acids ◽  
Gut Microbiota ◽  
Barrier Function ◽  
Unsaturated Fatty Acids ◽  
Intestinal Barrier ◽  
Dietary Fats ◽  
Intestinal Barrier Function ◽  
Metabolic Endotoxemia

A high-fat diet and elevated levels of free fatty acids are known risk factors for metabolic syndrome, insulin resistance, and visceral obesity. Although these disease associations are well established, it is unclear how different dietary fats change the risk of insulin resistance and metabolic syndrome. Here, we review emerging evidence that insulin resistance and fat storage are linked to changes in the gut microbiota. The gut microbiota and intestinal barrier function, in turn, are highly influenced by the composition of fat in the diet. We review findings that certain fats (for example, long-chain saturated fatty acids) are associated with dysbiosis, impairment of intestinal barrier function, and metabolic endotoxemia. In contrast, other fatty acids, including short-chain and certain unsaturated fatty acids, protect against dysbiosis and impairment of barrier function caused by other dietary fats. These fats may promote insulin sensitivity by inhibiting metabolic endotoxemia and dysbiosis-driven inflammation. During dysbiosis, the modulation of metabolism by diet and microbiota may represent an adaptive process that compensates for the increased fuel demands of an activated immune system.

scholarly journals Gut Microbiota Markers for Antipsychotics Induced Metabolic Disturbance in Drug Naïve Patients with First Episode Schizophrenia – A 24 Weeks Follow-up Study

2021 ◽  
Author(s):  
Xue Li ◽  
Xiuxia Yuan ◽  
Lijuan Pang ◽  
Yu Miao ◽  
Shuying Wang ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Density Lipoprotein ◽  
Metabolic Disturbance ◽  
Metabolic Parameters ◽  
Lipoprotein Cholesterol ◽  
First Episode ◽  
Model Assessment ◽  
Microbial Composition ◽  
Drug Naïve ◽  
Risperidone Treatment

AbstractBackgroundWhile cardiometabolic adverse effects associated with antipsychotic treatment is an important clinical challenge, the underlying mechanisms are unknown. Here we investigated if changes in gut microbial composition associate with the metabolic disturbance induced by the risperidone treatment of schizophrenia.MethodsNinety-four first episode, drug naïve schizophrenia patients (SZ), and 100 healthy controls (HCs) were enrolled at baseline. Six metabolic parameters (glucose, homeostasis model assessment of insulin resistance (HOMA-IR), Total cholesterol (Total-C), Low-density lipoprotein cholesterol (LDL-C), High-density lipoprotein cholesterol (HDL-C) and triglycerides) and body mass index (BMI) were measured for all participants. Gut microbial composition (microbials) was determined by fecal samples using 16S ribosomal RNA sequencing. Both the metabolic parameters and the gut microbiota were analyzed at baseline (all participants) and after 12 and 24 weeks of risperidone treatment (patients).ResultsThe glucose was significantly higher in SZ than HCs at baseline (p = 0.005). After 24-weeks treatment with risperidone, the levels of BMI, glucose, HOMA-IR, Total-C, LDL-C, HDL-C and triglyceride, were significant changed compared to baseline (p < 0.01). Six microbials showed significant changes in abundance after 24 weeks of risperidone treatment in SZ (p < 0.05), and four of these (Bacteroidetes, Proteobacteria, Christensenellaceae, and Enterobacteriaceae) were associated with the changes in metabolic parameters (p < 0.05). At baseline, the abundance of the microbials Christensenellaceae and Enterobacteriaceae were significantly associated with changes in triglyceride, BMI and HOMA-IR after 24-week risperidone treatment.ConclusionsChanges in gut microbial composition induced by risperidone treatment may be a key pathway underlying the metabolic disturbances observed in SZ patients. While these findings warrant replication in independent samples, they provide insight into the role of microbiota in SZ treatment, which can form the basis for development of better SZ treatment strategies.

scholarly journals Yogurt improves insulin resistance and liver fat in obese women with nonalcoholic fatty liver disease and metabolic syndrome: a randomized controlled trial

2019 ◽  
Vol 109 (6) ◽  
pp. 1611-1619 ◽  
Author(s):  
Yang Chen ◽  
Rennan Feng ◽  
Xue Yang ◽  
Jiaxing Dai ◽  
Min Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Gut Microbiota ◽  
Fatty Liver Disease ◽  
Liver Fat ◽  
Microbiota Composition ◽  
Obese Women ◽  
Nonalcoholic Fatty Liver ◽  
And Oxidative Stress ◽  
Gut Microbiota Composition

ABSTRACT Background Because consumption of conventional yogurt has beneficial effects in a healthy population, and insulin resistance (IR) is the mutual pathogenesis in nonalcoholic fatty liver disease (NAFLD) and metabolic syndrome (MetS), we hypothesized that yogurt would ameliorate IR in patients with NAFLD and MetS. Objectives The aim of this study was to investigate the effects of yogurt on IR and secondary endpoints including liver fat, gut microbiota, and serum biomarkers of inflammation and oxidative stress in obese women with NAFLD and MetS. Methods One hundred obese women aged 36–66 y with both NAFLD and MetS were randomly assigned to consume 220 g/d of either conventional yogurt or milk for 24 wk. At baseline and week 24, we measured anthropometric indices, serum glucose, insulin, lipids, and cytokines in all participants, and liver fat and gut microbiota in 20 participants randomly selected from each group. Results Forty-eight participants from the yogurt group and 44 from the milk group completed the intervention. Compared with milk, yogurt significantly decreased the homeostasis model assessment of insulin resistance (−0.53; 95% CI: −1.03, −0.02), fasting insulin (−2.77 mU/L; 95% CI: −4.91, −0.63 mU/L), 2-h insulin (−25.5 mU/L; 95% CI: −33.0, −17.9 mU/L), 2-h area under the curve for insulin (−29.4 mU/L · h; 95% CI: −44.0, −14.8 mU/L · h), alanine aminotransferase (−4.65 U/L; 95% CI: −8.67, −0.64 U/L), intrahepatic lipid (−3.44%; 95% CI: −6.19%, −0.68%), and hepatic fat fraction (−3.48%; 95% CI: −6.34%, −0.63%). Yogurt also decreased serum LPS (−0.31 EU/mL; 95% CI: −0.48, −0.14 EU/mL), fibroblast growth factor 21 (−57.76 pg/mL; 95% CI: −86.32, −29.19 pg/mL), lipids, and biomarkers of inflammation and oxidative stress, and altered gut microbiota composition. Mediation analysis showed that yogurt may improve IR by reducing serum lipids, inflammation, oxidative stress, and LPS. Conclusions Yogurt was better than milk at ameliorating IR and liver fat in obese Chinese women with NAFLD and MetS, possibly by improving lipid metabolism, reducing inflammation, oxidative stress, and LPS, and changing the gut microbiota composition. This trial was registered at www.chictr.org.cn as ChiCTR-IPR-15006801.

scholarly journals Vitamin D Supplementation Reduces Both Oxidative DNA Damage and Insulin Resistance in the Elderly with Metabolic Disorders

2019 ◽  
Vol 20 (12) ◽  
pp. 2891 ◽  
Author(s):  
Sylwia Wenclewska ◽  
Izabela Szymczak-Pajor ◽  
Józef Drzewoski ◽  
Mariusz Bunk ◽  
Agnieszka Śliwińska
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Vitamin D ◽  
Dna Damage ◽  
Metabolic Disorders ◽  
Oxidative Dna Damage ◽  
Intervention Group ◽  
Density Lipoprotein ◽  
Vitamin D Supplementation ◽  
Metabolic Parameters

Background: Research evidence indicates that vitamin D deficiency is involved in the pathogenesis of insulin resistance (IR) and associated metabolic disorders including hyperglycemia and dyslipidemia. It also suggested that vitamin D deficiency is associated with elevated levels of oxidative stress and its complications. Therefore, the aim of our study was to determine the effect of vitamin D supplementation on DNA damage and metabolic parameters in vitamin D deficient individuals aged >45 with metabolic disorders. Material and Methods: Of 98 initially screened participants, 92 subjects deficient in vitamin D were included in the study. They were randomly assigned to the following group: with vitamin D supplementation (intervention group, n = 48) and without supplementation (comparative group, n = 44). The patients from both groups were divided into two subgroups according to the presence or absence of type 2 diabetes (T2DM). The intervention group was treated with 2000 International Unit (IU) cholecalciferol/day between October and March for three months. At baseline and after three-month supplementation vitamin D concentration (25-OH)D3 and endogenous and oxidative DNA damage were determined. In addition, fast plasma glucose (FPG), fasting insulin, HbA1c and lipid fraction (total cholesterol (TC), low-density lipoprotein cholesterol (LDL), high-density lipoprotein cholesterol (HDL), triglyceride (TG)), as well as anthropometric measurements (weight, height) were gathered. The following IR-related parameters were calculated Homeostatic Model Assesment – Insulin Resistance (HOMA-IR) and TG/HDL ratio. Results: Three-month vitamin D supplementation increased the mean vitamin D concentration to generally accepted physiological level independently of T2DM presence. Importantly, vitamin D exposure decreased the level of oxidative DNA damage in lymphocytes of patients of intervention group. Among studied metabolic parameters, vitamin D markedly increased HDL level, decreased HOMA-IR, TG/HDL ratio. Furthermore, we found that HbA1c percentage diminished about 0.5% in T2DM patients supplemented with vitamin D. Conclusion: The current study demonstrated that daily 2000I U intake of vitamin D for three months decreased the level of oxidative DNA damage, a marker of oxidative stress, independently on T2DM presence. Furthermore, vitamin D reduced metabolic parameters connected with IR and improved glucose and lipid metabolism. Therefore, our results support the assertion that vitamin D, by reducing oxidative stress and improving of metabolic profile, may decrease IR and related diseases.

scholarly journals Genistein stimulates insulin sensitivity through gut microbiota reshaping and skeletal muscle AMPK activation in obese subjects

2020 ◽  
Vol 8 (1) ◽  
pp. e000948 ◽  
Author(s):  
Martha Guevara-Cruz ◽  
Einar T Godinez-Salas ◽  
Monica Sanchez-Tapia ◽  
Gonzalo Torres-Villalobos ◽  
Edgar Pichardo-Ontiveros ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Insulin Sensitivity ◽  
Gut Microbiota ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Oral Glucose ◽  
Model Assessment ◽  
Metabolic Endotoxemia

ObjectiveObesity is associated with metabolic abnormalities, including insulin resistance and dyslipidemias. Previous studies demonstrated that genistein intake modifies the gut microbiota in mice by selectively increasing Akkermansia muciniphila, leading to reduction of metabolic endotoxemia and insulin sensitivity. However, it is not known whether the consumption of genistein in humans with obesity could modify the gut microbiota reducing the metabolic endotoxemia and insulin sensitivity.Research design and methods45 participants with a Homeostatic Model Assessment (HOMA) index greater than 2.5 and body mass indices of ≥30 and≤40 kg/m2 were studied. Patients were randomly distributed to consume (1) placebo treatment or (2) genistein capsules (50 mg/day) for 2 months. Blood samples were taken to evaluate glucose concentration, lipid profile and serum insulin. Insulin resistance was determined by means of the HOMA for insulin resistance (HOMA-IR) index and by an oral glucose tolerance test. After 2 months, the same variables were assessed including a serum metabolomic analysis, gut microbiota, and a skeletal muscle biopsy was obtained to study the gene expression of fatty acid oxidation.ResultsIn the present study, we show that the consumption of genistein for 2 months reduced insulin resistance in subjects with obesity, accompanied by a modification of the gut microbiota taxonomy, particularly by an increase in the Verrucomicrobia phylum. In addition, subjects showed a reduction in metabolic endotoxemia and an increase in 5′-adenosine monophosphate-activated protein kinase phosphorylation and expression of genes involved in fatty acid oxidation in skeletal muscle. As a result, there was an increase in circulating metabolites of β-oxidation and ω-oxidation, acyl-carnitines and ketone bodies.ConclusionsChange in the gut microbiota was accompanied by an improvement in insulin resistance and an increase in skeletal muscle fatty acid oxidation. Therefore, genistein could be used as a part of dietary strategies to control the abnormalities associated with obesity, particularly insulin resistance; however, long-term studies are needed.

scholarly journals Lipocalin 2 deficiency-induced gut microbiota dysbiosis evokes metabolic syndrome in aged mice

2020 ◽  
Vol 52 (8) ◽  
pp. 314-321
Author(s):  
Vishal Singh ◽  
Sarah Galla ◽  
Rachel M. Golonka ◽  
Andrew D. Patterson ◽  
Benoit Chassaing ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Fasting Blood Glucose ◽  
Lipocalin 2 ◽  
Metabolic Markers ◽  
Aged Mice ◽  
Gut Dysbiosis ◽  
Clinical Biomarker ◽  
Compositional Changes

Lipocalin 2 (Lcn2) is a multifunctional innate immune protein that limits microbial overgrowth. Our previous study demonstrated that the gut microbiota directly induces intestinal Lcn2 production, and Lcn2-deficient ( Lcn2−/−) mice exhibit gut dysbiosis. Coincidentally, gut dysbiosis is associated with metabolic syndrome pathogenesis, and elevated Lcn2 levels has been considered a potential clinical biomarker of metabolic syndrome. Yet whether Lcn2 mitigates or exacerbates metabolic syndrome remains inconclusive. Our objective was to determine whether Lcn2 deficiency-induced compositional changes in gut microbiota contribute to gain in adiposity in aged mice. Utilizing Lcn2−/− mice and their wild-type (WT) littermates, we measured metabolic markers, including fasting blood glucose, serum lipids, fat pad weight, and insulin resistance at ages 3, 6, and 9 mo old. Relative to WT mice, aged Lcn2−/− mice exhibited a gain in adiposity associated with numerous features of metabolic syndrome, including insulin resistance and dyslipidemia. Surprisingly, supplementation with a high-fat diet did not further aggravate metabolic syndrome that spontaneously occurs in Lcn2−/− mice by 6 mo of age. Interestingly, chow-fed Lcn2−/− mice displayed marked differences in the bacterial abundance and metabolomic profile of the gut microbiota compared with WT mice. Overall, our results demonstrate that Lcn2 is essential to maintain metabolic and gut microbiotal homeostasis, where deficiency induces spontaneous delayed onset of metabolic syndrome.

scholarly journals Gut Microbiota’s Relationship with Liver Disease and Role in Hepatoprotection by Dietary Natural Products and Probiotics

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1457 ◽  
Author(s):  
Xiao Meng ◽  
Sha Li ◽  
Ya Li ◽  
Ren-You Gan ◽  
Hua-Bin Li
Keyword(s):  
Oxidative Stress ◽  
Natural Products ◽  
Gut Microbiota ◽  
Beneficial Effects ◽  
Gut Dysbiosis ◽  
Fatty Acid Accumulation ◽  
Acid Accumulation ◽  
Liver Health ◽  
Hepatoprotective Effects ◽  
Gut Microorganisms

A variety of dietary natural products have shown hepatoprotective effects. Increasing evidence has also demonstrated that gut microorganisms play an important role in the hepatoprotection contributed by natural products. Gut dysbiosis could increase permeability of the gut barrier, resulting in translocated bacteria and leaked gut-derived products, which can reach the liver through the portal vein and might lead to increased oxidative stress and inflammation, thereby threatening liver health. Targeting gut microbiota modulation represents a promising strategy for hepatoprotection. Many natural products could protect the liver from various injuries or mitigate hepatic disorders by reverting gut dysbiosis, improving intestinal permeability, altering the primary bile acid, and inhibiting hepatic fatty acid accumulation. The mechanisms underlying their beneficial effects also include reducing oxidative stress, suppressing inflammation, attenuating fibrosis, and decreasing apoptosis. This review discusses the hepatoprotective effects of dietary natural products via modulating the gut microbiota, mainly focusing on the mechanisms of action.

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