Insulin Resistance https://greenmedinfo.com/category/keywords/Insulin%20Resistance en An update of the beneficial effects of nuts and dried fruits on type 2 diabetes. https://greenmedinfo.com/article/update-beneficial-effects-nuts-and-dried-fruits-type-2-diabetes n/a PMID:  Nutrients. 2017 Jun 28 ;9(7). Epub 2017 Jun 28. PMID: 28657613 Abstract Title:  Nuts and Dried Fruits: An Update of Their Beneficial Effects on Type 2 Diabetes. Abstract:  Nuts and dried fruit are essential foods in the Mediterranean diet. Their frequent consumption has been associated with the prevention and/or the management of such metabolic conditions as type 2 diabetes (T2D), metabolic syndrome and cardiovascular diseases. Several previous reviews of epidemiological studies and clinical trials have evaluated the associations of nuts and/or dried fruit with various metabolic disorders. However, no reviews have focused on the mechanisms underlying the role of nuts and/or dried fruit in insulin resistance and T2D. This review aims to report nut and dried-fruit nutritional interventions in animals and humans, and to focus on mechanisms that could play a significant role in the prevention and treatment of insulin resistance and T2D. https://greenmedinfo.com/article/update-beneficial-effects-nuts-and-dried-fruits-type-2-diabetes#comments Diabetes Mellitus: Type 2 Fruit: All Insulin Resistance Nuts Diabetes mellitus: Type 2 Fruit: All Insulin Resistance nuts Review Thu, 20 Jul 2017 00:18:25 +0000 greenmedinfo 150714 at https://greenmedinfo.com Aspartames break down product phenylalanine, can inhibit the protective effects of intestinal alkaline phosphatase. https://greenmedinfo.com/article/aspartames-break-down-product-phenylalanine-can-inhibit-protective-effects-int n/a PMID:  Appl Physiol Nutr Metab. 2016 Nov 18:1-7. Epub 2016 Nov 18. PMID: 27997218 Abstract Title:  Inhibition of the gut enzyme intestinal alkaline phosphatase may explain how aspartame promotes glucose intolerance and obesity in mice. Abstract:  Diet soda consumption has not been associated with tangible weight loss. Aspartame (ASP) commonly substitutes sugar and one of its breakdown products is phenylalanine (PHE), a known inhibitor of intestinal alkaline phosphatase (IAP), a gut enzyme shown to prevent metabolic syndrome in mice. We hypothesized that ASP consumption might contribute to the development of metabolic syndrome based on PHE&#039;s inhibition of endogenous IAP. The design of the study was such that for the in vitro model, IAP was added to diet and regular soda, and IAP activity was measured. For the acute model, a closed bowel loop was created in mice. ASP or water was instilled into it and IAP activity was measured. For the chronic model, mice were fed chow or high-fat diet (HFD) with/without ASP in the drinking water for 18 weeks. The results were that for the in vitro study, IAP activity was lower (p&lt;0.05) in solutions containing ASP compared with controls. For the acute model, endogenous IAP activity was reduced by 50% in the ASP group compared with controls (0.2± 0.03 vs 0.4 ± 0.24) (p = 0.02). For the chronic model, mice in the HFD + ASP group gained more weight compared with the HFD + water group (48.1 ± 1.6 vs 42.4 ± 3.1, p = 0.0001). Significant difference in glucose intolerance between the HFD ± ASP groups (53 913 ± 4000.58 (mg·min)/dL vs 42 003.75 ± 5331.61 (mg·min)/dL, respectively, p = 0.02). Fasting glucose and serum tumor necrosis factor-alpha levels were significantly higher in the HFD + ASP group (1.23- and 0.87-fold increases, respectively, p = 0.006 and p = 0.01). In conclusion, endogenous IAP&#039;s protective effects in regard to the metabolic syndrome may be inhibited by PHE, a metabolite of ASP, perhaps explaining the lack of expected weight loss and metabolic improvements associated with diet drinks. https://greenmedinfo.com/article/aspartames-break-down-product-phenylalanine-can-inhibit-protective-effects-int#comments Insulin Resistance Obesity Artificial Sweeteners Aspartame Obesogenic Artificial Sweeteners aspartame Insulin Resistance obesity Risk Factors Animal Study Tue, 27 Dec 2016 17:15:19 +0000 greenmedinfo 141025 at https://greenmedinfo.com Diabetes: An Entirely Preventable & Reversible Condition https://greenmedinfo.com/blog/diabetes-entirely-preventable-reversible-condition <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2018<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="" src="http://gallery.mailchimp.com/7f494613c5ad4db1b93e647ad/images/DownloadedFile.jpeg" style="border-width: 0px; border-style: solid; width: 275px; height: 183px;" title="Diabetes: An Entirely Preventable &amp; Reversible Condition" /></p> <p><span style="font-size:14px;"><span style="font-family:verdana,geneva,sans-serif;">The title of this article may sound like heresy to those who have been schooled to believe that when diabetes "happens" to you, it is with you for life. There is far more to the story than both drug and naturally-based palliative medicine normally touches upon.&nbsp;</span></span></p><p><a href="https://greenmedinfo.com/blog/diabetes-entirely-preventable-reversible-condition" target="_blank">read more</a></p> https://greenmedinfo.com/blog/diabetes-entirely-preventable-reversible-condition#comments Diabetes Mellitus: Type 1 Diabetes Mellitus: Type 2 Hyperglycemia Insulin Resistance Blood Sugar Problems Diabetes Mellitus: Type 1 Diabetes mellitus: Type 2 hyperglycemia Insulin Resistance Fri, 24 Feb 2012 20:30:25 +0000 Sayer Ji 73036 at https://greenmedinfo.com Evidence of insulin-dependent signalling mechanisms produced by Citrus sinensis. https://greenmedinfo.com/article/evidence-insulin-dependent-signalling-mechanisms-produced-citrus-sinensis n/a PMID:  Food Chem Toxicol. 2018 Mar 31. Epub 2018 Mar 31. PMID: 29614383 Abstract Title:  Evidence of insulin-dependent signalling mechanisms produced by Citrus sinensis (L.) Osbeck fruit peel in an insulin resistant diabetic animal model. Abstract:  Citrus sinensis (L.) Osbeck is extensively cultivated worldwide and one of the most consumed fruits in the world. We evaluated the therapeutic properties of the methanol extract from Citrus sinensis fruit peel (CSMe) in high-fat diet-fed streptozotocin-induced insulin-resistant diabetic rats. Body weight, food intake, and water consumption were analysed. Biochemical and molecular biologic indices, and the expression of insulin receptor-induced signalling molecules were assessed to identify possible mechanisms. In addition, we conducted histology of pancreatic and adipose tissues. UHPLC-MS/MS analysis showed the presence of 17 dietary phenolics at substantial concentrations. High-fat diet-fed streptozotocin-induced diabetic rats administered CSMe (50 and 100 mg/kg) had reduced fasting blood glucose (56.1% and 55.7%, respectively) and plasma insulin levels (22.9% and 32.7%, respectively) compared with untreated diabetic control rats. CSMe reversed the biochemical abnormalities in diabetic rats, showed cytoprotective activity, and increased the intensity of the positive immunoreactions for insulin in pancreatic islets. CSMe treatment increased the expression of PPARγ in the adipose tissue and signalling molecules GLUT4 and insulin receptor. Our data suggest that CSMe could optimize glucose uptake of adipose tissues through the insulin-dependentsignalling cascade mechanism and it should be investigated in the management of individuals with type 2 diabetes mellitus. https://greenmedinfo.com/article/evidence-insulin-dependent-signalling-mechanisms-produced-citrus-sinensis#comments Insulin Resistance Sweet Orange Hypoglycemic Agents Hypoglycemic Agents Insulin Resistance Sweet Orange Animal Study Mon, 09 Apr 2018 18:51:10 +0000 greenmedinfo 162376 at https://greenmedinfo.com Genistein significantly improves glucose control and insulin sensitivity in postmenopausal women. https://greenmedinfo.com/article/genistein-significantly-improves-glucose-control-and-insulin-sensitivity-postm n/a PMID:  Maturitas. 2017 Mar ;97:44-52. Epub 2016 Dec 28. PMID: 28159061 Abstract Title:  The effect of genistein on glucose control and insulin sensitivity in postmenopausal women: A meta-analysis. Abstract:  Preclinical studies have revealed the beneficial effects of genistein in pancreaticβ-cell functions. The results of randomized controlled trials (RCTs) in assessing the effects of genistein on glucose metabolism are inconsistent, however. The aim of this meta-analysis is to evaluate the effects of genistein on glucose control and insulin sensitivity in postmenopausal women. Thisstudy searched the Medline, PubMed, and Cochrane databases, and ClinicalTrials.gov for trials from January 1970 to February 2016. We included RCTs that investigated the effects of genistein on glucose control and insulin metabolism in postmenopausal women. We also performed pooled analyses with weighted mean difference (WMD) and 95% confidence intervals (CI) according to the RevMan 5.3 software with the random-effects model. Seven eligible RCTs with 670 participants were included in the meta-analysis. Compared with placebos, genistein exhibited significant effects in lowering fasting glucose levels (WMD, -6.35mg/dL [95% CI, -10.78 to -1.93]; P=0.005), fasting insulin concentrations (WMD, -1.92μIU/mL [95% CI, -3.04 to -0.79]; P=0.0008), and HOMA-IR values (WMD, -0.74 [95% CI, -1.21 to -0.28]; P=0.002). Genistein significantly improves glucose control and insulin sensitivity in postmenopausal women. Long-term treatment may have greater effects than short-term use. The role and safety of genistein in glucose control in postmenopausal women require further investigation. https://greenmedinfo.com/article/genistein-significantly-improves-glucose-control-and-insulin-sensitivity-postm#comments Genistein Insulin Resistance Postmenopausal Complications Hypoglycemic Agents Genistein Hypoglycemic Agents Insulin Resistance Meta Analysis Postmenopausal Complications Risk Reduction Mon, 06 Feb 2017 21:38:54 +0000 greenmedinfo 143081 at https://greenmedinfo.com Insulin induces the expression of delta-5 desaturase (FADS1) in a dose-dependent manner which may explain insulin's regulation of dihomo-gamma-linoleic acid to inflammatory arachidonic acid. https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic PMID:  Scand J Clin Lab Invest. 2011 Jul ;71(4):330-9. Epub 2011 Mar 17. PMID: 21413848 Abstract Title:  Insulin induces fatty acid desaturase expression in human monocytes. Abstract:  Increasing evidence suggests that fatty acid desaturases, rate-limiting enzymes in unsaturated fatty acid biosynthesis, are important factors in the pathogenesis of lipid-induced insulin resistance. The conversion of dihomogamma linolenic acid (DGLA) into arachidonic acid (AA) in human plasma phospholipids has been shown to be regulated by insulin, suggesting a role for insulin in fatty acid desaturase 1 regulation. However insulin&#039;s role in monocyte inflammation associated with obesity and lifestyle disease development is uncertain. We therefore investigated if insulin is able to induce expression of stearoyl-CoA desaturase (SCD,Δ9 desaturase), fatty acid desaturase 1 (FADS1, Δ5 desaturase), and fatty acid desaturase 2 (FADS2, Δ6 desaturase), as well as the sterol regulatory element binding transcription factor 1-c (SREBP-1c) in monocytes. Here, for the first time, we demonstrate that THP-1 monocytes are insulin-responsive in inducing expression of SCD, FADS1, and FADS2 in a time- and dose-dependent manner. Understanding secondary consequences of postprandial hyperinsulinemia may open up new strategies for prevention and/or treatment of obesity-related metabolic complications. <p><a href="https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic" target="_blank">read more</a></p> https://greenmedinfo.com/article/insulin-induces-expression-delta-5-desaturase-fads1-dose-dependent-manner-whic#comments Endocrine Disruptor: Insulin Resistance Inflammatory Insulin arachidonic acid Dose Response High Sugar Diet hyperinsulinemia Inflammation Insulin Resistance In Vitro Study Thu, 25 Jul 2019 16:39:59 +0000 greenmedinfo 191864 at https://greenmedinfo.com Litchi semen constituents can improve glycolipid metabolism and insulin resistance, and increase insulin sensitivity to cure T2DM. https://greenmedinfo.com/article/litchi-semen-constituents-can-improve-glycolipid-metabolism-and-insulin-resist n/a PMID:  Zhong Yao Cai. 2015 Jul ;38(7):1466-71. PMID: 26946845 Abstract Title:  [Effect and Mechanism of Litchi Semen Effective Constituents on Insulin Resistance in Rats with Type 2 Diabetes Mellitus]. Abstract:  OBJECTIVE: To observe the effect of Litchi Semen Effective Constituents (LSEC) on insulin resistance (IR) in rats with Type 2 Diabetes Mellitus(T2DM), and to explore its mechanism. METHOD: T2DM models in rats with IR were induced by high-fat feeding combined with streptozocin, then the rats were randomly divided into four groups: model group, LSEC high-dose group (1. 87 g/kg), LSEC low-dose group(0. 47 g/kg) and rosiglitazone group(3. 87 x 10(-3) g/kg), blank group was established as control. After medication for four weeks, effects of LSEC on glucose or lipid metabolism and insulin resistance were investigated, histopathology and ultrastructure changes of pancreatic tissues were observed,Stem-loop Real-time fluorescence quantitative RT-PCR was used for evaluation of GRP78 mRNA and CHOP mRNA levels in pancreatic tissue of rats. RESULT: LSEC of high-dose group obviously improved fasting blood glucose, serum TG level and glucose tolerance in T2DM rats (P&lt;0. 05 or P&lt;0. 01). ISI was increased, HOMA-IR index was decreased, histopathology change of pancreatic tissue were alleviated, damaged organelle, such as endoplasmic reticulum and mitochondria were repaired in both groups of LSEC. Expression levels of GRP78 mRNA of both groups of LSEC and CHOP mRNA of high-dose group in pancreatic tissue were obviously lower than those of model group (P&lt;0. 01). CONCLUSION: LSEC can improve glycolipid metabolism and IR, increase insulin sensitivity to cure T2DM, its effects may be attributed, at least in part, to inhibit the expression of GRP78 mRNA and CHOP mRNA. https://greenmedinfo.com/article/litchi-semen-constituents-can-improve-glycolipid-metabolism-and-insulin-resist#comments Diabetes Mellitus: Type 2 Diabetes Mellitus: Type 2: Prevention Insulin Resistance Litchi Insulin Sensitizers MicroRNA modulator Pancreato Protective Agents Diabetes mellitus: Type 2 Diabetes Mellitus: Type 2: Prevention Insulin Resistance Insulin Sensitizers Litchi Plant Extracts Animal Study Tue, 31 Jan 2017 16:54:58 +0000 greenmedinfo 142805 at https://greenmedinfo.com Magnesium Improves Metabolic Profile In Metabolically Obese, Normal-Weight Individuals https://greenmedinfo.com/blog/magnesium-improves-metabolic-profile-metabolically-obese-normal-weight <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2014<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><br /> <img alt="Oral Magnesium Improves Metabolic Profile In Metabolically Obese, Normal-Weight Individuals" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/stebu/images/Magnesium_Deficiency.jpg" style="width: 400px; height: 250px;" /></p> <h1> Introduction:</h1> <p>Some normal weight individuals show obesity-related characteristics such as <strong><a href="/disease/insulin-resistance">insulin resistance</a></strong>, elevated fasting blood sugar levels, high triglyceride levels, and&nbsp;<strong><a href="http://doctormurray.com/high-blood-pressure/" rel="nofollow">high blood pressure</a></strong>. Although eating a high carbohydrate diet is linked to these findings, a new study shows that <strong><a href="/disease/magnesium-deficiency">low magnesium</a></strong> status contributes to this disorder, and that magnesium supplementation can improve the metabolic profile in these subjects.</p><p><a href="https://greenmedinfo.com/blog/magnesium-improves-metabolic-profile-metabolically-obese-normal-weight" target="_blank">read more</a></p> https://greenmedinfo.com/blog/magnesium-improves-metabolic-profile-metabolically-obese-normal-weight#comments Insulin Resistance Kidney Diseases Liver Disease Magnesium Magnesium Deficiency Potassium Insulin Resistance Kidney Diseases Liver Disease Magnesium Magnesium Deficiency potassium Mon, 27 Oct 2014 18:30:15 +0000 doctormurray 115129 at https://greenmedinfo.com Many Faces of Insulin Resistance https://greenmedinfo.com/blog/many-faces-insulin-resistance <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2019<br/><strong><a href="/greenmedinfocom-re-post-guidelines">Visit our Re-post guidelines</a></strong></div><p class="rtecenter"><img alt="" src="//cdn.greenmedinfo.com/sites/default/files/ckeditor/blank.justin/images/ManyFacesofInsulinResistance.jpg" /></p> <p><span style="font-size:18px;"><em><strong>Insulin resistance is a state where cells cannot take properly sugar from blood to use it as an energy source. Cells become resistant to the action of insulin. It therefore takes more insulin to keep blood sugar in balance. People with insulin resistance syndrome will consequently have normal blood sugar levels but elevated insulin level</strong></em></span></p><p><a href="https://greenmedinfo.com/blog/many-faces-insulin-resistance" target="_blank">read more</a></p> https://greenmedinfo.com/blog/many-faces-insulin-resistance#comments Anthocyanins Blood Pressure: High Cancers Cholesterol Coconut Oil Curcuminoids Dementia Diabetes Exercise Flavonoids Heart Disease Herbs: General Insulin Resistance Lethargy Metabolic Diseases Obesity Olive Oil Polyphenols Prediabetes Vegetables: All Blood Sugar Problems Cancer Health Guide: Herbs and Traditional Knowledge Health Guide: Obesity and Dieting Health Guides: Healing Foods Insulin Sugar healing foods Insulin Resistance natural health Mon, 04 Dec 2017 21:04:24 +0000 Dr.Antti 156870 at https://greenmedinfo.com Native probiotic strains MTCC 5690 and MTCC 5689 appear to have potential against insulin resistance and type 2 diabetes. https://greenmedinfo.com/article/native-probiotic-strains-mtcc-5690-and-mtcc-5689-appear-have-potential-against n/a PMID:  Eur J Nutr. 2016 Oct 18. Epub 2016 Oct 18. PMID: 27757592 Abstract Title:  Improvement in glucose tolerance and insulin sensitivity by probiotic strains of Indian gut origin in high-fat diet-fed C57BL/6J mice. Abstract:  PURPOSE: Diabetes and obesity are characterized by glucose intolerance, fat deposition, inflammation, and dyslipidemia. Recent reports postulated that distinct gut microbiota alterations were observed in obese/diabetic subjects and modulating gut microbiota beneficially through specific probiotics could be a potential therapeutic option for type 2 diabetes/obesity. Therefore, we attempted to study the efficacy of probiotics of Indian gut origin (Lactobacillus plantarum MTCC5690 and Lactobacillus fermentum MTCC5689) along with a positive control, Lactobacillus rhamnosus (LGG) on glucose/lipid homeostasis in high-fat-diet-induced diabetic animal model. METHODS: C57BL/6J male mice were divided into seven groups (n = 6 per group) comprising feeding on: (1) Normal Pellet Diet (NPD), (2) High-Fat Diet (HFD), (3) HFD with LGG, (4) HFD with MTCC5690, (5) HFD with MTCC5689, (6) HFD with metformin, and 7) HFD with vildagliptin for a period of 6 months. Biochemical markers, glucose tolerance, insulin resistance,and GLP-1 and LPS levels were assessed by standard protocols. Gut integrity was measured by intestinal permeability test. Transcriptional levels of tight junction proteins (TJPs) were probed in small intestinal tissues while inflammatory signals and other pathway specific genes were profiled in liver, visceral adipose tissue, and skeletal muscle. RESULTS: Mice fed with HFD became insulin resistant, glucose intolerant, hyperglycemic, and dyslipidemic. Diabetic mice were characterized to exhibit decreased levels of GLP-1, increased gut permeability, increased circulatory levels of LPS, decrease in the gene expression patterns of intestinal tight junction markers (occludin and ZO-1), and increased proinflammatory gene markers (TNFα and IL6) in visceral fat along with decreased mRNA expression of FIAF and adiponectin. Diabetic mice also exhibited increased mRNA expression of ER stress markers in skeletal muscle. In addition, liver from HFD-fed diabetic mice showed increased gene expressions of proinflammation, lipogenesis, and gluconeogenesis. Probiotic interventions (most prominently the MTCC5689) resisted insulin resistance and development of diabetes in mice under HFD feeding and beneficially modulated all the biochemical and molecular alterations in a mechanistic way in several tissues. The metabolic benefits offered by the probiotics were also more or less similar to that of standard drugs such as metformin and vildagliptin. CONCLUSION: Native probiotic strains MTCC 5690 and MTCC 5689 appear to have potential against insulin resistance and type 2 diabetes with mechanistic, multiple tissue-specific mode of actions. https://greenmedinfo.com/article/native-probiotic-strains-mtcc-5690-and-mtcc-5689-appear-have-potential-against#comments Diabetes Mellitus: Type 2 Insulin Resistance Lactobacillus fermentum Lactobacillus plantarum Lactobacillus rhamnosus Probiotics Diabetes mellitus: Type 2 Insulin Resistance Lactobacillus fermentum Lactobacillus plantarum Lactobacillus rhamnosus probiotics Risk Reduction Animal Study Thu, 08 Jun 2017 02:13:16 +0000 greenmedinfo 148844 at https://greenmedinfo.com Prior lactation reduces future diabetic risk through sustained postweaning effects on insulin sensitivity. https://greenmedinfo.com/article/prior-lactation-reduces-future-diabetic-risk-through-sustained-postweaning-eff n/a PMID:  Am J Physiol Endocrinol Metab. 2017 Mar 1 ;312(3):E215-E223. Epub 2016 Dec 13. PMID: 27965206 Abstract Title:  Prior lactation reduces future diabetic risk through sustained postweaning effects on insulin sensitivity. Abstract:  Breastfeeding for≥12 mo is recommended for optimal infant nutrition but may hold maternal benefits as well. Indeed, lactation has been associated with lower long-term risk of diabetes in the mother, but the mechanism by which it imparts sustained postweaning effects on glucose tolerance remains unclear. In this context, we postulated that lactation could potentially induce postweaning beneficial effects on glucose tolerance by modifying the natural history of insulin sensitivity and/or pancreatic β-cell function over time. Thus, in this study, we evaluated the relationships between duration of lactation [≤3 mo (n = 70), 3-12 mo (n = 140), and ≥12 mo (n = 120)] and trajectories of insulin sensitivity/resistance, β-cell function, and glycemia over the first 3 yr postpartum in a cohort of 330 women comprising the full spectrum of glucose tolerance in pregnancy, who underwent serial metabolic characterization, including oral glucose tolerance tests, at 3 mo, 1 yr, and 3 yr postpartum. The prevalence of dysglycemia (pre-diabetes/diabetes) at 3 yr postpartum was lower in women who breastfed for ≥12 mo (12.5%) than in those who breastfed for ≤3 mo (21.4%) or for 3-12 mo (25.7%)(overall P = 0.028). On logistic regression analysis, lactation for ≥12 mo independently predicted a lower likelihood of prediabetes/diabetes at 3 yr postpartum (OR = 0.37, 95% CI 0.18-0.78, P = 0.009). Notably, lactation for ≥12 mo predicted lesser worsening of insulin sensitivity/resistance (P&lt;0.0001), fasting glucose (P&lt;0.0001), and 2-h glucose (P = 0.011) over 3 yr compared with lactation≤3 mo but no differences in β-cell function (P ≥ 0.37). It has thus emerged that adherence to current breastfeeding recommendations reduces future diabetic risk through sustained postweaning effects on insulin sensitivity/resistance but not β-cell function. https://greenmedinfo.com/article/prior-lactation-reduces-future-diabetic-risk-through-sustained-postweaning-eff#comments Insulin Resistance Prediabetes Breastfeeding breastfeeding Insulin Resistance Prediabetes Risk Reduction Human Study Sat, 24 Jun 2017 00:16:57 +0000 greenmedinfo 149568 at https://greenmedinfo.com Tartary buckwheat flavonoids ameliorate high fructose-induced insulin resistance and oxidative stress. https://greenmedinfo.com/article/tartary-buckwheat-flavonoids-ameliorate-high-fructose-induced-insulin-resistan n/a PMID:  Food Funct. 2017 Jul 17. Epub 2017 Jul 17. PMID: 28714504 Abstract Title:  Tartary buckwheat flavonoids ameliorate high fructose-induced insulin resistance and oxidative stress associated with the insulin signaling and Nrf2/HO-1 pathways in mice. Abstract:  The present study was conducted to explore the effects of a purified tartary buckwheat flavonoid fraction (TBF) on insulin resistance and hepatic oxidative stress in mice fed high fructose in drinking water (20%) for 8 weeks. The results indicated that continuous administration of TBF dose-dependently improved the insulin sensitivity and glucose intolerance in high fructose-fed mice. TBF treatment also reversed the reduced level of insulin action on the phosphorylation of insulin receptor substrate-1 (IRS-1), protein kinase B (Akt) and phosphatidylinositol 3-kinase (PI3K), as well as the translocation of glucose transporter type 4 (GLUT4) in the insulin-resistant liver. Furthermore, TBF was found to exert high antioxidant capacity as it acts as a shield against oxidative stress induced by high fructose by restoring the antioxidant status, and modulating nuclear factor E2 related factor 2 (Nrf2) translocation to the nucleus with subsequently up-regulated antioxidative enzyme protein expression. Histopathological examinations revealed that impaired pancreatic/hepatic tissues were effectively restored in high fructose-fed mice following TBF treatment. Our results show that TBF intake is effective in preventing the conversion of high fructose-induced insulin resistance and hepatic oxidative stress in mice by improving the insulin signaling molecules and the Nrf2 signal pathway in the liver. https://greenmedinfo.com/article/tartary-buckwheat-flavonoids-ameliorate-high-fructose-induced-insulin-resistan#comments Buckwheat Flavonoids High Fructose Diet Insulin Resistance Antioxidants Heme oxygenase-1 up-regulation Nrf2 activation Antioxidants Buckwheat Flavonoids High Fructose Diet Insulin Resistance Animal Study Wed, 09 Aug 2017 15:59:27 +0000 greenmedinfo 151387 at https://greenmedinfo.com The current review summarizes the existing in vitro and in vivo studies examining the anti-diabetic effects of rosemary extract. https://greenmedinfo.com/article/current-review-summarizes-existing-vitro-and-vivo-studies-examining-anti-diabe n/a PMID:  Nutrients. 2017 Sep 1 ;9(9). Epub 2017 Sep 1. PMID: 28862678 Abstract Title:  Rosemary Extract as a Potential Anti-Hyperglycemic Agent: Current Evidence and Future Perspectives. Abstract:  Type 2 diabetes mellitus (T2DM), a disease on the rise and with huge economic burden to health care systems around the globe, results from defects in insulin action (termed insulin resistance) combined with impaired insulin secretion. Current methods of prevention and treatments for insulin resistance and T2DM are lacking in number and efficacy and, therefore, there is a need for new preventative measures and targeted therapies. In recent years, chemicals found in plants/herbs have attracted attention for their use as functional foods or nutraceuticals for preventing and treating insulin resistance and T2DM. Rosemary is an evergreen shrub indigenous to the Mediterranean region and South America, which contains various polyphenols. Rosemary extract and its polyphenolic constituents have been reported to have antioxidant, anti-inflammatory, anticancer, and anti-hyperglycemic properties. The current review summarizes the existing in vitro and in vivo studies examining the anti-diabetic effects of rosemary extract and its polyphenolic components and highlights the known mechanism of action. https://greenmedinfo.com/article/current-review-summarizes-existing-vitro-and-vivo-studies-examining-anti-diabe#comments Diabetes Mellitus: Type 2 Insulin Resistance Rosemary Anti-Inflammatory Agents Antioxidants Hypoglycemic Agents Anti-Inflammatory Agents Antioxidants Diabetes mellitus: Type 2 Hypoglycemic Agents Insulin Resistance Plant Extracts rosemary Animal Study Fri, 25 May 2018 01:27:18 +0000 greenmedinfo 164769 at https://greenmedinfo.com These findings suggested that berberine may reduce insulin resistance. https://greenmedinfo.com/article/these-findings-suggested-berberine-may-reduce-insulin-resistance n/a PMID:  Exp Clin Endocrinol Diabetes. 2018 Jan 24. Epub 2018 Jan 24. PMID: 29365334 Abstract Title:  Berberine Modulates Gut Microbiota and Reduces Insulin Resistance via the TLR4 Signaling Pathway. Abstract:  Berberine, a natural compound extracted from several Chinese herbs including Coptis chinensis, has been shown to have anti-obesity effects and prevents insulin resistance in high-fat diet (HFD)-fed obese rats by modulating the gut microbiota; however, the molecular mechanisms underlying these activities remain unknown. We investigated the effects of berberine on obesity and insulin resistance by examining the lipopolysaccharide (LPS)/toll-like receptor 4 (TLR4)/tumor necrosis factor (TNF)-α signaling pathway in livers of HFD-fed obese rats. Our results showed that 8-week berberine (200 mg/kg) treatment significantly reduced fasting blood glucose, triglyceride, low-density lipoprotein-cholesterol and insulin resistance in HFD-fed obese rats. However, berberine had no significant effects on body weight, visceral fat mass or the visceral fat to body weight ratio. Berberine also attenuated HFD-induced hepatic steatosis. A prolonged HFD altered the gut microbiota composition by reducing protective bacteria like Bifidobacterium and increasing gram negative bacteria like Escherichia coli, which resulted in increased LPS release into plasma. Berberine reversed these effects and inhibited LPS-induced TLR4/TNF-α activation, resulting in increased insulin receptor and insulin receptor substrate-1 expression in the liver. These findings suggested that berberine may reduce insulinresistance, at least in part by modulating the gut microbiota along with inhibiting LPS/TLR4/TNF-α signaling in the liver. https://greenmedinfo.com/article/these-findings-suggested-berberine-may-reduce-insulin-resistance#comments Berberine Insulin Resistance Anti-Inflammatory Agents Gastrointestinal Agents Hypoglycemic Agents Hypolipidemic Anti-Inflammatory Agents Berberine Gastrointestinal Agents Hypoglycemic Agents Hypolipidemic Insulin Resistance Animal Study Wed, 31 Jan 2018 03:48:47 +0000 greenmedinfo 159030 at https://greenmedinfo.com These results suggest that tangeretin improves insulin resistance by attenuating obesity-induced inflammation in adipose tissue. https://greenmedinfo.com/article/these-results-suggest-tangeretin-improves-insulin-resistance-attenuating-obesi n/a PMID:  Dev Reprod. 2017 Mar ;21(1):93-100. Epub 2017 Mar 31. PMID: 28484748 Abstract Title:  Tangeretin Improves Glucose Uptake in a Coculture of Hypertrophic Adipocytes and Macrophages by Attenuating Inflammatory Changes. Abstract:  Obesity is characterized by a state of chronic low-grade inflammation and insulin resistance, which are aggravated by the interaction between hypertrophic adipocytes and macrophages. In this study, we investigated the effects of tangeretin on inflammatory changes and glucose uptake in a coculture of hypertrophic adipocytes and macrophages. Tangeretin decreased nitric oxide production and the expression of interleukin (IL)-6, IL-1β, tumor necrosis factor-α, inducible nitric oxide synthase, and cyclooxygenase-2 in a coculture of 3T3-L1 adipocytes and RAW 264.7 cells. Tangeretin also increased glucose uptake in the coculture system, but did not affect the phosphorylation of insulin receptor substrate (IRS) and Akt. These results suggest that tangeretin improves insulin resistance by attenuating obesity-induced inflammation in adipose tissue. https://greenmedinfo.com/article/these-results-suggest-tangeretin-improves-insulin-resistance-attenuating-obesi#comments Inflammation Insulin Resistance Obesity Tangeretin Anti-Inflammatory Agents Cyclooxygenase 2 Inhibitors Insulin Sensitizers Interleukin-1 beta downregulation Interleukin-6 Downregulation Nitric Oxide Inhibitor Anti-Inflammatory Agents Inflammation Insulin Resistance obesity Tangeretin In Vitro Study Tue, 23 Jan 2018 15:31:37 +0000 greenmedinfo 158680 at https://greenmedinfo.com