High Sugar Diet https://greenmedinfo.com/category/keywords/High%20Sugar%20Diet en 4 Sugar Alternatives That Won't Poison You https://greenmedinfo.com/blog/4-sugar-alternatives-wont-poison-you <div class="copyright">This article is copyrighted by GreenMedInfo LLC, 2022<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/DietWithoutDeprivation.jpg" style="width: 600px; height: 315px;" title="4&nbsp;Sugar Alternatives That Won't Poison You" /></p> <p><span style="font-size:18px;"><em><strong>You may think that staying slim and eating healthfully means NO sweets, but guess what? There are natural and delicious sweeteners that won't wreck your diet, and even have therapeutic 'side benefits'</strong></em></span></p> <p><span style="letter-spacing: 0px;">No arena of health and wellness is more debatable than what we </span><strong style="letter-spacing: 0px;"><em>should </em></strong><span style="letter-spacing: 0px;">be eating. Looking back through time, the foods that constitute a healthy diet have changed so dramatically, you can literally mark the passage of time by the coming and going of dietary fads.</span></p><p><a href="https://greenmedinfo.com/blog/4-sugar-alternatives-wont-poison-you" target="_blank">read more</a></p> https://greenmedinfo.com/blog/4-sugar-alternatives-wont-poison-you#comments Cardiovascular Disease Dental Caries Diabetes Honey Hypertension Molasses Nonalcoholic fatty liver disease (NAFLD) Obesity Overweight Stevia Xylitol GMOs High Fructose Corn Syrup Sugar Sugary soda Artificial Sweeteners GMO High Fructose Corn Syrup High Sugar Diet toxicity from artificial sweeteners Thu, 03 Nov 2022 13:01:16 +0000 Sayer Ji 152956 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 Krill oil treatment was associated with the alleviation of hyperlipidemia in animals. https://greenmedinfo.com/article/krill-oil-treatment-was-associated-alleviation-hyperlipidemia-animals n/a PMID:  Front Microbiol. 2017 ;8:905. Epub 2017 May 17. PMID: 28567037 Abstract Title:  Modulation of the Gut Microbiota by Krill Oil in Mice Fed a High-Sugar High-Fat Diet. Abstract:  Multiple lines of evidence suggest that the gut microbiota plays vital roles in metabolic diseases such as hyperlipidemia. Previous studies have confirmed that krill oil can alleviate hyperlipidemia, but the underlying mechanism remains unclear. To discern whether krill oil changes the structure of the gut microbiota during the hyperlipidemia treatment, 72 mice were acclimatized with a standard chow diet for 2 weeks and then randomly allocated to receive a standard chow diet (control group, n = 12) or a high-sugar-high-fat (HSHF) diet supplemented with a low (100μg/g·d, HSHF+LD group, n = 12), moderate (200 μg/g·d, HSHF+MD group, n = 12) or high dosage of krill oil (600 μg/g·d, HSHF+HD group, n = 12), simvastatin (HSHF+S group, n = 12) or saline (HSHF group, n = 12) continuously for 12 weeks. The resulting weight gains were attenuated, the liver indexand the low-density lipoprotein, total cholesterol and triglyceride concentrations showed a stepwise reduction in the treated groups compared with those of the control group. A dose-dependent modulation of the gut microbiota was observed after treatment with krill oil. Low- and moderate- doses of krill oil increased the similarity between the composition of the HSHF diet-induced gut microbiota and that of the control, whereas the mice fed the high-dose exhibited a unique gut microbiota structure that was different from that of the control and HSHF groups. Sixty-five key operational taxonomicunits (OTUs) that responded to the krill oil treatment were identified using redundancy analysis, of which 26 OTUs were increased and 39 OTUs were decreased compared with those of the HSHF group. In conclusion, the results obtained in this study suggest that the structural alterations in the gut microbiota induced by krill oil treatment were dose-dependent and associated with the alleviation of hyperlipidemia. Additionally, the high-dose krill oil treatment showed combined effects on the alleviation of hyperlipidemia and obesity. https://greenmedinfo.com/article/krill-oil-treatment-was-associated-alleviation-hyperlipidemia-animals#comments High Fat Diet High Sugar Diet Hyperlipidemia Krill Obesity Gastrointestinal Agents Hypolipidemic Anti-Obesity Agents Gastrointestinal Agents high fat diet High Sugar Diet hyperlipidemia Hypolipidemic Krill obesity Animal Study Fri, 01 Sep 2017 20:28:52 +0000 greenmedinfo 152590 at https://greenmedinfo.com Sulforaphane delays fibroblast aging in vitro by decreasing glycolysis and reducing oxidative stress. https://greenmedinfo.com/article/sulforaphane-delays-fibroblast-aging-vitro-decreasing-glycolysis-and-reducing- PMID:  Oxid Med Cell Longev. 2018 ;2018:5642148. Epub 2018 Nov 22. PMID: 30595796 Abstract Title:  Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage. Abstract:  Increased cell senescence contributes to the pathogenesis of aging and aging-related disease. Senescence of human fibroblastsmay be delayed by culture in low glucose concentration. There is also accumulating evidence of senescence delay by exposure to dietary bioactive compounds that activate transcription factor Nrf2. The mechanism of cell senescence delay and connection between these responses is unknown. We describe herein that the cruciferous vegetable-derived metabolite, sulforaphane (SFN), activates Nrf2 and delays senescence of human MRC-5 and BJ fibroblasts. Cell senescence is associated with a progressive and marked increased rate of glucose metabolism through glycolysis. This increases mitochondrial dysfunction and overwhelms defences against reactive metabolites, leading to increasing proteomic and genomic oxidative damage. Increased glucose entry into glycolysis in fibroblast senescence is mainly mediated by increased hexokinase-2. SFN delayed senescence by decreasing glucose metabolism on the approach to senescence, exhibiting a caloric restriction mimetic-like activity and thereby decreased oxidative damage to cell protein and DNA. This was associated with increased expression of thioredoxin-interacting protein, curbing entry of glucose into cells; decreased hexokinase-2, curbing entry of glucose into cellular metabolism; decreased 6-phosphofructo-2-kinase, downregulating formation of allosteric enhancer of glycolysis fructose-2,6-bisphosphate; and increased glucose-6-phosphate dehydrogenase, downregulating carbohydrate response element- (ChRE-) mediated transcriptional enhancement of glycolysis by Mondo/Mlx. SFN also enhanced clearance of proteins cross-linked by transglutaminase which otherwise increased in senescence. This suggests that screening of compounds to counter senescence-associated glycolytic overload may be an effective strategy to identify compounds with antisenescence activity and health beneficial effects of SFN in longevity may involve delay of senescence through glucose and glycolytic restriction response. <p><a href="https://greenmedinfo.com/article/sulforaphane-delays-fibroblast-aging-vitro-decreasing-glycolysis-and-reducing-" target="_blank">read more</a></p> https://greenmedinfo.com/article/sulforaphane-delays-fibroblast-aging-vitro-decreasing-glycolysis-and-reducing-#comments Aging Oxidative Stress Sulforaphane Nrf2 activation calorie restriction High Sugar Diet Isothiocyanates Human In Vitro Fri, 26 Jul 2019 13:40:18 +0000 greenmedinfo 191950 at https://greenmedinfo.com