2016

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Agaricus bisporus-Derived Glucosamine Hydrochloride Regulates VEGF through BMP Signaling to Promote Zebrafish Vascular Development and Impairment Repair
Agaricus bisporus-Derived Glucosamine Hydrochloride Regulates VEGF through BMP Signaling to Promote Zebrafish Vascular Development and Impairment Repair
Glucosamine hydrochloride (GAH) is a natural component of glycoproteins present in almost all human tissues and participates in the construction of human tissues and cell membranes. GAH has a wide range of biological activities, particularly in anti-inflammatory and osteogenic damage repair. At present, little is known about how GAH functions in angiogenesis. To determine the role of GAH on vascular development and impairment repair, we used the inhibitors VRI, DMH1, and dorsomorphin (DM) to construct vascular-impaired models in Tg(kdrl: mCherry) transgenic zebrafish. We then treated with GAH and measured its repair effects on vascular impairment through fluorescence intensity, mRNA, and protein expression levels of vascular-specific markers. Our results indicate that GAH promotes vascular development and repairs impairment by regulating the vascular endothelial growth factor (VEGF) signaling pathway through modulation of bone morphogenetic protein (BMP) signaling. This study provides an experimental basis for the development of GAH as a drug to repair vascular diseases.
·mdpi.com·
Agaricus bisporus-Derived Glucosamine Hydrochloride Regulates VEGF through BMP Signaling to Promote Zebrafish Vascular Development and Impairment Repair
Nanogels with covalently bound and releasable trehalose for autophagy stimulation in atherosclerosis | Journal of Nanobiotechnology | Full Text
Nanogels with covalently bound and releasable trehalose for autophagy stimulation in atherosclerosis | Journal of Nanobiotechnology | Full Text
Atherosclerosis, cholesterol-driven plaque formation in arteries, is a complex multicellular disease which is a leading cause of vascular diseases. During the progression of atherosclerosis, the autophagic function is impaired, resulting in lipid accumulation-mediated foam cell formation. The stimulation of autophagy is crucial for the recovery of cellular recycling process. One of the potential autophagy inducers is trehalose, a naturally occurring non-reducing disaccharide. However, trehalose has poor bioavailability due to its hydrophilic nature which results in poor penetration through cell membranes. To enhance its bioavailability, we developed trehalose-releasing nanogels (TNG) for the treatment of atherosclerosis. The nanogels were fabricated through copolymerization of 6-O-acryloyl-trehalose with the selected acrylamide-type monomers affording a high trehalose conjugation (~ 58%, w/w). TNG showed a relatively small hydrodynamic diameter (dH, 67 nm) and a uniform spherical shape and were characterized by negative ζ potential (-18 mV). Thanks to the trehalose-rich content, TNG demonstrated excellent colloidal stability in biological media containing serum and were non-hemolytic to red blood cells. In vitro study confirmed that TNG could stimulate autophagy in foam cells and enhance lipid efflux and in vivo study in ApoE−/− mice indicated a significant reduction in atherosclerotic plaques, while increasing autophagic markers. In conclusion, TNG hold great promise as a trehalose delivery system to restore impaired autophagy-mediated lipid efflux in atherosclerosis and subsequently reduce atherosclerotic plaques. Graphical abstract
·jnanobiotechnology.biomedcentral.com·
Nanogels with covalently bound and releasable trehalose for autophagy stimulation in atherosclerosis | Journal of Nanobiotechnology | Full Text
Strategies for the Development of Glycomimetic Drug Candidates - PMC
Strategies for the Development of Glycomimetic Drug Candidates - PMC
Carbohydrates are a structurally-diverse group of natural products which play an important role in numerous biological processes, including immune regulation, infection, and cancer metastasis. Many diseases have been correlated with changes in the composition ...
·ncbi.nlm.nih.gov·
Strategies for the Development of Glycomimetic Drug Candidates - PMC
Peace in the Middle East. Is it Possible? - YouTube
Peace in the Middle East. Is it Possible? - YouTube
This is an excerpt from a Prophecy Watchers podcast titled "The Biblical Plan for Mideast Peace" which previously aired here on 11/30/23.Thanks For Watching...
·youtube.com·
Peace in the Middle East. Is it Possible? - YouTube
RxSugar® The World’s Best Tasting, Keto, Non-GMO Natural Sugar & Syrup
RxSugar® The World’s Best Tasting, Keto, Non-GMO Natural Sugar & Syrup
Non-GMO Project Verified, Keto Certified, Grain-Free/Gluten-Free Certified, FODMAP Friendly Certified, Kosher, Halal, Plant-Based and Naturally Vegan. RxSugar®. There Is No Substitute™. RxSugar® is Sugar Reimagined®! Live Swealthy™ - Sweet & Healthy!
·rxsugar.com·
RxSugar® The World’s Best Tasting, Keto, Non-GMO Natural Sugar & Syrup
Allulose Sweetener Granules – Micro Ingredients
Allulose Sweetener Granules – Micro Ingredients
Micro Ingredients Pure Allulose Sweetener, 3 Pounds (48 Ounces), Plant Based Brown Sugar Alternative, No After Taste, Keto Diet and Vegan Friendly. Fine Granules, Keto Friendly, Sugar Alternative, Zero Calorie Sweetener. Great for Tea, Coffee, Drinks, Baking, Cooking and More. Scoop included to get the measurement ever
·microingredients.com·
Allulose Sweetener Granules – Micro Ingredients
Allulose Crystalized Powder
Allulose Crystalized Powder
BulkSupplements Allulose is a natural sweetener perfect for baking and adding sweetness to food and drinks without all of the excess sugar. It can also replace other sweeteners in recipes, allowing you to eat the same treats but with fewer calories and carbohydrates! This allulose is gluten free and filler free, making it safe for people with dietary restrictions. It's also incredibly easy to use - just substitute one cup of your usual sweetener with two-thirds of a cup of BulkSupplements Allulose and enjoy the same flavor without all of the unhealthy sugar content. If you're looking for a sugar substitute or want to cut down on your daily calorie intake, then try BulkSupplements Allulose today! You won't regret it!
·bulksupplements.com·
Allulose Crystalized Powder
D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance
D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance
D-allulose, a rare sugar, has been proposed to have potential benefits in addressing metabolic disorders such as obesity and type 2 diabetes (T2D). However, the precise mechanisms underlying these effects remain poorly understood. We aimed to elucidate the mechanisms by which D-allulose influences obesity-induced insulin resistance. We conducted gene set enrichment analysis on the liver and white adipose tissue of mice exposed to a high-fat diet (HFD) along with the white adipose tissue of individuals with obesity. Our study revealed that D-allulose effectively suppressed IFN-γ, restored chemokine signaling, and enhanced macrophage function in the livers of HFD-fed mice. This implies that D-allulose curtails liver inflammation, alleviating insulin resistance and subsequently impacting adipose tissue. Furthermore, D-allulose supplementation improved mitochondrial NADH homeostasis and translation in both the liver and white adipose tissue of HFD-fed mice. Notably, we observed decreased NADH homeostasis and mitochondrial translation in the omental tissue of insulin-resistant obese subjects compared to their insulin-sensitive counterparts. Taken together, these results suggest that supplementation with allulose improves obesity-induced insulin resistance by mitigating the disruptions in macrophage and mitochondrial function. Furthermore, our data reinforce the crucial role that mitochondrial energy expenditure plays in the development of insulin resistance triggered by obesity.
·mdpi.com·
D-Allulose Ameliorates Dysregulated Macrophage Function and Mitochondrial NADH Homeostasis, Mitigating Obesity-Induced Insulin Resistance