|
Search Term: " PP "
Understanding Benfotiamine: The Fat-Soluble, Bioavailable and Physiologically Active Form of Thiamine   
Date:
July 27, 2023 12:12 PM
What if there existed a form of thiamine that was more bioavailable and physiologically active than the conventional form we all know about? Well, that form does exist, and it is called Benfotiamine. Benfotiamine has been gaining popularity lately, especially among people dealing with diabetes and other metabolic disorders. But what exactly is Benfotiamine, and what makes it different? Lets explore Benfotiamine, its bioavailability, and its physiological effects. Thiamine, also known as Vitamin B1, is a nutrient that plays a crucial role in energy production, nerve function, and metabolism. It is a water-soluble vitamin, which means it dissolves in water and is not stored by the body. However, conventional forms of thiamine have a limited ability to cross cell membranes and are easily excreted out of the body, rendering it ineffective for some individuals. This is where Benfotiamine comes in; it is a modified form of Vitamin B1 that is fat-soluble, highly bioavailable, and because cells are wraPPed in lipid fat this form of B1 is capable of crossing cell membranes with ease. Since our cell membranes are composed of lipids, fat-soluble nutrients can easily penetrate the cell barrier and get into living cells where the vitamin is needed. Upon entering the bloodstream, benfotiamine is converted to thiamin pyrophosphate (TPP), the biologically active co-enzyme of thiamin, which is responsible for energy metabolism. By raising the blood levels of TPP, benfotiamine has been shown to suPPort glucose metabolism, reduce oxidative stress and inflammation, and protect against the damage caused by high levels of advanced glycation end products (AGEs). In addition to its bioavailability, benfotiamine has been shown to have several physiological effect on the body. One of the key enzymes that benfotiamine influences is transketolase, which is involved in the pentose phosphate pathway, a metabolic pathway that generates NADPH, a vital molecule that protects cells against oxidative stress. By stimulating transketolase, benfotiamine suPPorts the diversion of excess glucose to the pentose phosphate pathway, thereby reducing the production of reactive oxygen species and increasing the production of NADPH. Another significant benefit of benfotiamine is that it helps protect the nervous system. Chronic high blood glucose levels are known to cause oxidative stress and to damage the peripheral and central nervous systems. However, benfotiamine has been shown to help lower oxidative stress markers and reduce the risk of nerve damage. This can in turn help reduce pain, numbness, and tingling sensations associated with nerve damage, making it a promising adjunct therapy for people with diabetic neuropathy. In Summary: benfotiamine is a modified and bioavailable form of thiamine that offers unique benefits compared to conventional forms of Vitamin B1. Its fat-solubility enables it to cross cell membranes, raise levels of thiamin pyrophosphate, stimulate the transketolase enzyme, and suPPort proper glucose metabolism. Its notable effects on the nervous system make it an attractive therapeutic agent for people with diabetic neuropathy. If you're seeking an alternative and highly effective form of thiamine, benfotiamine is definitely worth considering. Give it a try today!
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=6580) Benfotiamine raises the blood level of thiamine pyrophosphate (TPP)  
Date:
August 02, 2005 03:52 PM
Benefits Benfotiamine raises the blood level of thiamine pyrophosphate (TPP), the biologically active co-enzyme of thiamine.4 Thiamine and its Co-enzyme, TPP Thiamine (vitamin B1) plays an essential part in the metabolism of glucose, through actions of it co-enzyme TPP (thiamine pyrophosphate). TPP is formed by the enzymatically-catalyzed addition of two phosphate groups donated by ATP to thiamine. TPP also goes by the name "thiamine diphosphate." In the cytoplasm of the cell, glucose, a 6-carbon sugar, is metabolized to pyruvic acid, which is converted into acetyl-CoA, otherwise known as "active acetate." Acetyl CoA enters the mitochondrion, where it serves as the starting substrate in the Kreb’s cycle (citric acid cycle). The Krebs cycle is the primary source of cellular metabolic energy. TPP, along with other co-enzymes, is essential for the removal of CO2 from pyruvic acid, which in turn is a key step in the conversion of pyruvic acid to acetyl CoA. CO2 removal from pyruvic acid is called "oxidative decarboxylation," and for this reason, TPP was originally referred to as "cocarboxylase." TPP is thus vital to the cell’s energy suPPly. Benfotiamine helps maintain healthy cells in the presence of blood glucose. Acting as a biochemical "super-thiamin," it does this through several different cellular mechanisms, as discussed below. Benfotiamine and Glucose Metabolism Benfotiamine normalizes cellular processes fueled by glucose metabolites. As long as glucose remains at normal levels, excess glucose metabolites do not accumulate within the cell. The bulk of the cell’s glucose suPPly is converted to pyruvic acid, which serves as substrate for production of acetyl CoA, the primary fuel for the Krebs cycle. Of the total amount of metabolic energy (in the form of ATP) released from food, the Krebs cycle generates about 90 percent.5 In the presence of elevated glucose levels, the electron transport chain, the final ATP-generating system in the mitochondrion, produces larger than normal amounts of the oxygen free radical "superoxide." This excess superoxide inhibits glyceraldehyde phosphate dehydrogenase (GAPDH), as key enzyme in the conversion of glucose to pyruvic acid, resulting in an excess of intermediate metabolites known as "triosephosphates." Increase triosephophate levels trigger several cellular mechanisms that result in potential damage to vascular tissue. Cells particularly vulnerable to this biochemical dysfunction are found in the retina, kidneys and nerves. Benfotiamine has been shown to block three of these mechanisms: the hexosamine pathway, the diaglycerol-protein kinease C pathway and the formation of Advanced Glycation End-poducts. As discussed below, benfotiamine does this by activating transketolase, a key thiamin-dependent enzyme.6 Benfotiamine stimulates tranketolase, a cellular enzyme essential for maintenance of normal glucose metabolic pathways.* Transketolase diverts the excess fructose-6-phosphate and glyceraldehydes-3-phosphate, (formed by the inhibition of GAPDH, as mentioned above), into production of pentose-5-phosphates and erythrose-4-phosphate and away from the damaging pathways. Benfotiamine activates transketolase activity in bovine aortic endothelial cells incubated in glucose.6 To test benfotiamine’s ability to counteract these metabolic abnormalities caused by elevated blood glucose, studies have been done in diabetic rats. Benfotiamine increases transketolase activity in the retinas of diabetic rats, while concomitantly decreasing hexosamine pathway activity, protein kinase C activity and AGE formation.6 Benfotiamine and Protein glycation Benfotiamine controls formation of Advanced Glycation End-products (AGEs). AGEs have an affinity for proteins such as collagen, the major structural protein in connective tissue. AGEs are formed through abnormal linkages between proteins and glucose. This occurs via a non-enzymatic glycosylation reaction similar to the "browning reaction" that takes place in stored food.7 At high glucose concentrations, glucose attaches to lysine, forming a Schiff base, which in turn forms "early glycosylation products." Once blood glucose levels return to normal levels, the amount of these early glycosylation products decreases, and they are not particularly harmful to most tissue proteins. On long-lived proteins such as collagen, however, early glycosylation products are chemically rearranged into the damaging Advanced Glycation End-products. AGE formation on the collagen in coronary arteries causes increased vascular permeability. This vessel "leakiness" allows for abnormal cross-linking between plasma proteins and other proteins in the vessel wall, comprising vascular function and potentially occluding the vessel lumen. A number of other potentially harmful events may also occur, including production of cytokines that further increase vascular permeability. Endothelin-1, a strong vasoconstrictor, is over produced, increasing the possibility of thrombosis and generation of oxygen free radicals is stimulated.8 It is vitally important to suPPort normal glucose metabolic pathways so that formation of AGEs is minimized. Benfotiamine, in the test tube (in vitro) prevents AGE formation in endothelial cells cultured in high glucose by decreasing the glucose metabolites that produce AGEs.9 Endothelial cells make up the membranes that line the inner walls of organs and blood vessels. In a rat study comparing the effects of Benfotiamine with water-soluble thiamin, Benfotiamine inhibited AGE formation in diabetic rats while completely preventing formation of "glycooxidation products," which are toxic by products of chronic elevated blood glucose. AGE levels were not significantly altered by thiamin.10 Benfotiamine also normalized nerve function in the animals. After three months of administration, "nerve conduction velocity (NCV)," a measure of nerve function, was increased by both benfotiamine and thiamin; at six months, NCV was normalized by benfotiamine, whereas thiamin produced no further increases in this parameter. Dysfunctional glucose metabolic pathways leading to AGE formation occurs in endothelial cells of the kidneys. In a recent animal study, benfotiamine was administered to rats with elevated glucose levels. Benfotiamine increased transketolase activity in the kidney filtration system of these rats, while at the same time shifting triosephophates into the pentose pathway and preventing protein leakage.11 Safety Benfotiamine has an excellent tolerability profile and can be taken for long periods without adverse effects.3,12 The statements in this fact sheet have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease. Scientific References 1. Bitsch R, Wolf M, Möller J. Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamin derivative. Ann Nutr Metab 1991;35(2):292-6. 2. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997; 52(4):319-20. 3. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther 1996;34(2):47-50. 4. Frank T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfontiamine. Eur J Clin Pharmacol. 2000;56(3):251-7. 5. Pike RL, Brown ML. Nutrition, An Integrated APProach, 3rd Ed. New York:MacMillan; 1986:467. 6. Hammes H-P, Du X, Edlestein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic neuropathy. Nat Med 2003;9(3):294-99. 7. Monnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen in diabetes mellitus. Proc Natl Acad Sci 1984;81(2):583-7. 8. Brownlee M. The pathological implications of protein glycation. Clin Invest Med 1995;18(4):275-81. 9. Pomero F, Molinar Min A, La Selva M, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol 2001;38(3):135-8. 10. Stracke H, Hammes HP, Werkman D, et al. Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes 2001;109(6):300-6. 11. Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes 2003;52(8):2110-20. 12. Bergfeld R, MatsumaraT, Du X, Brownlee M. Benfotiamin prevents the consequences of hyperglycemia induced mitochondrial overproduction of reactive oxygen specifies and experimental diabetic neuropathy (Abstract) Diabetologia 2001; 44(SuPPl1):A39.
(https://vitanetonline.com:443/forums/Index.cfm?CFApp=1&Message_ID=721) | ||||||||||||||||||||
