• Phosphatidylserine and kidney function

    Phosphatidylserine and kidney function

    What Is Phosphatidylserine? Phosphatidylserine PS is one of the naturally-occurring molecules present all through the body.

    phosphatidylserine and kidney function

    Although the human body can produce this substance at its own, the majority of this nutrient can be attained through the diet. Phosphatidylserine PS is an essential component in all our cells; specifically, it is a major component of the cell membrane.

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    The cell membrane is a kind of "skin" that surrounds living cells. Besides keeping cells intact, this membrane performs vital functions such as moving nutrients into cells and pumping waste products out of them. PS plays an important role in many of these functions. So to maintain those levels it is prescribed as a supplement with treatment. It is widely used for this purpose in Italy, Scandinavia, and other parts of Europe. PS has also been marketed as a "brain booster" for people of all ages, said to sharpen memory and increase thinking ability.

    Effect of Phosphatidylserine on Alzheimer's Disease. Phosphatidylserine PSin studies of severe mental decline, appears to have been equally effective whether the cause was Alzheimer's disease or something entirely unrelated, such as multiple small strokes. This certainly suggests that PS may have a positive impact on the brain that is not specific to any one condition.

    From this observation, it is not a great leap to suspect that it might be useful for much less severe problems with memory and mental function, such as those that seem to occur in nearly all of us who are older than Indeed, one double-blind study did find that animal-source phosphatidylserine could improve mental function in individuals with relatively mild age-related memory loss.

    Overall, the evidence for animal-source PS in dementia is fairly strong. Double-blind studies involving a total of more than 1, people suggest that phosphatidylserine is an effective treatment for Alzheimer's disease and other forms of dementia. The largest of these studies followed elderly subjects in northeastern Italy over a course of 6 months. All suffered from moderate to severe mental decline, as measured by standard tests. Treatment consisted of either mg daily of PS or placebo.

    The group that took PS did significantly better in both behavior and mental function than the placebo group. Symptoms of depression also improved. These results agree with those of numerous other smaller double-blind studies involving a total of more than people with Alzheimer's and other types of age-related dementia. And, finally, the promising study results were published in the November issue of the "Journal of Clinical Biochemistry and Nutrition.

    phosphatidylserine and kidney function

    Memory scores increased in all groups, and those with the lowest starting scores improved the most. Improvements occurred mostly in delayed verbal recall, an aspect of memory associated with early stages of dementia.

    There were no adverse effects, and the researchers concluded that phosphatidylserine is a safe and helpful supplement for improving memory for some people.

    Supplements containing phosphatidylserine are now derived from soy extracts. Early studies, though promising, were based on cow-derived supplements. There are reasons to expect that plant-source PS should function very similarly to PS made from cows' brains, and some animal studies suggest that it is indeed effective. However, in preliminary trials, soy-based PS and cabbage-based PS failed to prove beneficial and did not show the same level of effectiveness.

    Are There Side Effects?To browse Academia. Skip to main content. Log In Sign Up. Dwayne Sutton. Paul Tchounwou. Download Free PDF. Free PDF. Download PDF Package. Premium PDF Package. This paper. A short summary of this paper. Sutton, and Paul B. Paul B. Email: paul. A comprehensive analysis of published data indicates that inorganic mercury is one of the most environmentally abundant toxic metals, is a potent and selective nephrotoxicant that preferentially accumulates in the kidneys, and is known to produce cellular injury in the kidneys.

    Binding sites are present in the proximal tubules, and it is in the epithelial cells of these tubules that toxicants such as inorganic mercury are reabsorbed. This can affect the enzymatic activity and the structure of various proteins.

    Mercury may alter protein and membrane structure and function in the epithelial cells and this alteration may result in long term residual effects. This research was therefore designed to evaluate the dose-response relationship in human renal proximal tubule HK-2 cells following exposure to inorganic mercury.

    The distribution and function of phosphatidylserine in cellular membranes

    Cytotoxicity was evaluated using the MTT assay for cell viability. The Annexin-V assay was performed by flow cytometry to determine the extent of phosphatidylserine externalization. Cytotoxicity experiments yielded a LD50 value of 4. The percentages of cells undergoing early apoptosis were 0.Lactadherin was used to quantify PS exposure on MPs and their original cells.

    Fibrin production was determined by turbidity. PS exposure and fibrin strands were observed using confocal microscopy. In vitroBCs and endothelial cells exposed more PS in hypoglycemia or hyperglycemia.

    Interestingly, reconstitution experiments showed that hypoglycemia-treated cells could be further activated or injured when recovery is obtained reaching hyperglycemia. Blockade of PS could become a novel therapeutic modality for the prevention of thrombosis in these patients.

    phosphatidylserine and kidney function

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    phosphatidylserine and kidney function

    Sign In. Advanced Search. Search Menu. Skip Nav Destination Article Navigation. Close mobile search navigation Article Navigation. Volume Article Navigation. Phosphatidylserine on microparticles and associated cells contributes to the hypercoagulable state in diabetic kidney disease Muxin YuMuxin Yu. Oxford Academic. Google Scholar. Rujuan Xie. Correspondence and offprint requests to: Rujuan Xie; E-mail: xierujuanhydyy Yan Zhang.

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    Comments 0.You may have noticed phosphatidylserine being added to shakes in the gym or taken by people you know as part of a balanced lifestyle.

    Indeed, studies have been done on phosphatidylserine, but the positive properties of it are becoming more widely known and appreciated. But what is it, and how can it benefit you?

    If you live a hectic lifestyle, this could be your new favourite supplement. Phosphatidylserine is a key component of your cell membranes. It is a major part of the lipids that make up essential parts of your cells.

    It helps to cover and protect the cell and helps the cells communicate. Phosphatidylserine is found in a number of foods. It is found in high amounts of fish such as mackerel and herring, as well as in offal such as chicken hearts and pig kidney.

    The highest dose by far is in bovine brain. Not easy things to mix in your shakes and eat on the go! Another source of phosphatidylserine is soya lechtin. It is safer, as it carries no risk of infectious disease from animals and is vegetarian and vegan-friendly. Cortisol is a stress hormone which naturally occurs in the body. It is released when the body feels under stress. This can be stress from work or lifestyle, but it can also be caused by exercise, particularly heavy resistance exercises.

    This is often surprising to people who often only link exercise with feel-good endorphin hormones. However, stress hormones and their effects are vital to consider in a healthy active lifestyle. Cortisol is a hormone that effects many different functions throughout the body. Cortisol effects blood sugar levels, metabolism and water retention.

    High cortisol levels can be linked to weight gain in your abdomen, face and chest. So if you are stressed and not seeing the results you should from your workout and balanced diet, cortisol could be to blame. Not only that, but cortisol also affects memory formulation. So if you struggle to get your workout together and keep having to stop to go over your workout plan, it could be your stress levels.Aims: The present studies assessed the possibility that exposure to oxalate leads to alterations in membrane structure that promote crystal binding to renal epithelial cells.

    Specifically, we determined whether oxalate exposure produces a redistribution of membrane phosphatidylserine PS and an increase in the binding of 14 C-oxalate crystals to renal epithelial cells.

    Oxalate exposure also increased PS at the surface of phospholipid vesicles, suggesting that oxalate may interact directly with PS. The oxalate concentrations that increased superficial PS also increased binding of 14 C-oxalate crystals to MDCK cells, and the increased crystal binding was blocked by annexin V.

    Conclusions: These findings provide direct evidence that oxalate exposure promotes both a redistribution of PS and an increase in crystal binding in renal epithelial cells and support the notion that oxalate toxicity may contribute to the development of stone disease by altering the properties of the renal epithelial cell membrane.

    Abstract Aims: The present studies assessed the possibility that exposure to oxalate leads to alterations in membrane structure that promote crystal binding to renal epithelial cells. Publication types Research Support, U.

    Gov't, P. Substances Oxalates Phosphatidylserines.Diabetic kidney disease DKD is an important public health problem. Podocyte injury is a central event in the mechanism of DKD development. Podocytes are terminally differentiated, highly specialized glomerular visceral epithelial cells critical for the maintenance of the glomerular filtration barrier.

    Although potential mechanisms by which diabetic milieu contributes to irreversible loss of podocytes have been described, identification of markers that prognosticate either the development of DKD or the progression to end-stage kidney disease ESKD have only recently made it to the forefront.

    Several novel biomarkers indicating glomerular or tubular damage precede microalbuminuria, suggesting that the latter develops when significant kidney injury has already occurred.

    Because podocyte injury plays a key role in DKD pathogenesis, identification of markers of early podocyte injury or loss may play an important role in the early diagnosis of DKD. Such biomarkers in the urine include podocyte-released microparticles as well as expression of podocyte-specific markers. DKD is a glomerular disease, damaging the glomerular filtration barrier, a tripartite system consisting of fenestrated endothelial cells, the glomerular basement membrane, and podocytes.

    This barrier is critical to the selective filtration of water and solutes; it impedes the passage of macromolecules, such as albumin. Furthermore, podocyte injury with eventual podocyte loss is a critical event in the development and eventual progression of DKD.

    The hallmark histological changes associated with DKD comprise basement membrane thickening, podocyte loss, and mesangial expansion, with eventual nodular sclerosis in the later stages [ 34 ].

    These late stages are often associated with arterial hyalinosis and tubulointerstitial fibrosis [ 4 ]. The changes also cause microalbuminuria that can eventually progress to macroalbuminuria. Twelve percent of patients with diabetes mellitus type 1 develop macroalbuminuria after an average diabetes duration of 29 years [ 5 ].

    Currently, albuminuria is the most widely used earliest clinical marker of DKD. Albuminuria is independently associated with increased cardiovascular morbidity and mortality and may be the best predictor of a future decline in glomerular filtration rate GFR [ 6 ].

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    The risk of developing DKD strongly correlates with the duration of diabetes [ 8 ]. Hyperglycemia generates reactive oxygen radicals and advanced glycation end-products, which bind to advanced glycation end-product receptors, triggering downstream signaling that facilitates production of reactive oxygen species, activates inflammatory cells, increases synthesis of angiotensin II, and causes a release of growth factors.

    The currently available forms of medical therapy capable of reducing proteinuria and delaying the progression of DKD are angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and sodium-glucose cotransporter-2 inhibitors [ 9—12 ].

    VEGF-A is necessary for the normal development of glomerular capillaries and for maintenance of podocytes via Akt signaling. In later stages of diabetic nephropathy, podocytes are lost; as a result, VEGF-A synthesis is reduced negatively affecting podocyte health, endothelial fenestration, and glomerular basement membrane composition [ 1314 ].

    Podocytes are terminally differentiated, highly specialized glomerular visceral epithelial cells that consist of a cell body primary processes and branching foot processes. Podocytes are characterized by a high rate of vesicular traffic as evidenced by multiple coated vesicles and coated pits along the basolateral domain of these cells.

    Podocytes have high capacity for protein synthesis and posttranslational modifications because of a well-developed endoplasmic reticulum and a large Golgi apparatus [ 19 ]. A multiprotein complex, the SD plays an important role in blood filtration and podocyte signal transduction. Podocytes participate in regulating GFR: when podocytes contract, they close filtration slits and, thus, reduce the surface area available for filtration [ 19—21 ]. Although terminally differentiated, the cells are highly dynamic, interacting with the glomerular basement membrane and communicating through signaling at the slit diaphragm [ 19—21 ].

    Podocyte loss is a key factor contributing to DKD progression [ 22—24 ]. Because podocytes are terminally differentiated cells, their loss is an irreversible event that leads to a decline in the function of the glomerular filtration barrier [ 2125 ]. An important component of effacement mechanism is dysregulation of nephrin production. Nephrin is an essential transmembrane protein in the slit diaphragm complex involved in podocyte survival [ 26—29 ].

    The expression of nephrin and its mRNA are decreased in diabetic nephropathy; the decrease results in aberrant rearrangement of actin and breakdown of the slit diaphragm and leads to foot process effacement [ 32 ]. Nephrin is also important in regulating podocyte insulin sensitivity; its cytoplasmic domain enables the docking of glucose transporters GLUT1 and GLUT4 with vesicle-associated membrane protein-2, thus facilitating insulin signaling [ 3334 ].

    These molecules are key regulators of actin cytoskeleton remodeling, functioning as molecular switches: they toggle between active and inactive states to coordinate signaling and either promote or inhibit cell motility [ 3536 ]. Diabetic milieu have been shown to stimulate Rho-GTPase activity, resulting in podocyte actin remodeling and proteinuria. Mutations in specific guanine exchange factors and GTPase activating proteins of the Rho-family GTPases can result in cytoskeletal rearrangement and foot process effacement [ 35—38 ].

    Podocytes adhere to the glomerular basement membrane via alpha3beta1 integrin and dystroglycans. The expression of alpha3beta1 has been shown to be decreased in patients with diabetes and in rats with streptozotocin-induced diabetes, thereby contributing to detachment of podocytes from the GBM [ 3940 ].Phosphatidylserine abbreviated Ptd-L-Ser or PS is a phospholipid and is a component of the cell membrane.

    It is a key pathway for viruses to enter cells via apoptotic mimicry. Phosphatidylserine is a phospholipid —more specifically a glycerophospholipid —which consists of two fatty acids attached in ester linkage to the first and second carbon of glycerol and serine attached through a phosphodiester linkage to the third carbon of the glycerol. Phosphatidylserine sourced from plants differs in fatty acid composition from that sourced from animals.

    In the plasma membrane, PS is localized exclusively in the cytoplasmic leaflet where it forms part of protein docking sites necessary for the activation of several key signaling pathways. These include the Akt, protein kinase C PKC and Raf-1 signaling that is known to stimulate neuronal survival, neurite growth, and synaptogenesis [2—7]. Modulation of the PS level in the plasma membrane of neurons has a significant impact on these signaling processes. Phosphatidylserine is biosynthesized in bacteria by condensing the amino acid serine with CDP cytidine diphosphate -activated phosphatidic acid.

    Only small amounts are found in dairy products and vegetables, with the exception of white beans and soy lecithin. Table 1. Phosphatidylserine content in different foods.

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    Therefore, the results of studies using phosphatidylserine from different sources cannot be generalized. In May, the Food and Drug Administration gave "qualified health claim" status to phosphatidylserine thus allowing labels to state "consumption of phosphatidylserine may reduce the risk of dementia and cognitive dysfunction in the elderly" along with the disclaimer "very limited and preliminary scientific research suggests that phosphatidylserine may reduce the risk of cognitive dysfunction in the elderly.

    More recent reviews have suggested that the relationship may be more robust, [12] [13] though the mechanism remains unclear. Initially, phosphatidylserine supplements were derived from bovine cortex. However, due to the risk of potential transfer of infectious diseases such as bovine spongiform encephalopathy or "mad cow disease"soy-derived supplements became an alternative.

    Svennerholm L. Distribution and fatty acid composition of normal human brain. J Lipid Res. Docosahexaenoic acid: a positive modulator of Akt signaling in neuronal survival. Phosphatidylserine is a critical modulator for Akt activation. J Cell Biol. Inhibition of neuronal apoptosis by docosahexaenoic acid n-3 : Role of phosphatidylserine in antiapoptotic effect.

    J Biol Chem.


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