Temat: AMP-activated kinase - Katalog OPAC zbiorów

Skocz do pozycji: 1.

Tytuł:: Metformin reduces NAD(P)H oxidase activity in mouse cultured podocytes through purinergic dependent mechanism by increasing extracellular ATP concentration
Autorzy:: Piwkowska, Agnieszka
Rogacka, Dorota
Jankowski, Maciej
Angielski, Stefan
Powiązania:: https://bibliotekanauki.pl/articles/1039452.pdf
Data publikacji:: 2013
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: AMP-activated kinase
free radicals
metformin
NAD(P)H oxidase
podocytes
purinoceptors
Opis:: Hyperglycemia affects the functioning numbers of podocytes and leads to a gradual decline of renal function. The normalization of glucose level is a principle therapeutic goal in diabetic patients and metformin is a popular hypoglycemic drug used in type 2 diabetes mellitus. Metformin activates AMP-activated kinase (AMPK) and decreases NAD(P)H oxidase activity in podocytes leading to reduction of free radical generation. Similar effects are observed after activation of P2 receptors. Therefore, we investigated whether metformin increases extracellular ATP concentration and affects the activities of NAD(P)H oxidase and AMPK through P2 receptors. Experiments were performed on cultured mouse podocytes. NAD(P)H oxidase activity was measured by chemiluminescence and changes in AMPK activity were estimated by immunoblotting against AMPKα-Thr172-P. Metformin increased extracellular ATP concentration by reduction of ecto-ATPase activity, decreased NAD(P)H oxidase activity and increased AMPK phosphorylation. A P2 receptor antagonist, suramin (300 µM), prevented metformin action on NAD(P)H oxidase and AMPK phosphorylation. The data suggests a novel mechanism of metformin action, at least in podocytes. Metformin, which increases extracellular ATP concentration leads to activation of P2 receptors and consequent modulation of the podocytes' metabolism through AMPK and NAD(P)H oxidase which, in turn, may affect podocyte functioning.
Źródło:: Acta Biochimica Polonica; 2013, 60, 4; 607-612
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Ganoderma lucidum extract stimulates glucose uptake in L6 rat skeletal muscle cells
Autorzy:: Jung, Kyung
Ha, Eunyoung
Kim, Mi-Ja
Uhm, Yoon
Kim, Hye
Hong, Seung-Jae
Chung, Joo-Ho
Yim, Sung-Vin
Powiązania:: https://bibliotekanauki.pl/articles/1041224.pdf
Data publikacji:: 2006
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: Ganoderma lucidum extract
skeletal muscle
phosphatidylinositol 3-kinase
AMP-activated protein kinase
glucose uptake
Opis:: The effect of Ganoderma lucidum extract on glucose uptake was studied in L6 rat skeletal muscle cells. G. lucidum extract increased glucose uptake about 2-fold compared to control. The extract stimulated the activity of phosphatidylinositol (PI) 3-kinase which is a major regulatory molecule in the glucose uptake pathway. About 7-fold increased activity of a PI 3-kinase was observed after treatment with G. lucidum extract, whereas PI 3-kinase inhibitor, LY294002, blocked the G. lucidum extract-stimulated PI 3-kinase activity in L6 skeletal muscle cells. Protein kinase B, a downstream mediator of PI 3-kinase, was also activated by G. lucidum extract. We then assessed the activity of AMP-activated protein kinase (AMPK), another regulatory molecule in the glucose uptake pathway. G. lucidum extract increased the phosphorylation level of both AMPK α1 and α2. Activity of p38 MAPK, a downstream mediator of AMPK, was also increased by G. lucidum extract. Taken together, these results suggest that G. lucidum extract may stimulate glucose uptake, through both PI 3-kinase and AMPK in L6 skeletal muscle cells thereby contributing to glucose homeostasis.
Źródło:: Acta Biochimica Polonica; 2006, 53, 3; 597-601
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki