Regular ArticleDecreased Expression of Adenosine Kinase in Streptozotocin-Induced Diabetes Mellitus Rats
References (40)
- et al.
Am. J. Med.
(1985) J. Biol. Chem.
(1992)- et al.
Cell Signal
(1993) - et al.
Biochem. Biophys. Res. Commun.
(1990) - et al.
Biochim. Biophys. Acta
(1992) - et al.
J. Biol. Chem.
(1951) - et al.
Kidney. Int.
(1996) - et al.
Biochim. Biophys. Acta.
(1996) - et al.
Biochem. Biophys. Res. Commun.
(1997) - et al.
Diabetologia
(1980)
Hypertension
Int. J. Biochem.
Am. J. Physiol.
Contrib. Nephrol.
Am. J. Physiol.
Cardiovasc. Res.
Hypertension
Circulation
Cited by (48)
Adenosine kinase: An epigenetic modulator in development and disease
2021, Neurochemistry InternationalCitation Excerpt :As a regulator of adenosine, maladaptive changes in ADK expression have been implicated in a number of pathologies, including epilepsy, brain injury, stroke, diabetes, and cancer (Boison, 2013; Boison and Yegutkin, 2019). Initially, the role of ADK in those pathologies has been linked to its role as regulator of the tissue tone of adenosine, which determines the degree of adenosine receptor activation (Aronica et al., 2011; Giglioni et al., 2008; Li et al., 2008a; Masino et al., 2011; Pawelczyk et al., 2000; Saitoh et al., 2004; Sakowicz-Burkiewicz et al., 2006; Tsuchiya et al., 2012). However, ADK is also a well-characterized key regulator of the transmethylation pathway (Bjursell et al., 2011; Boison et al., 2002; Moffatt et al., 2002; Williams-Karnesky et al., 2013; Xu et al., 2017a, 2017b), which suggests additional functions of ADK beyond its role as a regulator of adenosine receptor activation.
“Adenosine an old player with new possibilities in kidney diseases”: Preclinical evidences and clinical perspectives
2021, Life SciencesCitation Excerpt :Induction of diabetes resulted in reduced activity and transcript levels of AK in kidneys of rats. Moreover these changes were consistent after 5 and 10 days of streptozotocin administration in these rats [99]. However, this study could not find any difference in ADA activity in diabetic rat kidneys.
Adenosine kinase and cardiovascular fetal programming in gestational diabetes mellitus
2020, Biochimica et Biophysica Acta - Molecular Basis of DiseaseGlioma progression in diabesity
2019, Molecular Aspects of MedicineCitation Excerpt :On the other hand, a profound reduction in the plasma insulin concentration in streptozotocin-induced diabetes results in elevated ADAs activity in these tissues (Fulzele et al., 2015; Rutkiewicz and Gorski, 1990). Also, AK is decreased in the kidney of diabetic rats leading to a local increase in adenosine concentration (Pawelczyk et al., 2000). All together these studies suggest that the local concentration of adenosine may be affected by the plasma concentration of insulin and its biological actions on ADAs and AK activity in target organs and tissues (Fulzele et al., 2015).
Adenosine contribution to normal renal physiology and chronic kidney disease
2017, Molecular Aspects of MedicineCitation Excerpt :Thus CD73 would be useful as a marker of CKD progression in the clinic. Other studies on adenosine metabolizing enzymes found that the expression of ecto-adenosine kinase (adenosine → AMP) was significantly lower in diabetic rat kidney (Pawelczyk et al., 2000; Sakowicz and Pawelczyk, 2002). Using different experimental approaches, it was suggested that increased adenosine and signaling is a common event in the pathogenesis of non-diabetic chronic kidney disease (Dai et al., 2011).
Adenosine receptors and diabetes: Focus on the A<inf>2B</inf> adenosine receptor subtype
2015, Pharmacological ResearchCitation Excerpt :Accordingly the inhibition of AK reduced renal inflammation and oxidative stress in MLDS-induced diabetes, allowing the speculation that these effects were due to an increase of adenosine [117]. A downregulation of AK was observed in MLDS-diabetes, that was restored following insulin treatment [69,118]. This effect was found to be associated with inhibition of T lymphocytes proliferation [69].
- 1
To whom correspondence should be addressed. Fax: (58) 344-9653. E-mail: [email protected].