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Lack of insulin impairs Mg2+ homeostasis and transport in cardiac cells of streptozotocin-injected diabetic rats
Journal of cellular biochemistry, 2008-06, Vol.104 (3), p.1034-1053
Reed, Grant
Cefaratti, Christie
Berti-Mattera, Liliana N.
Romani, Andrea
2008
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Reed, Grant
Cefaratti, Christie
Berti-Mattera, Liliana N.
Romani, Andrea
Titel
Lack of insulin impairs Mg2+ homeostasis and transport in cardiac cells of streptozotocin-injected diabetic rats
Ist Teil von
Journal of cellular biochemistry, 2008-06, Vol.104 (3), p.1034-1053
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2008
Quelle
MEDLINE
Beschreibungen/Notizen
Serum and tissue Mg2+ content are markedly decreased in diabetic patients and animals. At the tissue level, Mg2+ loss progresses over time and affects predominantly heart, liver and skeletal muscles. In the present study, alterations in Mg2+ homeostasis and transport in diabetic cardiac ventricular myocytes were evaluated. Cardiac tissue and isolated cardiac ventricular myocytes from diabetic animals displayed a decrease in total Mg2+ content that affected all cellular compartments. This decrease was associated with a marked reduction in cellular protein and ATP content. Diabetic ventricular myocytes were unable to mobilize Mg2+ following β‐adrenergic receptor stimulation or addition of cell permeant cyclic‐AMP. Sarcolemma vesicles purified from diabetic animals, however, transported Mg2+ normally as compared to vesicles from non‐diabetic animals. Treatment of diabetic animals with exogenous insulin for 2 weeks restored ATP and protein levels as well as Mg2+ homeostasis and transport to levels comparable to those observed in non‐diabetic animals. These results suggest that in diabetic cardiac cells Mg2+ homeostasis and extrusion via β‐adrenergic/cAMP signaling are markedly affected by the concomitant decrease in protein and ATP content. As Mg2+ regulates numerous cellular enzymes and functions, including protein synthesis, these results provide a new rationale to interpret some aspects of the cardiac dysfunctions observed under diabetic conditions. J. Cell. Biochem. 104: 1034–1053, 2008. © 2008 Wiley‐Liss, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0730-2312
eISSN: 1097-4644
DOI: 10.1002/jcb.21690
Titel-ID: cdi_proquest_miscellaneous_70739462
Format
–
Schlagworte
Adenosine Triphosphate - chemistry
,
Adenosine Triphosphate - metabolism
,
adrenergic signaling
,
Animals
,
Biological Transport
,
cardiac cells
,
Diabetes Mellitus, Experimental - drug therapy
,
Diabetes Mellitus, Type 1 - metabolism
,
Homeostasis
,
insulin
,
Insulin - metabolism
,
Magnesium - metabolism
,
Male
,
Mg2+ distribution
,
Mg2+ extrusion
,
Myocardium - cytology
,
Rats
,
Rats, Sprague-Dawley
,
Receptors, Adrenergic - metabolism
,
Signal Transduction
,
Streptozocin - pharmacology
,
type-I diabetes
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