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Can Malaria cause Diabetes?

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One Response to “Can Malaria cause Diabetes?”

  1. aneurodoc125 says:

    Actually, there is an article saying it may reverse type II diabetes. It does not cause Diabetes to my knowlege. I would appreciate a reference from the responder that says it can.

    Reversal of Type 2 Diabetes in Mice by Products of Malaria Parasites: II. Role of Inositol Phosphoglycans (IPGs)

    References and further reading may be available for this article. To view references and further reading you must purchase this article.

    K. M. Elaseda, 1, K. A. Gumaaa, J. B. de Souzab, H. Rahmounea, J. H. L. Playfairb and T. W. Rademacherc

    a Rademacher Group Ltd, Arthur Stanley House, 6th Floor, 40-50 Tottenham Street, London, W1P 9PG, United Kingdom

    b Department of Immunology, Molecular Medicine Unit, UCL Medical School, Windeyer Building, 46 Cleveland Street, London, W1P 6DB, United Kingdom

    c Department of Molecular Pathology, Molecular Medicine Unit, UCL Medical School, Windeyer Building, 46 Cleveland Street, London, W1P 6DB, United Kingdom

    Received 5 February 2001; revised 29 March 2001. Available online 22 February 2002.

    Abstract
    We have previously shown that infection with Plasmodium yoelii malaria or injection of extracts from malaria-parasitized red cells induces hypoglycemia in normal mice and normalizes the hyperglycemia in mice made moderately diabetic with streptozotocin. Inositol phosphoglycans (IPGs) are released outside cells by hydrolysis of membrane-bound glycosylphosphatidylinositols (GPIs), and act as second messengers mediating insulin action. The C57BL/Ks-db/db and C57BL/6J-ob/ob mice offer good models for studies on human obesity and Type 2 diabetes. In the present study, we show that a single iv injection of IPG-A or IPG-P extracted from P. yoelii significantly (P < 0.02) lowers the blood glucose in STZ-diabetic, db/db, and in ob/ob mice for at least 4–6 h. Using rat white adipocytes, IPG-P increased lipogenesis by 20–30% in the presence and absence of maximal concentrations of insulin (10−8 M) (P < 0.01) and stimulated pyruvate dehydrogenase (PDH) phosphatase in a dose-related manner. Both IPG-A and IPG-P inhibited c-AMP-dependent protein kinase (PKA) in a dose-related manner. Compositional analysis of IPGs after 24 h hydrolysis revealed the presence of myo-inositol, phosphorus, galactosamine, glucosamine, and glucose in both IPG-A and IPG-P. However, hydrolysis of IPGs for 4 h highlighted differences between IPG-A and IPG-P. There are some functional similarities between P. yoelii IPGs and those previously described for mammalian liver. However, this is the first report of the hypoglycemic effect of IPGs in murine models of Type 2 diabetes. We suggest that IPGs isolated from P. yoelii, when fully characterized, may provide structural information for the synthesis of new drugs for the management of diabetes mellitus.

    Author Keywords: diabetes; malaria; glucose; inositol phosphoglycans; lipogenesis

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