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  • 1. Dludla, Phiwayinkosi V.
    et al.
    Nkambule, Bongani B.
    Tiano, Luca
    Louw, Johan
    Jastroch, Martin
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. Helmholtz-Zentrum München, German Research Center for Environmental Health (GmbH), Germany; German Center for Diabetes Research (DZD), Germany.
    Mazibuko-Mbeje, Sithandiwe E.
    Uncoupling proteins as a therapeutic target to protect the diabetic heart2018In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 137, p. 11-24Article, review/survey (Refereed)
    Abstract [en]

    Myocardial remodeling and dysfunction caused by accelerated oxidative damage is a widely reported phenomenon within a diabetic state. Altered myocardial substrate preference appears to be the major cause of enhanced oxidative stress-mediated cell injury within a diabetic heart. During this process, exacerbated free fatty acid flux causes an abnormal increase in mitochondrial membrane potential leading to the overproduction of free radical species and subsequent cell damage. Uncoupling proteins (UCPs) are expressed within the myocardium and can protect against free radical damage by modulating mitochondrial respiration, leading to reduced production of reactive oxygen species. Moreover, transgenic animals lacking UCPs have been shown to be more susceptible to oxidative damage and display reduced cardiac function when compared to wild type animals. This suggests that tight regulation of UCPs is necessary for normal cardiac function and in the prevention of diabetes-induced oxidative damage. This review aims to enhance our understanding of the pathophysiological mechanisms relating to the role of UCPs in a diabetic heart, and further discuss known pharmacological compounds and hormones that can protect a diabetic heart through the modulation of UCPs.

  • 2. El-Seedi, Hesham R.
    et al.
    Khalifa, Shaden A. M.
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Taher, Eman A.
    Farag, Mohamed A.
    Saeed, Aamer
    Gamal, Mohamed
    Hegazy, Mohamed-Elamir F.
    Youssef, Diaa
    Musharraf, Syed G.
    Alajlani, Muaaz M.
    Xiao, Jianbo
    Efferth, Thomas
    Cardenolides: Insights from chemical structure and pharmacological utility2019In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 141, p. 123-175Article, review/survey (Refereed)
    Abstract [en]

    Cardiac glycosides (CGs) are a class of naturally occurring steroid-like compounds, and members of this class have been in clinical use for more than 1500 years. They have been used in folk medicine as arrow poisons, abortifacients, heart tonics, emetics, and diuretics as well as in other applications. The major use of CGs today is based on their ability to inhibit the membrane-bound Na+/K+ -ATPase enzyme, and they are regarded as an effective treatment for congestive heart failure (CHF), cardiac arrhythmia and atrial fibrillation. Furthermore, increasing evidence has indicated the potential cytotoxic effects of CGs against various types of cancer. In this review, we highlight some of the structural features of this class of natural products that are crucial for their efficacy, some methods of isolating these compounds from natural resources, and the structural elucidation tools that have been used. We also describe their physicochemical properties and several modern biotechnological approaches for preparing CGs that do not require plant sources.

  • 3. Mukaida, Saori
    et al.
    Evans, Bronwyn A.
    Bengtsson, Tore
    Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
    Hutchinson, Dana S.
    Sato, Masaaki
    Adrenoceptors promote glucose uptake into adipocytes and muscle by an insulin-independent signaling pathway involving mechanistic target of rapamycin complex 22017In: Pharmacological Research, ISSN 1043-6618, E-ISSN 1096-1186, Vol. 116, p. 87-92Article in journal (Refereed)
    Abstract [en]

    Uptake of glucose into skeletal muscle and adipose tissue plays a vital role in metabolism and energy balance. Insulin released from beta-islet cells of the pancreas promotes glucose uptake in these target tissues by stimulating translocation of CLUT4 transporters to the cell surface. This process is complex, involving signaling proteins including the mechanistic (or mammalian) target of rapamycin (mTOR) and Akt that intersect with multiple pathways controlling cell survival, growth and proliferation. mTOR exists in two forms, mTOR complex 1 (mTORC1), and mTOR complex 2 (mTORC2). mTORC1 has been intensively studied, acting as a key regulator of protein and lipid synthesis that integrates cellular nutrient availability and energy balance. Studies on mTORC2 have focused largely on its capacity to activate Akt by phosphorylation at Ser473, however recent findings demonstrate a novel role for mTORC2 in cellular glucose uptake. For example, agonists acting at beta(2)-adrenoceptors (ARs) in skeletal muscle or beta(3)-ARs in brown adipose tissue increase glucose uptake in vitro and in vivo via mechanisms dependent on mTORC2 but not Akt. In this review, we will focus on the signaling pathways downstream of beta-ARs that promote glucose uptake in skeletal muscle and brown adipocytes, and will highlight how the insulin and adrenergic pathways converge and interact in these cells. The identification of insulin-independent mechanisms that promote glucose uptake should facilitate novel treatment strategies for metabolic disease.

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