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Most relevant scientific articles
• Mir-Coll J., Durán J., Slebe F., García-Rocha M., Gomis R., Gasa R. et al. genetic models rule out a major role of beta cell glycogen in the control of glucose homeostasis. Diabetologia. 2016:1-9.
• Slebe F., Rojo F., Vinaixa M., García -Rocha M., Testoni G., Guiu M. et al. FoxA and LIPg endothelial lipase control the uptake of extracellular lipids for breast cancer growth. nature Communications. 2016;7.
• Díaz-Lobo M., Concia A.L., Gómez L., Clapes P., Fita I., Guinovart J.J. et al. Inhibitory properties of 1,4-dideoxy-1,4-imino-d-arabinitol (DAB) derivatives acting on glycogen metabolising enzymes. Organic and Biomolecular Chemistry. 2016;14(38):9105-9113.
• Maldonado R., Mancilla H., Villarroel-Espindola F., Slebe F., Slebe J.C., Mendez R. et al. glycogen Synthase in Sertoli Cells: More Than glycogenesis? Journal of Cellular Biochemistry. 2016.
• Krag T.O., Pinos T., Nielsen T.L., Durán J., García-Rocha M., Andreu A.L. et al. Differential glucose metabolism in mice and humans affected by McArdle disease. American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2016;311(2):R307-R314.
Highlights
• Glycogen accumulation in beta cells of diabetic patients has been proposed to partly mediate glucotoxicity-induced beta cell dysfunction. We studied glucose homeostasis in mice with (1) defective glycogen synthesis and (2) excessive glycogen accumulation in beta cells. Our results demonstrated that glycogen metabolism is not required for the maintenance of beta cell function. Furthermore, glycogen accumulation in beta cells alone is not sufficient to trigger the dysfunction or loss of these cells (Mir-Coll et al., Diabetologia 2016).
• To examine the involvement of the hepatic branch of the vagus nerve in the regulation of food intake and glucose homeostasis by liver glycogen, we performed vagotomy on mice that overaccumulate glycogen in the liver. Our results confirmed that this regulation of food intake and glucose homeostasis by liver glycogen is dependent on the hepatic branch of the vagus nerve (López-Soldado et al, second revision in Diabetologia).
• Glycogenin (GYG) is considered to be indispensable for the synthesis of glycogen, acting as primer
of the glucose chain. We generated a gYg-KO mouse. Surprisingly, gYg-KO mice not only maintain their ability to synthesise glycogen, but accumulate high levels of the polysaccharide in skeletal and cardiac muscle. Recently, several patients with GYG1 loss of function that are affected by high glycogen storage in muscle fibers have been identified. Our results contribute to understanding this new type
of glycogenosis and challenge the role of GYG in glycogen metabolism (Testoni et al, in revision in Cell
Metabolism).
• We found that breast cancer cells are dependent on a mechanism to supply precursors for intracellular
lipid production that are derived from extracellular sources and that the endothelial lipase LIPG fulfils this function. The downregulation of LIPg in transformed cells results in decreased proliferation and impaired synthesis of intracellular lipids (Slebe et al., Nature Communications 2016).
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