Abstract: The present invention relates to a kit-of-parts comprising at least one mitochondrial uncoupler and at least one cationic amphiphilic drug and its use in medicine. The invention further relates to a pharmaceutical composition comprising at least one mitochondrial uncoupler and at least one cationic amphiphilic drug for use in medicine. Moreover, the invention is directed to the kit-of-parts and the pharmaceutical composition for use in the treatment of cancer, in particular glioma, pancreatic cancer, small cell lung cancer, metastatic prostate cancer, liver cancer and triple-negative breast cancer.

Abstract: The present invention relates to composition comprising an inhibitor of miR-379 or a portion or fragment thereof and an inhibitor of miR-541 or a portion or fragment thereof, and/or an inhibitor of the target site of miR-379 or a portion or fragment thereof and an inhibitor of the target site of miR-541 or a portion or fragment thereof, and/or a combination of an inhibitor of miR-379 or a portion or fragment thereof and an inhibitor of the target site of miR-541 or a portion or fragment thereof or a combination of an inhibitor of the target site of miR-379 or a portion or fragment thereof and an inhibitor of miR-541 or a portion or fragment thereof. The present invention also relates to the respective composition for use in treating or preventing a metabolic disease, a disease related to a metabolic disorder, and/or cancer.

Abstract: The present invention relates to oligonucleotide inhibitors of the TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in a mammal.

Abstract: The present invention relates to oligonucleotide inhibitors of the TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in a mammal.

Abstract: The present invention relates to oligonucleotide inhibitors of the TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in a mammal.

Abstract: The present invention discloses microRNAs (miR) involved in the regulation of the lipid and glucose metabolism. Several conserved miR molecules were found as direct targets of the glucocorticoid hormone/glucocorticoid receptor signaling axis. Hence, the present invention pertains to inhibitors of these miRs—such as antimiRs and blockmiRs—as well as isolated miR molecules or miR expression constructs for the treatment or prevention of metabolic disorders caused by deregulated glucocorticoid signaling, such as insulin resistance, the metabolic syndrome, obesity and/or diabetes type II. Particular preferred embodiments of the invention pertain to antagonists or agonists of a miR of the conserved miR-379-410 cluster, particularly of miR-379.

Abstract: The present invention relates to modulators, in particular inhibitors, of TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in mammal. The present invention further relates to screening methods in order to identify these modulators, the use of modulators as identified in the diagnosis of these diseases, as well as kits, comprising materials for performing the methods according to the present invention.

Abstract: The present invention relates to oligonucleotide inhibitors of the TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in a mammal.

Abstract: The present invention discloses microRNAs (miR) involved in the regulation of the lipid and glucose metabolism. Several conserved miR molecules were found as direct targets of the glucocorticoid hormone/glucocorticoid receptor signaling axis. Hence, the present invention pertains to inhibitors of these miRs—such as antimiRs and blockmiRs—as well as isolated miR molecules or miR expression constructs for the treatment or prevention of metabolic disorders caused by deregulated glucocorticoid signaling, such as insulin resistance, the metabolic syndrome, obesity and/or diabetes type II. Particular preferred embodiments of the invention pertain to antagonists or agonists of a miR of the conserved miR-379-410 cluster, particularly of miR-379.

Abstract: The present invention relates to modulators, in particular inhibitors, of TSC22D4 activity or expression and their uses for the prevention, treatment, and/or regulation of insulin resistance, metabolic syndrome and/or diabetes and/or for improving insulin sensitivity in mammal. The present invention further relates to screening methods in order to identify these modulators, the use of modulators as identified in the diagnosis of these diseases, as well as kits, comprising materials for performing the methods according to the present invention.

Abstract: The present invention describes modulator of protein kinase B (PKB)/Akt proteins, exemplified by the Tribbles (TRB) family. An exemplary member of the TRB family, TRB-3, binds to Akt and inhibits its catalytic activity, in turn causing altered regulation of glucose metabolism pathways. TRB-3 expression is strongly induced in the fasting state, and upregulated in mouse models of type II, causing disruptions in insulin signaling. Accordingly, the present invention further provides compositions and methods for disrupting the interaction between such a modulator and PKB/Akt protein kinases. Also provided are methods of determining if a subject has a predisposition to impaired glucose regulation and methods for treating diabetes mellitus using invention compositions.

Abstract: In accordance with the present invention, it has been discovered that CREB regulates hepatic gluconeogenesis via the co-activator, PGC-1. PGC-1 potentiated glucocorticoid induction of the gene for PEPCK, the rate limiting enzyme in gluconeogenesis, via the glucocorticoid response unit in the promoter, indicating that activation of PGC-1 by CREB in liver contributes to the pathogenesis of diabetes mellitus. In accordance with the above discoveries, the present invention provides a method of identifying a compound that modulates gluconeogenesis. The invention method comprises contacting CREB and a nucleic acid comprising a PGC-1 promoter with a test compound, and determining if the test compound modulates binding between CREB and the PGC-1 promoter.