Searchable abstracts of presentations at key conferences in endocrinology

ea0065oc1.5 | Metabolism and Obesity | SFEBES2019

Prolyl-hydroxylase 3 maintains β-cell glucose-sensing under metabolic stress

Cuozzo Federica , Nasteska Daniela , Thakker Alpesh , Westbrook Rebecca , Bakar Rula Bany , Cantley James , Tennant Daniel , Hodson David J

Aims: Prolyl-4 hydroxylase domain protein 3 (PHD3) is an alpha ketoglutarate-dependent dioxygenase involved in the oxygen-dependent regulation of cell phenotype. While PHD3 has been reported to suppress insulin sensitivity in the liver, little is known about effects of the enzyme in insulin-secreting β-cells.Methods: βPHD3−/− mice were generated by crossing the Ins1Cre driver line with animals bearing a floxed Egln3</...

ea0044p187 | Obesity and Metabolism | SFEBES2016

NAD+ supplementation normalises central carbon metabolism in skeletal muscle: a mechanistic insight into the energetic consequences of age-related NAD+ decline

Oldacre-Bartley Lucy , Fletcher Rachel , Hollinshead Kate , Elhassan Yasir , Doig Craig , Tennant Daniel , Ludwig Christian , Lavery Gareth

A decline in skeletal muscle nicotinamide adenine dinucleotide (NAD+) can decrease mitochondrial function and energy metabolism in age-related metabolic disease. Restoration of NAD+ using the precursor nicotinamide riboside (NR) may serve to support age and disease driven impairment of mitochondrial energy metabolism. Manipulating NAD+, and consequently cellular pyridine nucleotide NAD(P)(H) pools, may impact the flux of glucose through intermediary energy metabolism pathways....

ea0050s5.2 | Beyond paragangliomas | SFEBES2017

Identification of novel therapeutic targets in SDH-mutated cancers: tracing dysfunction

Lussey-Lepoutre Charlotte , Hollinshead Kate E R , Ludwig Christian , Menara Melanie , Morin Aurelie , Gimenez-Roqueplo Anne-Paule , Favier Judith , Tennant Daniel A

Since the discovery of mutations in succinate dehydrogenase (SDH) complex early this century, it has been shown that tumours underpinned by deficiencies in this metabolic enzyme will demonstrate altered cell metabolism. However, the precise nature of these changes remains poorly described. The metabolic network within cells is highly redundant, with multiple pathways capable of synthesising the required building blocks for cell growth. By the very fact that SDH-deficient cells...

ea0050s5.2 | Beyond paragangliomas | SFEBES2017

Identification of novel therapeutic targets in SDH-mutated cancers: tracing dysfunction

Lussey-Lepoutre Charlotte , Hollinshead Kate E R , Ludwig Christian , Menara Melanie , Morin Aurelie , Gimenez-Roqueplo Anne-Paule , Favier Judith , Tennant Daniel A

Since the discovery of mutations in succinate dehydrogenase (SDH) complex early this century, it has been shown that tumours underpinned by deficiencies in this metabolic enzyme will demonstrate altered cell metabolism. However, the precise nature of these changes remains poorly described. The metabolic network within cells is highly redundant, with multiple pathways capable of synthesising the required building blocks for cell growth. By the very fact that SDH-deficient cells...