Regulation of Hepatic Energy Metabolism and Gluconeogenesis by BAD

Giménez-Cassina, Alfredo; García-Haro, Luisa; Choi, Cheol Soo; Osundiji, Mayowa A.; Lane, Elizabeth A.; Hu, Huang; Yıldırım, Muhammed A.; Szlyk, Benjamin; Fisher, Jill K.; Polak, Klaudia; Patton, Elaura; Wiwczar, Jessica; Godes, Marina; Lee, Dong Hoon; Robertson, Kirsten; Kim, Sheene; Kulkarni, Ameya; Distefano, Alberto; Samuel, Varman T.; Cline, Gary W.; Kim, Young–Bum; Shulman, Gerald I.; Danial, Nika N.

doi:10.1016/j.cmet.2013.12.001

Cited by 69 publications

(102 citation statements)

References 43 publications

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“…The assessment of lactate production as an indication of glycolytic flux was performed as previously described with slight modifications63. Cells were seeded in M12 well plates, at a density of 50× 10E5 cells per well.…”

Section: Methodsmentioning

confidence: 99%

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Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness

Peng

Giménez-Cassina

Petrus

et al. 2016

Sci Rep

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Recently thioredoxin reductase 1 (TrxR1), encoded by Txnrd1, was suggested to modulate glucose and lipid metabolism in mice. Here we discovered that TrxR1 suppresses insulin responsiveness, anabolic metabolism and adipocyte differentiation. Immortalized mouse embryonic fibroblasts (MEFs) lacking Txnrd1 (Txnrd1−/−) displayed increased metabolic flux, glycogen storage, lipogenesis and adipogenesis. This phenotype coincided with upregulated PPARγ expression, promotion of mitotic clonal expansion and downregulation of p27 and p53. Enhanced Akt activation also contributed to augmented adipogenesis and insulin sensitivity. Knockdown of TXNRD1 transcripts accelerated adipocyte differentiation also in human primary preadipocytes. Furthermore, TXNRD1 transcript levels in subcutaneous adipose tissue from 56 women were inversely associated with insulin sensitivity in vivo and lipogenesis in their isolated adipocytes. These results suggest that TrxR1 suppresses anabolic metabolism and adipogenesis by inhibition of intracellular signaling pathways downstream of insulin stimulation.

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Section: Methodsmentioning

confidence: 99%

“…Oxygen consumption rate (OCR) in real time on MEFs was performed using an Extracellular Flux Analyzer X24-3 (Seahorse Bioscience, Billerica, MA, USA) as previously described63. Cells were seeded at a density of 50x 10E3 cells/well.…”

Section: Methodsmentioning

confidence: 99%

Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness

Peng

Giménez-Cassina

Petrus

et al. 2016

Sci Rep

Self Cite

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“…In addition to apoptotic cell death, the extended Bcl-2 family of proteins (Aouacheria et al, 2015), interact to exert many effects in healthy cells that are distinct from apoptotic processes (Chau et al, 2000; Chen et al, 2011; Cheng et al, 1996; Chipuk et al, 2005; Fannjiang et al, 2003; Gimenez-Cassina et al, 2014; Hosoi et al, 2017; White et al, 2005; Yi et al, 2011). In this capacity, Bcl-2 family proteins interact physically or functionally with a remarkably broad range of other proteins and lipids, the full extent of which is difficult to assimilate and comprehend.…”

Section: Introductionmentioning

confidence: 99%

Connecting mitochondrial dynamics and life-or-death events via Bcl-2 family proteins

Aouacheria

Baghdiguian

Lamb

et al. 2017

Neurochemistry International

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The morphology of a population of mitochondria is the result of several interacting dynamical phenomena, including fission, fusion, movement, elimination and biogenesis. Each of these phenomena is controlled by underlying molecular machinery, and when defective can cause disease. New understanding of the relationships between form and function of mitochondria in health and disease is beginning to be unraveled on several fronts. Studies in mammals and model organisms have revealed that mitochondrial morphology, dynamics and function appear to be subject to regulation by the same proteins that regulate apoptotic cell death. One protein family that influences mitochondrial dynamics in both healthy and dying cells is the Bcl-2 protein family. Connecting mitochondrial dynamics with life-death pathway forks may arise from the intersection of Bcl-2 family proteins with the proteins and lipids that determine mitochondrial shape and function. Bcl-2 family proteins also have multifaceted influences on cells and mitochondria, including calcium handling, autophagy and energetics, as well as the subcellular localization of mitochondrial organelles to neuronal synapses. The remarkable range of physical or functional interactions by Bcl-2 family proteins is challenging to assimilate into a cohesive understanding. Most of their effects may be distinct from their direct roles in apoptotic cell death and are particularly apparent in the nervous system. Dual roles in mitochondrial dynamics and cell death extend beyond BCL-2 family proteins. In this review, we discuss many processes that govern mitochondrial structure and function in health and disease, and how Bcl-2 family proteins integrate into some of these processes.

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“…For instance, phosphorylated BAD can promote hepatic glycolysis by activating glucokinase in response to the fed state. 44 Also, proteins from the BCL2 family have been shown to modulate the balance between mitochondrial fission and fusion. In this regard, mitochondrial fission has been generally associated with apoptotic cell death.…”

Section: Mitochondrial Dynamics and Cell Deathmentioning

confidence: 99%

Mitochondrial dynamics and cancer

et al. 2017

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Cancer is among the leading causes of death worldwide, and the number of new cases continues to rise. Despite recent advances in diagnosis and therapeutic strategies, millions of cancer-related deaths occur, indicating the need for better therapies and diagnostic strategies. Mitochondria and metabolic alterations have been recognized as important for cancer progression. However, a more precise understanding of how to manipulate mitochondria-related processes for cancer therapy remains to be established. Mitochondria are highly dynamic organelles which continually fuse and divide in response to diverse stimuli. Participation in the aforementioned processes requires a precise regulation at many levels that allows the cell to couple mitochondrial activity to nutrient availability, biosynthetic demands, proliferation rates, and external stimuli. The many functions of these organelles are intimately linked to their morphology. Recent evidence suggests an important link between mitochondrial morphology and disease, including neurodegenerative, inflammatory diseases and cancer. Here, we review recent advances in the understanding of mitochondrial dynamics with a special focus on its relationship to tumor progression.

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Regulation of Hepatic Energy Metabolism and Gluconeogenesis by BAD

Cited by 69 publications

References 43 publications

Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness

Thioredoxin reductase 1 suppresses adipocyte differentiation and insulin responsiveness

Connecting mitochondrial dynamics and life-or-death events via Bcl-2 family proteins

Mitochondrial dynamics and cancer

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