Showing papers in "Cell Metabolism in 2012"

TL;DR: Mice under tRF consume equivalent calories from HFD as those with ad lib access yet are protected against obesity, hyperinsulinemia, hepatic steatosis, and inflammation and have improved motor coordination.

TL;DR: Mice treated with a moderate dose of resveratrol showed increased mitochondrial biogenesis and function, AMPK activation, and increased NAD(+) levels in skeletal muscle, whereas SIRT1 knockouts displayed none of these benefits, whereas a mouse overexpressing Sirt1 mimicked these effects.

TL;DR: It is shown that NR supplementation in mammalian cells and mouse tissues increases NAD(+) levels and activates SIRT1 and SIRT3, culminating in enhanced oxidative metabolism and protection against high-fat diet-induced metabolic abnormalities.

TL;DR: The metabolic responses of a MYC-inducible human Burkitt lymphoma model P493 cell line to aerobic and hypoxic conditions, and to glucose deprivation, are determined using stable isotope-resolved metabolomics to demonstrate an alternative energy-generating glutaminolysis pathway involving a glucose-independent TCA cycle.

TL;DR: Progress in understanding conserved, molecular mechanisms of skeletal muscle atrophy/hypertrophy has provided a downstream platform for circumventing the variations and redundancy in upstream mediators and may ultimately translate into new targeted therapies.

TL;DR: New findings that lipolytic products and intermediates participate in cellular signaling processes and that “lipolytic signaling” is particularly important in many nonadipose tissues unveil a previously underappreciated aspect of lipolysis, which may be relevant for human disease.

TL;DR: This Perspective develops a model to explain how lipids and BCAA may synergize to promote metabolic diseases and predicts incident diabetes and intervention outcomes and uniquely responsive to therapeutic interventions.

TL;DR: Results provide evidence that acute gene activation is associated with a dynamic change in DNA methylation in skeletal muscle and suggest that DNA hypomethylation is an early event in contraction-induced gene activation.

TL;DR: Recent findings related to this interconnected network of eicosanoids and inositol phospholipids are reviewed from the perspective of immunity and metabolic disease.

TL;DR: The IRE1α-TXNIP pathway is used in the terminal UPR to promote sterile inflammation and programmed cell death and may be targeted to develop effective treatments for cell degenerative diseases.

TL;DR: It is shown that PPARγ ligands require full agonism to induce a brown fat gene program preferentially in subcutaneous white adipose cells, and that compounds that stabilize PRDM16 protein may represent a plausible therapeutic pathway for the treatment of obesity and diabetes.

TL;DR: It is demonstrated that brown adipocytes that are induced by β3-adrenergic receptor activation in abdominal WAT arise from the proliferation and differentiation of cells expressing platelet-derived growth factor receptor alpha, CD34, and Sca-1 (PDGFRα(+) cells).

TL;DR: Recent progress in understanding the molecular connection between metabolism and epigenetic modifications of chromatin implicated in a variety of diseases including cancer is summarized.

TL;DR: It is reported that thioredoxin-interacting protein (TXNIP) is a critical signaling node that links ER stress and inflammation and is a potential therapeutic target for diabetes and ER stress-related human diseases such as Wolfram syndrome.

TL;DR: The results suggest that the metabolic profiles of tumors are likely to depend on both the genotype and tissue of origin and have implications regarding the design of therapies targeting tumor metabolism.

TL;DR: The genes and mechanisms implicated in these two aging model systems and key remaining issues that need to be addressed for their optimization are reviewed.

TL;DR: This review discusses from a historical perspective the most important discoveries produced over the last decade supporting a role for ceramide and its metabolites in the pathogenesis of insulin resistance and other obesity-associated metabolic diseases.

TL;DR: A mechanism-based strategy to therapeutically suppress atherosclerosis progression and its clinical sequelae is suggested, suggesting a protective process in oxidatively stressed macrophages relevant to plaque necrosis.

TL;DR: Dysregulated cholesterol metabolism in NAFLD is demonstrated which may contribute to disease severity and cardiovascular risks and is associated with increased SREBP-2 maturation, HMG CoA reductase (HMGCR) expression and decreased phosphorylation of HMGCR.

TL;DR: Modulation of SKN-1/Nrf and DAF-16/FoxO may be generally important in the effects of TOR signaling in vivo and that these transcription factors mediate an opposing relationship between growth signals and longevity is concluded.

TL;DR: Results show that autophagy becomes dysfunctional in Atherosclerosis and its deficiency promotes atherosclerosis in part through inflammasome hyperactivation.

TL;DR: Defining the mechanisms regulating macrophage metabolic activity and orchestration of metabolism by macrophages is crucial to pathology and therapeutic intervention.

TL;DR: It is found that CARKL-dependent metabolic reprogramming is required for proper M1- and M2-like macrophage polarization and a rate-limiting requirement for appropriate glucose flux in macrophages polarization is uncovered.

TL;DR: GBM cells utilize mitochondrial glucose oxidation during aggressive tumor growth in vivo, and many of these same activities were conserved in cells cultured ex vivo from the tumors.

TL;DR: Mammalian target of rapamycin complex 2 regulates hepatic glucose and lipid metabolism via insulin-induced Akt signaling to control whole-body metabolic homeostasis and has implications for emerging drug therapies that target mTORC2.

TL;DR: The cellular functions of ER are reviewed, how perturbation of ER homeostasis contributes to metabolic dysregulation and potential causative mechanisms of ER stress in obesity are considered, and a conceptual framework of metabolic roundabout is suggested to integrate key mechanisms of insulin resistance and metabolic diseases.

TL;DR: Genetic evidence that pathological circulating hyperinsulinemia drives diet-induced obesity and its complications is provided and white adipose tissue is reprogrammed to express uncoupling protein 1 and increase energy expenditure.

TL;DR: The saturated FA palmitate induces β cell dysfunction in vivo by activating inflammatory processes within islets by accessing the TLR4/MyD88 pathway and producing chemokines that recruit CD11b(+)Ly-6C(+) M1-type proinflammatory monocytes/macrophages to the islets.

TL;DR: Sterol regulatory element-binding protein (SREBP) transcription factors regulate cellular lipogenesis and lipid homeostasis and the discovery of functions for SREBPs in type II diabetes, cancer, immunity, neuroprotection, and autophagy is revealed.

TL;DR: The pathways utilized by the heart to acquire FAs from the circulation and to store triglyceride intracellularly are reviewed and the known relationships between heart lipid metabolism and dysfunction in humans will be summarized.