PubMed Journal Database | Cell metabolism 
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Showing PubMed Articles 1–25 of 140 from Cell metabolism
Anaerobicizing into pluripotency.
Reprogramming involves multiple layers of molecular regulation, yet it remains relatively unknown how the cell's metabolism is changing and/or contributing to this process. In this issue of Cell Metabolism, Folmes et al. (2011) demonstrate that reprogramming induces a bioenergetic transition from an oxidative to a glycolytic state, and provide evidence to suggest that these changes may precede pluripotency.
The smoking gun in nicotine-induced anorexia.
Hypothalamic pro-opiomelanocortin (POMC) neurons are the major source of anorectic melanocortin peptides in the brain. A recent study (Mineur et al., 2011) demonstrates that nicotine directly stimulates arcuate POMC neurons through nicotinic acetylcholinergic α3β4 receptors, suggesting a new mechanism to understand the inverse relationship between tobacco smoking and body weight.
Aged worms erase epigenetic history.
Defining the molecular events that precipitate multisystem decline is an important component of aging research. In this issue, Jin et al. (2011) show that increased expression of the histone demethylase, utx-1, causes genome-wide decreases in histone H3K27 trimethylation, which includes the insulin/IGF-1 signaling (IIS) pathway that promotes aging.
MicroRNAs (miRNAs) have recently been found to be critical regulators of metabolic homeostasis. A study in Nature by Trajkovski et al. (2011) shows that the highly related miRNAs miR-103 and miR-107 modulate insulin sensitivity and glucose homeostasis in obese mice. These miRNAs might represent therapeutic targets to ameliorate obesity-associated insulin resistance.
The logic linking protein acetylation and metabolism.
Protein acetylation now rivals phosphorylation in frequency of occurrence but is incompletely understood. A picture is presented in which protein acetylation is linked to available energy via the NAD-dependent deacetylases. This model suggests that protein acetylation regulates metabolic strategy and also helps store energy in cells.
Dietary restriction and aging: a unifying perspective.
Dietary restriction (DR) and mutations in nutrient signaling pathways can extend healthy life span in diverse organisms. Studying the interaction between these interventions should reveal mechanisms of aging, but has yielded some apparently contradictory results. A multidimensional representation of nutrition, called the geometric framework, can better describe the responses of life span and other traits, including metabolism, and can reconcile these apparent contradictions. We provide examples showing that...
Epigenetic modifications are thought to be important for gene expression changes during development and aging. However, besides the Sir2 histone deacetylase in somatic tissues and H3K4 trimethylation in germlines, there is scant evidence implicating epigenetic regulations in aging. The insulin/IGF-1 signaling (IIS) pathway is a major life span regulatory pathway. Here, we show that progressive increases in gene expression and loss of H3K27me3 on IIS components are due, at least in part, to increased activi...
Autophagy in Hypothalamic AgRP Neurons Regulates Food Intake and Energy Balance.
Macroautophagy is a lysosomal degradative pathway that maintains cellular homeostasis by turning over cellular components. Here we demonstrate a role for autophagy in hypothalamic agouti-related peptide (AgRP) neurons in the regulation of food intake and energy balance. We show that starvation-induced hypothalamic autophagy mobilizes neuron-intrinsic lipids to generate endogenous free fatty acids, which in turn regulate AgRP levels. The functional consequences of inhibiting autophagy are the failure to upr...
Reduced expression of the Indy (I'm Not Dead, Yet) gene in D. melanogaster and its homolog in C. elegans prolongs life span and in D. melanogaster augments mitochondrial biogenesis in a manner akin to caloric restriction. However, the cellular mechanism by which Indy does this is unknown. Here, we report on the knockout mouse model of the mammalian Indy (mIndy) homolog, SLC13A5. Deletion of mIndy in mice (mINDY(-/-) mice) reduces hepatocellular ATP/ADP ratio, activates hepatic AMPK, induces PGC-1α, inhi...
Ryanodine receptor oxidation causes intracellular calcium leak and muscle weakness in aging.
Age-related loss of muscle mass and force (sarcopenia) contributes to disability and increased mortality. Ryanodine receptor 1 (RyR1) is the skeletal muscle sarcoplasmic reticulum calcium release channel required for muscle contraction. RyR1 from aged (24 months) rodents was oxidized, cysteine-nitrosylated, and depleted of the channel-stabilizing subunit calstabin1, compared to RyR1 from younger (3-6 months) adults. This RyR1 channel complex remodeling resulted in "leaky" channels with increased open prob...
Alternative mRNA splicing provides transcript diversity and may contribute to human disease. We demonstrate that expression of several genes regulating RNA processing is decreased in both liver and skeletal muscle of obese humans. We evaluated a representative splicing factor, SFRS10, downregulated in both obese human liver and muscle and in high-fat-fed mice, and determined metabolic impact of reduced expression. SFRS10-specific siRNA induces lipogenesis and lipid accumulation in hepatocytes. Moreover, Sfr...
Opposing activities of acetyltransferases and deacetylases help regulate energy balance. Mice heterozygous for the acetyltransferase CREB binding protein (CBP) are lean and insulin sensitized, but how CBP regulates energy homeostasis is unclear. In one model, the main CBP interaction with the glucagon-responsive factor CREB is not limiting for liver gluconeogenesis, whereas a second model posits that Ser436 in the CH1 (TAZ1) domain of CBP is required for insulin and the antidiabetic drug metformin to inhibi...
TRIC-A Channels in Vascular Smooth Muscle Contribute to Blood Pressure Maintenance.
TRIC channel subtypes, namely TRIC-A and TRIC-B, are intracellular monovalent cation channels postulated to mediate counter-ion movements facilitating physiological Ca(2+) release from internal stores. Tric-a-knockout mice developed hypertension during the daytime due to enhanced myogenic tone in resistance arteries. There are two Ca(2+) release mechanisms in vascular smooth muscle cells (VSMCs); incidental opening of ryanodine receptors (RyRs) generates local Ca(2+) sparks to induce hyperpolarization, whil...
Cardiotrophin-1 is a key regulator of glucose and lipid metabolism.
Cardiotrophin-1 (CT-1) is a member of the gp130 family of cytokines. We observed that ct-1(-/-) mice develop mature-onset obesity, insulin resistance, and hypercholesterolemia despite reduced calorie intake. Decreased energy expenditure preceded and accompanied the development of obesity. Acute treatment with rCT-1 decreased blood glucose in an insulin-independent manner and increased insulin-stimulated AKT phosphorylation in muscle. These changes were associated with stimulation of fatty acid oxidation, an...
Neuropeptide and peptide hormone secretion from neural and endocrine cells occurs by Ca(2+)-triggered dense-core vesicle exocytosis. The membrane fusion machinery consisting of vesicle and plasma membrane SNARE proteins needs to be assembled for Ca(2+)-triggered vesicle exocytosis. The related Munc13 and CAPS/UNC31 proteins that prime vesicle exocytosis are proposed to promote SNARE complex assembly. CAPS binds SNARE proteins and stimulates SNARE complex formation on liposomes, but the relevance of SNARE bi...
The bioenergetics of somatic dedifferentiation into induced pluripotent stem cells remains largely unknown. Here, stemness factor-mediated nuclear reprogramming reverted mitochondrial networks into cristae-poor structures. Metabolomic footprinting and fingerprinting distinguished derived pluripotent progeny from parental fibroblasts according to elevated glucose utilization and production of glycolytic end products. Temporal sampling demonstrated glycolytic gene potentiation prior to induction of pluripote...
Different metabolic responses of human brown adipose tissue to activation by cold and insulin.
We investigated the metabolism of human brown adipose tissue (BAT) in healthy subjects by determining its cold-induced and insulin-stimulated glucose uptake and blood flow (perfusion) using positron emission tomography (PET) combined with computed tomography (CT). Second, we assessed gene expression in human BAT and white adipose tissue (WAT). Glucose uptake was induced 12-fold in BAT by cold, accompanied by doubling of perfusion. We found a positive association between whole-body energy expenditure and BAT...
Saturated Fatty Acids and snoRNAs: Partners in Crime.
Lipotoxicity describes the process of cellular dysfunction in response to lipid overload. In this issue of Cell Metabolism, Michel and colleagues (2011) provide evidence for a role of snoRNAs in palmitate-induced oxidative stress.
Inflaming hypothalamic neurons raises blood pressure.
Obesity and hypertension are strongly associated, and neural dysfunction has been implicated in both. The hypothalamus integrates signals regulating blood pressure and energy homeostasis. A recent paper in Nature Medicine (Purkayastha et al., 2011) suggests that obesity and hypertension are caused by inflammation in distinct hypothalamic neuronal populations.
Islets have a lot of nerve! Or do they?
The autonomic nervous system influences insulin and glucagon secretion. In this issue, Rodriguez-Diaz et al. (2011) show that mouse and human islets differ in their innervation patterns, yet the effect of neural activation on islet hormone secretion is similar. Key questions raised by this species difference have potential relevance to diabetic therapeutics.
Fluorescent green plaques: light at the end of the catheter?
The field of vascular molecular imaging is searching for the "holy grail" of an imaging technique that will quantitatively and reliably assess vulnerable coronary plaques. Fluorescence imaging with indocyanine green specifically identifies lipid-rich plaques in rabbits and in humans and represents a promising, though invasive, approach.
Hormonal regulation of hepatic glucose production in health and disease.
We review mechanisms that regulate production of glucose by the liver, focusing on areas of budding consensus, and endeavoring to provide a candid assessment of lingering controversies. We also attempt to reconcile data from tracer studies in humans and large animals with the growing compilation of mouse knockouts that display changes in glucose production. A clinical hallmark of diabetes, excessive glucose production remains key to its treatment. Hence, we attempt to integrate emerging pathways into the br...
Through unknown mechanisms, insulin activates the sterol regulatory element-binding protein (SREBP1c) transcription factor to promote hepatic lipogenesis. We find that this induction is dependent on the mammalian target of rapamycin (mTOR) complex 1 (mTORC1). To further define the role of mTORC1 in the regulation of SREBP1c in the liver, we generated mice with liver-specific deletion of TSC1 (LTsc1KO), which results in insulin-independent activation of mTORC1. Surprisingly, the LTsc1KO mice are protected fr...
Small Nucleolar RNAs U32a, U33, and U35a Are Critical Mediators of Metabolic Stress.
Lipotoxicity is a metabolic stress response implicated in the pathogenesis of diabetes complications and has been shown to involve lipid-induced oxidative stress. To elucidate the molecular mechanisms of lipotoxicity, we used retroviral promoter trap mutagenesis to isolate a cell line that is resistant to lipotoxic and oxidative stress. We show that loss of three box C/D small nucleolar RNAs (snoRNAs) encoded in the ribosomal protein L13a (rpL13a) locus is sufficient to confer resistance to lipotoxic and ox...
Innervation patterns of autonomic axons in the human endocrine pancreas.
The autonomic nervous system regulates hormone secretion from the endocrine pancreas, the islets of Langerhans, thus impacting glucose metabolism. The parasympathetic and sympathetic nerves innervate the pancreatic islet, but the precise innervation patterns are unknown, particularly in human. Here we demonstrate that the innervation of human islets is different from that of mouse islets and does not conform to existing models of autonomic control of islet function. By visualizing axons in three dimensions...
