ArticleProceedings of the National Academy of Sciences of the United States of America2006
Hypothalamic malonyl-CoA triggers mitochondrial biogenesis and oxidative gene expression in skeletal muscle: Role of PGC-1alpha.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 67 citations in OpenAlex.
- Associations of fatty acids in cerebrospinal fluid with peripheral glucose concentrations and energy metabolism.PloS one · 2012Trial
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- CPT1C deficiency in SF1 neurons impairs early metabolic adaptation to dietary fats, leading to obesity.Molecular metabolism · 2025Article
- The mRNA-lncRNA landscape of multiple tissues uncovers key regulators and molecular pathways that underlie heterosis for feed intake and efficiency in laying chickens.Genetics, selection, evolution : GSE · 2023Article
- Postnatal induction of muscle fatty acid oxidation in mice differing in propensity to obesity: a role of pyruvate dehydrogenase.International journal of obesity (2005) · 2020Article
- Fatty acid synthase regulates estrogen receptor-α signaling in breast cancer cells.Oncogenesis · 2017Article
- The central administration of C75, a fatty acid synthase inhibitor, activates sympathetic outflow and thermogenesis in interscapular brown adipose tissue.Pflugers Archiv : European journal of physiology · 2013Article
- Regulatory role of leptin in glucose and lipid metabolism in skeletal muscle.Indian journal of endocrinology and metabolism · 2012Article
- AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity.Journal of lipid research · 2012Article
- Mitochondrial biogenesis and increased uncoupling protein 1 in brown adipose tissue of mice fed a ketone ester diet.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012Article
- Transcriptional Regulation by Nuclear Corepressors and PGC-1α: Implications for Mitochondrial Quality Control and Insulin Sensitivity.PPAR research · 2012Article
- O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- MAPK phosphatase-1 facilitates the loss of oxidative myofibers associated with obesity in mice.The Journal of clinical investigation · 2009Article
- Insulin-stimulated cardiac glucose oxidation is increased in high-fat diet-induced obese mice lacking malonyl CoA decarboxylase.Diabetes · 2009Article
- Article
- Mitochondrial biogenesis and healthy aging.Experimental gerontology · 2008Review
- Hypothalamic malonyl-coenzyme A and the control of energy balance.Molecular endocrinology (Baltimore, Md.) · 2008Review
- Brain-specific carnitine palmitoyl-transferase-1c: role in CNS fatty acid metabolism, food intake, and body weight.Journal of neurochemistry · 2008Article
- Regulation of hypothalamic malonyl-CoA by central glucose and leptin.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Brain fatty acid synthase activates PPARalpha to maintain energy homeostasis.The Journal of clinical investigation · 2007Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous investigations show that intracerebroventricular administration of a potent inhibitor of fatty acid synthase, C75, increases the level of its substrate, malonyl-CoA, in the hypothalamus. The "malonyl-CoA signal" is rapidly transmitted to skeletal muscle by the sympathetic nervous system, increasing fatty acid oxidation, uncoupling protein-3 (UCP3) expression, and thus, energy expenditure. Here, we show that intracerebroventricular or intraperitoneal administration of C75 increases the number of mitochondria in white and red (soleus) skeletal muscle. Consistent with signal transmission from the hypothalamus by the sympathetic nervous system, centrally administered C75 rapidly (< or =2 h) up-regulated the expression (in skeletal muscle) of the beta-adrenergic signaling molecules, i.e., norepinephrine, beta3-adrenergic receptor, and cAMP; the transcriptional regulators peroxisomal proliferator activator regulator gamma coactivator 1alpha (PGC-1alpha) and estrogen receptor-related receptor alpha (ERRalpha); and the expression of key oxidative mitochondrial enzymes, including pyruvate dehydrogenase kinase, medium-chain length fatty acyl-CoA dehydrogenase, ubiquinone-cytochrome c reductase, cytochrome oxidase, as well as ATP synthase and UCP3. The role of PGC-1alpha in mediating these responses in muscle was assessed with C2C12 myocytes in cell culture. Consistent with the in vivo response, adenovirus-directed expression of PGC-1alpha in C2C12 muscle cells provoked the phosphorylation/inactivation and reduced expression of acetyl-CoA carboxylase 2, causing a reduction of the malonyl-CoA concentration. These effects, coupled with an increased carnitine palmitoyltransferase 1b, led to increased fatty acid oxidation. PGC-1alpha also increased the expression of ERRalpha, PPARalpha, and enzymes that support mitochondrial fatty acid oxidation, ATP synthesis, and thermogenesis, apparently mediated by an increased expression of UCP3.
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