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Metabolic Signaling and Disease
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Belly fat differs from thigh fat
Researchers discovered that the genes active in a person’s belly fat are significantly different from those in his or her thigh fat, a finding that could shift the way we approach unwanted belly fat—from banishing it to relocating it.
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Obesity research advances to clinical testing
Discoveries made in the laboratories of Sanford-Burnham will, for the first time, advance to the clinical research at the Florida Hospital – Sanford-Burnham Translational Research Institute for Metabolism and Diabetes (TRI).
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Super athletic mice burn more sugar
Sanford-Burnham scientists are unraveling a mechanism that re-programs metabolic genes in muscles in a way that increases their capacity to use sugar. When activated in mice, this metabolic re-programming dramatically improves exercise performance.
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Studying metabolic signaling and disease
Researchers in the Metabolic Signaling and Disease Program study how organs and cells work together to respond to biological and environmental challenges that lead to the development and progression of metabolic diseases such as diabetes and obesity. The program brings together investigators with complementary expertise in cell and molecular biology, chemistry, and physiology to understand mechanisms that regulate metabolic flow, energy expenditure, and appetite control. Since metabolic changes are also fundamental to many other pathological conditions, ranging from Alzheimer's disease to cancer, the basic principles of our research will also provide insight and therapeutic avenues for combating other major human diseases.
Research - Diabetes and Obesity - Metabolic Signaling: About |
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Mutidisciplinary teams within the program study how extrinsic and intrinsic cell signaling networks integrate with gene-regulatory mechanisms involved in energy generation and storage pathways to influence the biologic and physiologic mechanisms of metabolic disease. This holistic approach is essential to understanding how different organ systems communicate together to provide metabolic balance for the entire body.
How our research helps improve health
When the metabolic system is out of balance due to genetic, environmental, or dietary factors, diseases such as obesity and diabetes develop. An estimated 60 percent of the U.S. adult population is overweight or obese. By understanding the molecular regulatory mechanisms that maintain metabolic homeostasis, our scientists can identify new drug targets that will be exploited for novel therapies to reverse the extreme rise in the incidence of type 2 diabetes that has occurred over the past several decades.
Research - Diabetes and Obesity - Metabolic Signaling: How Our
Research Helps |
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Sterol regulatory element-binding proteins are essential for the metabolic programming of effector T cells and adaptive immunity.
Kidani Y, Elsaesser H, Hock MB, Vergnes L, Williams KJ, Argus JP, Marbois BN, Komisopoulou E, Wilson EB, Osborne TF, Graeber TG, Reue K, Brooks DG, Bensinger SJ.
Nat Immunol. 2013 May;14(5):489-99. doi: 10.1038/ni.2570. Epub 2013 Apr 7.
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Imbalance between Neutrophil Elastase and its Inhibitor α1-Antitrypsin in Obesity Alters Insulin Sensitivity, Inflammation, and Energy Expenditure.
Mansuy-Aubert V, Zhou QL, Xie X, Gong Z, Huang JY, Khan AR, Aubert G, Candelaria K, Thomas S, Shin DJ, Booth S, Baig SM, Bilal A, Hwang D, Zhang H, Lovell-Badge R, Smith SR, Awan FR, Jiang ZY.
Cell Metab. 2013 Apr 2;17(4):534-48. doi: 10.1016/j.cmet.2013.03.005.
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Multidomain integration in the structure of the HNF-4α nuclear receptor complex.
Chandra V, Huang P, Potluri N, Wu D, Kim Y, Rastinejad F.
Nature. 2013 Mar 21;495(7441):394-8. doi: 10.1038/nature11966. Epub 2013 Mar 13.
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Nine months of combined training improves ex vivo skeletal muscle metabolism in individuals with type 2 diabetes.
Sparks LM, Johannsen NM, Church TS, Earnest CP, Moonen-Kornips E, Moro C, Hesselink MK, Smith SR, Schrauwen P.
J Clin Endocrinol Metab. 2013 Apr;98(4):1694-702. doi: 10.1210/jc.2012-3874. Epub 2013 Mar 5.
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Integrating muscle cell biochemistry and whole-body physiology in humans:(31)P-MRS data from the InSight trial.
Edwards LM, Kemp GJ, Dwyer RM, Walls JT, Fuller H, Smith SR, Earnest CP.
Sci Rep. 2013;3:1182. doi: 10.1038/srep01182. Epub 2013 Jan 31.
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Central glucagon-like peptide 1 receptor-induced anorexia requires glucose metabolism-mediated suppression of AMPK and is impaired by central fructose.
Burmeister MA, Ayala J, Drucker DJ, Ayala JE.
Am J Physiol Endocrinol Metab. 2013 Apr;304(7):E677-85. doi: 10.1152/ajpendo.00446.2012. Epub 2013 Jan 22.
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