Homework 01 [email protected] (11) 99497 -7773 1 Esta p rimeir a tarefa visa verificar qual o seu nível e começar a mapear quais são as suas dificuldades de t radução. Traduza o texto abaixo. Use seu d icionár io e marqu e o tempo que a tarefa toma. Se não conseguir traduzir tudo, traduza o quanto der. Clues to how drug reverses obesity, diabetes, fatty liver disease A Researchers at the University of Michigan have identified how a promising drug in clinical trials for the treatment of obesity and related metabolic disorders improves the metabolism of sugar by generating a new signal between fat cells and the liver. In a ddition to illuminating how the drug, amlexanox, reverses obesity, diabetes and fatty liver disease, the findings suggest a new pathway for future treatments. The research was published Jan.12 in Nature Communications. B Investigators in the lab of Alan Saltiel, the Mary Sue Coleman Director of U-M's Life Sciences Institute, had previously discovered that this drug, which had been used in the treatment of asthma, also has the ability to cause weight loss and improve diabetes in obese mice. The current study revealed that amlexanox exerts its effects through a specialized type of fat cell by increasing the level of a second messenger molecule called cAMP. In turn, cAMP increases the rate by which cells "burn" fat so that the animal loses weight. But amlexan o x also triggers the release of the hormone interleukin-6 from these fat cells, which then travels in the circulation to the liver. In the livers of diabetic mice, interleukin-6 reduces production of glucose, so that ov erall blood suga r is lowered. "We know that amlexanox works to reverse obesity and insulin resistance in part by resolving chronic inflammation and increasing energy expenditure, but that's not the whole story of the drug's effects," said Shannon Reilly, first author of the study. "Understanding how the drug also enables crosstalk between fat cells and the liver in obese mice allows us to see more of the amlexan ox picture—and also sheds light on communica tion between different tissues in the body." C The finding is the latest piece of a complex obesity-inflammation-diabe tes puzzle that Saltiel lab investigators have been working to solve in order to find new treatments for metabolic disorders. Obesity lea ds to a state of chronic , low-grade inflamm ation in liver and fat tissue, which in turn increases the levels of a pair of kinases: IKK-ε and TBK1. In 2009, the Saltiel lab defined a key role of IKK-ε and TBK1 in the onset of obesity. In 2013, the researchers discovered that amlexanox, an off-patent drug currently prescr ibed for the treatment of asthma and other uses, reversed obesity, diabetes and fatty liver in mice. In research published in December 2013, the i nvestigators found that high levels of IKK-ε and TBK1 meant that certain receptors in the fa t cells of obes e mice we re unable to respond to neurotransm itters called catecholamines, which are generated by the sympathetic nervous system and promote "fat- burning." High levels of IKK-ε and TBK1 also resulted in lower levels of cAMP. Amlexano x reduces IKK-ε and TBK1, leading to higher cAMP , increased sensitivity to catec holamines and increased energy expenditure by the fat cells. The U-M study explains how increased cAMP in fat cells promo tes the secretion o f the hormone inter leukin-6, which signals the liver to stop producing glucose —thus improv ing overall blood sug ar levels in obe se diabetic mice.

HW01. Drug Reverses Obesity

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English Reading Homework for Pharmacology

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Homework 01

[email protected] (11) 99497-7773

1

Esta primeira tarefa visa verificar qual o seu nvel e comear a mapear quais so assuas dificuldades de traduo. Traduza o texto abaixo. Use seu dicionrio e marqueo tempo que a tarefa toma. Se no conseguir traduzir tudo, traduza o quanto der.Clues to how drug reverses obesity, diabetes, fatty liver disease

AResearchers at the University of Michigan have identified how a promising drug in clinical

trials for the treatment of obesity and related metabolic disorders improves the metabolism ofsugar by generating a new signal between fat cells and the liver. In addition to illuminating howthe drug, amlexanox, reverses obesity, diabetes and fatty liver disease, the findings suggest anew pathway for future treatments. The research was published Jan.12 in NatureCommunications.

BInvestigators in the lab of Alan Saltiel, the Mary Sue Coleman Director of U-M's Life

Sciences Institute, had previously discovered that this drug, which had been used in thetreatment of asthma, also has the ability to cause weight loss and improve diabetes in obesemice. The current study revealed that amlexanox exerts its effects through a specialized type offat cell by increasing the level of a second messenger molecule called cAMP. In turn, cAMPincreases the rate by which cells "burn" fat so that the animal loses weight. But amlexanox alsotriggers the release of the hormone interleukin-6 from these fat cells, which then travels in thecirculation to the liver. In the livers of diabetic mice, interleukin-6 reduces production ofglucose, so that overall blood sugar is lowered. "We know that amlexanox works to reverseobesity and insulin resistance in part by resolving chronic inflammation and increasing energyexpenditure, but that's not the whole story of the drug's effects," said Shannon Reilly, firstauthor of the study. "Understanding how the drug also enables crosstalk between fat cells andthe liver in obese mice allows us to see more of the amlexanox pictureand also sheds light oncommunication between different tissues in the body."

CThe finding is the latest piece of a complex obesity-inflammation-diabetes puzzle that Saltiel

lab investigators have been working to solve in order to find new treatments for metabolicdisorders. Obesity leads to a state of chronic, low-grade inflammation in liver and fat tissue,which in turn increases the levels of a pair of kinases: IKK- and TBK1. In 2009, the Saltiel labdefined a key role of IKK- and TBK1 in the onset of obesity. In 2013, the researchersdiscovered that amlexanox, an off-patent drug currently prescribed for the treatment of asthmaand other uses, reversed obesity, diabetes and fatty liver in mice. In research published inDecember 2013, the investigators found that high levels of IKK- and TBK1 meant that certainreceptors in the fat cells of obese mice were unable to respond to neurotransmitters calledcatecholamines, which are generated by the sympathetic nervous system and promote "fat-burning." High levels of IKK- and TBK1 also resulted in lower levels of cAMP. Amlexanoxreduces IKK- and TBK1, leading to higher cAMP, increased sensitivity to catecholamines andincreased energy expenditure by the fat cells. The U-M study explains how increased cAMP infat cells promotes the secretion of the hormone interleukin-6, which signals the liver to stopproducing glucosethus improving overall blood sugar levels in obese diabetic mice.