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Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
CLICK ON weeks 0 - 40 and follow along every 2 weeks of fetal development
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Home | Pregnancy Timeline | News Alerts |News Archive Jan 19, 2015

Amlexanox triggers the release of interleukin-6 from mouse fat cells, then travels to the
liver where in diabetic mice it reduces production of glucose, lowering blood sugar

 





 

 

How to reverse obesity and diabetes?

Researchers at the University of Michigan have identified how a promising drug improves the metabolism of sugar by generating a new signal between fat cells and the liver.

In addition to illuminating how the drug amlexanox reverses obesity, diabetes and fatty liver disease, the research suggests a new path for treatment. The work was published in Nature Communications.

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 drug Amlexanox affects a specialized fat cell by increasing the level of a molecule called cAMP. In turn, cAMP increases the rate by which cells "burn" fat so that the animal loses weight.

Amlexanox also triggers the release of the hormone interleukin-6 from these fat cells. Interleukin-6 then travels to the liver where it reduces production of glucose and lowers blood sugar in diabetic mice.


"We know that amlexanox works to reverse obesity and insulin resistance partly 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 enables crosstalk between fat cells and liver cells in obese mice expands our understanding of communication between different tissues in the body."

This finding is the latest piece of a complex obesity-inflammation-diabetes puzzle that Saltiel lab investigators have been working to solve in order to create new treatments for metabolic disorders.


Obesity leads to a state of chronic, low-grade inflammation in liver and fat tissue, which increases levels of a pair of kinases called IKK-ε and TBK1.

In 2009, Saltiel lab found a key role for IKK-ε and TBK1 in the onset of obesity. In 2013, researchers discovered amlexanox, an off-patent drug currently prescribed for treating asthma (and other uses) reversed obesity, diabetes and fatty liver in mice.


In research on obese mice published in December 2013, high levels of IKK-ε and TBK1 were found to reduce response to neurotransmitters called catecholamines. Generated by the sympathetic nervous system, catecholamines promote "fat-burning." In humans, the most abundant catecholamines are epinephrine, norepinephrine and dopamine, all part of our fight-or-flight response. High levels of IKK-ε and TBK1 also result in lower levels of cAMP.

The drug Amlexanox reduced IKK-ε and TBK1, leading to higher levels of cAMP, and increasing sensitivity to catecholamines — therefore increasing energy used by fat cells.


The U-M study showed how increasing cAMP in fat cells promotes secretion of the hormone interleukin-6.

Interleukin-6 then signals the liver to stop producing glucose thus improving overall blood sugar levels in obese and diabetic mice.


Abstract
The search for effective treatments for obesity and its comorbidities is of prime importance. We previously identified ?IKK-ε and ?TBK1 as promising therapeutic targets for the treatment of obesity and associated insulin resistance. Here we show that acute inhibition of ?IKK-ε and ?TBK1 with ?amlexanox treatment increases ?cAMP levels in subcutaneous adipose depots of obese mice, promoting the synthesis and secretion of the cytokine ?IL-6 from adipocytes and preadipocytes, but not from macrophages. ?IL-6, in turn, stimulates the phosphorylation of hepatic ?Stat3 to suppress expression of genes involved in gluconeogenesis, in the process improving ?glucose handling in obese mice. Preliminary data in a small cohort of obese patients show a similar association. These data support an important role for a subcutaneous adipose tissue–liver axis in mediating the acute metabolic benefits of ?amlexanox on ?glucose metabolism, and point to a new therapeutic pathway for type 2 diabetes.

Saltiel is also the John Jacob Abel Collegiate Professor in the Life Sciences and a professor of internal medicine and molecular and integrative physiology at the U-M Medical School.

Other authors of the study were Louise Chang, Maeran Uhm, BreAnne Poirier, Danielle Krause and Xiaoling Peng of the U-M Life Sciences Institute; Maryam Ahmadian, Ruth Yu, Michael Downes and Ronald Evans of the Gene Expression Laboratory, Salk Institute for Biological Sciences; Christopher Liddle of the Gene Expression Laboratory, Salk Institute for Biological Sciences, and the Storr Liver Unit, Westmead Millennium Institute and University of Sydney, Westmead Hospital; Brian Zamarron of the U-M Program in Immunology; Evgenia Korytnaya, Adam Neidert and Elif Oral of the U-M Department of Internal Medicine, Metabolism, Endocrine and Diabetes Division; and Carey Lumeng of the U-M Department of Pediatrics and Communicable Diseases.

Support for the research was provided by the National Institutes of Health and the Leona M. and Harry B. Helmsley Charitable Trust.

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