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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 Nov 20, 2013

 

Adult humans seem to contain brown adipose tissue (BAT) primarily behind the muscles of the lower neck and collarbone, as well as along the spine of the chest and abdomen.

After food consumption, absorbed fats and sugars are used to provide energy for daily functions, while excess calories are stored as fat in the white adipose tissue — mainly located under the skin of the buttocks and legs in women and around the internal organs in men.

BAT can be activated in response to various stimuli, including exposure to cold, to burn fat and sugars. This process seems to be more prominent in the young and lean than in the old and obese, and in women rather than in men.

Image Credit: Nature







WHO Child Growth Charts

 

 

 

Protein found that regulates burning of body fat

Muscle movements generate body heat. However, body heat can also be generated in another way: body fat contains a small number of brown adipose cells — special fat cells that can generate heat without muscle activity.


Brown fat cells use a protein known as UCP1 to enable babies and hibernating animals to keep warm without shivering.


A research team at the University of Veterinary Medicine (Vetmeduni Vienna) has found that a specific chemical compound, an aldehyde, can activate UCP1 under certain conditions, and that could also trigger fat burning. The data were published in the journal Plos One.

The uncoupling Protein 1 (UCP1) is found exclusively in brown adipose tissue. Until recently, it was thought that only babies and hibernating animals had brown adipose tissue, but now it is known that adults also have brown fat — though much reduced in volume. UCP1 could be useful in the fight against adult obesity:“If we can find out how to regulate this protein, we might also find a way to trigger fat burning in the body,” explains biophysicist Elena Pohl from the Unit of Physiology and Biophysics at the Vetmeduni Vienna.

UCP1 is located in the membrane of mitochondria, the power plants that fuel every single cell in the body. Cells that require a lot of energy, such as muscle cells, contain many mitochondria. But brown adipose tissue contains even more mitochondria than muscle tissue. In fact, it is the mitochondria that are responsible for the brown colour of this form of adipose tissue. Regular adipose tissue, which is the majority, is white.


UCP1 in mitochondria uses the cell’s energy to produce heat. If UCP1 is ‘turned off’ in mice, the animals will freeze. Hibernating animals would not survive the winter if they did not have this protein.


Elena Pohl and her research group are trying to find a way to regulate UCP1. In a project funded by the FWF, they have tested different substances reported to activate UCP1, under them also reactive aldehyde 4-hydroxy-2-nonenal (HNE).

Researchers were able to detect the activity of UCP1 by measuring the electrical conductivity of an artificial cell membrane. That membrane containing UCP1. The researchers dripped HNE onto the membrane and found that UCP1 can be activated by HNE only if combined with fatty acids.

“In this model, all the ‘players’ are known so we could determine clearly whether the substance influences the protein directly or not. The discovery helps to improve our understanding of the mechanisms that regulate UCP1 and may even lead us to a way to burn body fat,”
explains co-author Olga Jovanovic.

Reducing free radicals

Free radicals play an important role in many biological processes, but they also cause cellular damage and play a crucial role in the genesis of various diseases such as cancer, atherosclerosis and Alzheimer's disease. The research has shown that HNE, combined with fatty acids, also has the potential to minimize damaging free radicals by reducing the membrane potential.

“We want to examine the molecular mechanisms of UCP to better understand its' function. We are still examining various aldehydes and other UCPs as there are five different ones and all their functions are not yet fully understood. We hope that our work will contribute to the development of therapies for various diseases,”
says Olga Jovanovic.

Drugs in the battle against obesity

In the 1930s, a substance similar to UCP1 was developed that seemed to promise an easy way of losing weight. The substance was called 2,4-dinitrophenol and like UCP1, it worked as an uncoupler in the mitochondria of cells. Taken in the right amounts, the drug accelerates human metabolism by up to 50 percent. However, in some cases it caused serious and even lethal side effects and had to be withdrawn from the market.

“If we are able to regulate UCP1 in a controlled way, it might be different story,”
says Pohl.

Abstract
The production of reactive oxygen species (ROS) in mitochondria is very sensitive to the proton motive force and may be decreased by mild uncoupling, mediated e.g. by mitochondrial uncoupling proteins (UCPs). UCPs were conversely hypothesized to be activated by ROS. Conclusions from experiments studying the reactive product of lipid peroxidation 4-hydroxy-2-nonenal (HNE) in isolated mitochondria and UCP knock-out mice are highly controversial. Here we investigated the molecular mechanism of HNE action by evaluating the separate contributions of lipid and protein phases of the membrane and by comparing UCP1 and UCP2, which were reconstituted in planar lipid bilayers. We demonstrated that aldehyde does not directly activate either UCP1 or UCP2. However, HNE strongly potentiated the membrane conductance increase (Gm) mediated by different long-chain fatty acids in UCP-containing and in UCP-free membranes and this suggest the involvement of both lipid-mediated and protein-mediated mechanisms with FA playing the central role. Gm increase was concentration-dependent and exhibited a typical saturation kinetic with the binding constant 0.3 mM. By using Electron Paramagnetic Resonance, membrane fluidity change could be excluded as a cause for the HNE-mediated increase in the presence of FA. The impact of the HNE binding to definite positively charged UCP amino acid residues is discussed as a possible protein-mediated mechanism of the UCP activation.

The study "Fatty acids are key in 4-hydroxy-2-nonenal-mediated activation of uncoupling proteins 1 and 2," by Elena A. Malingriaux, Anne Rupprecht, Lars Gille, Olga Jovanovic, Petr Jezek, Martin Jaburek and Elena E. Pohl was published recently in the journal Plos One.