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3D imaging tracks Leptin

3D imaging technique tracks satiety hormone Leptin

3D images showed that leptin reaches the brain in sufficient quantities both in thin and in obese mice, thus cause of the eating disorder must therefore lie in the nerve cells themselves

Many overweight people lack the feeling of being full and it was believed that this was due to the disrupted transport of the satiety hormone leptin to the brain. However, a group of scientists from Helmholtz Zentrum München, Germany, have now shown with a new 3D imaging technique – which allows tracking the path of the hormone in the brain – that this is not the case. The findings were revealed in the paper, ‘Fluorescent blood brain barrier tracing shows intact leptin transport in obese mice’, published in the International Journal of Obesity.

Leptin is known to be an important satiety hormone that is produced by adipose tissue. The more fat there is in the body, the more leptin is released into the bloodstream. The hormone then crosses the blood-brain barrier to reach the brain’s satiety centres. There, it activates leptin receptors in nerve cells. The receptors, in turn, send signals to the brain to stop food intake. However, if the hormone no longer elicits a response in the satiety centres - Leptin resistance - people are always hungry, as if their fat stores were not already full. Leptin resistance is a major cause of overweight and obesity.

"In obese mice and humans, leptin is released from fatty tissue into the bloodstream in high concentrations but fails to activate the satiety centres in the brain,” said Luke Harrison, a doctoral student at Helmholtz Zentrum München and lead author of the study. “It has long been assumed that leptin resistance is caused by a disrupted transport process. Our innovative 3D technique enabled us to visualise the transport of leptin for the first time and to investigate whether this theory holds up.”

Working with biologists, pathologists and structural biologists, Harrison was able to disprove this assumption. Utilising the new imaging method, the research team headed by Dr Paul Pfluger, a partner in the German Center for Diabetes Research (DZD), showed that leptin reaches the brain in sufficient quantities both in thin and in obese mice (Figure 1). The cause of the eating disorder must therefore lie in the nerve cells themselves.

Figure 1: Stereoscopic 3D video of a mouse brain with green labelled leptin. For further information about the 3D video image, please click here

"We can now narrow down the cause of leptin resistance and focus our research on the molecular mechanisms within nerve cells," said Pfluger. "Once all the processes involved in our satiety behaviour have been elucidated, we will be able to develop new therapies for obesity and help overweight individuals lose weight. Restoring the body's response to leptin is an important step for obese patients in their efforts to regulate their food intake."

In fact, his research team has recently shown that the substance Celastrol, which is also used in traditional Chinese medicine, restores leptin sensitivity and lowers body weight. Initial approaches are now underway, and research at Helmholtz Zentrum München will be further intensified.

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