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Health Blog: Discovery of fat hormone leptin can win 2011 Nobel Prize

Submitted by John Wruyters on Mon, 2011-10-03 09:54
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One Canadian and one American scientist who discovered the hormone that regulates appetite have a good chance of winning the Nobel Prize for Medicine this week (October 2011).  Douglas Coleman and Jeffrey M. Friedman discovered the leptin appetite hormone back in 1995.

They not only discovered leptin, but also showed that leptin levels are either too high or too low in obese and diabetic people. Unfortunately nobody has been able to translate their discovery into a drug or treatment. Leptin has been good enough to make them a strong 2011 Nobel Prize candidate, but for obese people and diabetics the leptin hormone has never gone beyond a good theory.

 

NOBEL 2011 NEWS UPDATE

The 2011 Nobel Prize for Medicine did not go to the leptin researchers, but to 3 scientists researching the immune system.

Canadian born Steinman got half of the prize for researching the role of dendritic cells in immune response. Steinman passed away a few days prior to the announcement. He had pancreatic cancer for four years and prolonged his life with the very research that brought him the Nobel Prize.

The other half of the prize was shared by Beutler en Hoffmann who found genes and proteins in bacteria that trigger an immune response.

What is leptin?

Lepto means “lean” in Greek and it is a hormone that regulates appetite. It’s a protein made from 167 amino acids and is mainly produced by fat cells. The hormone targets mainly the hypothalamus in the brain. In a healthy signaling pathway we produce the hormone which tells the brain to turn off the hunger signal. The same hormone also regulates how much fat is burned. The leptin signaling pathway can be disrupted in two basic ways:

  1. The body misses the gene or the right amino acids to trigger the fat cells to produce enough leptin.
  2. The body does not have enough receptors in the brain to receive the leptin signal. The receptor deficiency is called leptin resistance.

The problem is similar to the happiness hormone serotonin: the drug Prozac increases the levels of serotonin, but that will only result in more happiness if there are enough serotonin receptors in the brain. Omega 3 has been shown to increase the number of these receptors.

Anti-obesity drug failed miserably

Leptin is not even close to becoming a drug like Prozac. Actually pharma giant Amgen purchased the rights to the leptin hormone from the universities and did a large scale clinical trial with obese people. Amgen had hoped that by administering the hormone as a drug, they could make obese people less hungry. The results were very disappointing. Only very few patients responded and lost weight. But for the overall group the trial failed miserably, and Amgen dropped the whole leptin research, because they couldn’t see a way to make the billions of dollars that they had hoped for.

Friedman understands why the trials failed. In a 2010 interview with American Society for Clinic. Investigation he says: “Even before leptin was tested in obese patients, we knew from animal studies that this hormone was not likely to be a panacea for every obese patient (…). Obesity is often associated with leptin resistance and (..) increasing already high levels was going to be of arguable benefit.”

Leptin works for some morbid obese

Friedman sees the future of his discovery in personalized medicine, where doctors can identify which obese people will respond to leptin. As an example: one study in 1997 showed that leptin injection can do wonders for some people. This study injected a morbid obese boy with leptin for 24 months. 

Stigma of being fat

What Friedman and Coleman did foremost for obese and diabetic patients is to reduce their stigma of being fat. Their research proved that the hormonal pathway can be majorly screwed up, and that this can have a genetic cause. Coleman in the 2010 interview:  “Two long-standing misconceptions were definitively laid to rest: obesity was not merely a behavioral problem but rather had a significant physiological component; and adipose tissue (fat tissue) was not merely a fat-storage site but rather an important endocrine (hormonal) organ.”

 

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John Wruyters
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John Wruyters's blog

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