Microorganisms and bacteria living in our intestines help with proper digestion of food by breaking down nutrients and helping our body absorb them better. Although much is known about the function of microorganisms, there is still much to study about the relationship between gut microorganisms and weight.  Scientists are particularly interested in the relationship between the kinds of gut microorganisms and amount of calories harvested from carbohydrates and sugars, as evidence to this could help with weight management. Researchers also want to find out how the various microorganism communities compare in different individuals.

A new study appearing online this week found that gut microorganisms are linked with obesity. Researchers found that obese individuals carried more hydrogen-producing and consuming microbes that could increase the amount of energy processed from their food.

The study also found that the kinds of microbe communities change after gastric bypass surgery-assisted weight loss. Changing the gut environment – its acidity, amount of stomach acid, even length of the intestine – can potentially change the types of microorganism that thrive inside.

More research is needed to confirm the results, especially regarding the effect on weight. It is not known whether microbial community in the gut is a cause or a consequence of obesity. But if gut microorganisms are found to contribute to weight problems, then it is possible to develop treatments for obesity or identify markers that can predict at risk individuals.

The study will be published online this week in the Proceedings of the National Academy of Sciences. [source: GenomeWeb]

Irochka - Fotolia.com

It’s the Sunday edition of Genetics and Health so let’s sum up some of the genetic research and news that came up this week.

A grand rounds lecture "Molecular Genetics of Colorectal Cancer" by Vincent Yang presents an overview on the role of genes in colorectal carcinoma, and shares initial findings on a cell cycle modulator gene.

The NY Times article, "Man Who Helped Set the Stage for Nobel-Winning Work Has Left Science" profiles Dr. Douglas C. Prasher, the scientist who provided the essential piece of evidence that helped the work of Nobel Price Chemistry winners Roger Y. Tsien and Martin Chalfie. You’ll be surprised to find out Dr. Prasher’s latest employment.

A "pleasure" gene is behind an obese person’s insatiable desire to eat more.

The Personal Genome Project is open for business and it’s looking for volunteers agree to make public their medical history AND DNA sequence. PGP is a nonprofit, volunteer database project by Harvard University.

Enlarged hearts are found often, but not exclusively, in those who are obese, have diabetes or high blood pressure. People with none of these underlying problems can be affected, as can elite athletes.  For example, a post-mortem diagnosed the problem in Cameroon football midfielder Marc-Vivien Foe, who died in 2003 after collapsing during an international match in France. Elite runner Olympic hopeful Ryan Shay died of complications involving an enlarged heart - the very condition that made him a great runner.

An international  research team headed up by Imperial College, UK say they have for the first time linked enlarged hearts with a gene, osteoglycin (Ogn).

Work carried out on rodents and some 30 humans indicated that Ogn - which has never before been linked with heart function - regulated the growth of the heart’s main pumping chamber, its left ventricle.  When this gene behaves abnormally the heart can become enlarged, putting the person at an increased risk of common heart diseases and heart attacks.

For further information, click on:

http://www3.imperial.ac.uk/newsandeventspggrp/imperialcollege/newssummary/news_29-4-2008-13-31-10

Elaine Warburton  www.geneticsandhealth.com

Scientists from Imperial College London and other international institutions have discovered a gene sequence that is associated with a 2cm expansion in waist circumference, a 2kg gain in weight, and a tendency to become resistant to insulin, which can lead to type 2 diabetes. The sequence is found in 50% of the UK population.

The study shows that the sequence is a third more common in those with Indian Asian than in those with European ancestry. This could provide a possible genetic explanation for the particularly high levels of obesity and insulin resistance in Indian Asians, who make up 25% of the world’s population, but who are expected to account for 40% of global cardiovascular disease by 2020.

The new gene sequence sits close to a gene called MC4R (Melancortin-4 Receptor), which regulates energy levels in the body by influencing how much we eat and how much energy we expend or conserve. The researchers believe the sequence is involved in controlling the MC4R gene, which has also been implicated in rare forms of extreme childhood obesity.

Elaine Warburton  www.geneticsandhealth.com
 

Many gene studies focus on WHICH genes cause a person’s risk of developing a disease (forward genetics) but few focus on HOW those genes can lead to disease.  Researchers at Merck and Co, deCODE genetics and academic centres in the US and France have focused on the latter and shed light on the complexity of common disease causes where multiple genetic changes are involved (functional genetics).

Two studies analysed DNA variations, patterns of gene expression in disease tissue, and clinical data on a large scale to identify which gene networks linked to metabolic disorders (a range of symptoms that are thought to cause obesity, diabetes and atherosclerosis or heart disease).

The first study on mouse livers looked at finding genes that might be linked to obesity, diabetes and heart disease.  The researchers created gene networks and located highly connected sub-networks of core genes that were known to be linked to obesity, diabetes and heart disease. They also identified, and validated at the experimental level, three new genes thought to cause obesity: Lpl, Pmp1l and Lactb.

The second study on over 1,000 human blood and fat tissue samples from Iceland, and using data from the first study, created a gene expression network of human obesity traits.  This human obesity network showed considerable overlap with the mouse network.

The researchers concluded that:

“A core network module in humans and mice was identified that is enriched for genes involved in the inflammatory and immune response and has been found to be causally associated to obesity-related traits.”

The next question is WHY?

Elaine Warburton  www.geneticsandhealth.com

Researchers at the Albert Einstein College of Medicine of Yeshiva University, in New York, claim they have found the genes responsible for storing fat in cells.  They have identified the FIT1 and FIT2 (Fat-Inducing Transcripts 1 and 2) genes that package fat in the form of lipid droplets.  Storing fat in lipid droplets is important for enabling cells to use fat as an energy source ….  but having high amounts of these droplets leads to obesity.

Obesity is a major cause of Type 2 diabetes, which is becoming a world epidemic. The discovery of genes that influence the development of obesity could help allow scientists and physicians to understand why some people gain weight more than others.

The study’s findings could open up a wealth of new avenues to understand and treat obesity and obesity-related conditions such as Type 2 diabetes.

Elaine Warburton

Body shape and fat distribution appear to be partially controlled by genes involved normal development. DNA chips were used to compare the levels of activity for three specific genes - Tbx15, Gpc4, and HoxA5. Intra-abdominal and subcutaneous fat taken from individuals of normal weight versus overweight or obese individuals were analyzed with these three genes appearing to be especially important in fat deposits and obesity.

Dr. Stephane Gesta:

The differences we found in gene expression were so distinct that we could identify the body mass index (level of obesity) and the waist/hip ratio (whether the fat is in the abdomen or under the skin) in the overweight population by the expression level of these genes. This finding suggests that the expression of these genes could be related to the pathogenesis of obesity.

An understanding of why some of us get larger while others don’t will eventually help us develop some form of drug therapy to help the most extreme cases. Of course, changing our lifestyle would be far less dramatic and invasive.

Eat right, exercise, and live healthily. I know it’s not easy to do, but at some point we just gotta suck it up and do it.

EurekAlert, April 10, 2006

This week’s genetics quote is from Choose to Lose: A Food Lover’s Guide to Permanent Weight Loss by Nancy and Ronald S. Goor.

Don’t Blame Mutant Genes

Why are we so fat? It is not because half of all Americans have psychological problems. It is not because our genes have mutated in the last twenty years so that we get fat just by sniffing cheeseburgers. It is not because we have slow metabolisms. It is not even that we have suddenly become gluttons. It is because our food system is so ultra high-fat and we can afford to revel in it.