FAT LOSS, BIOLOGICAL INFLUENCE: THE SATIETY GENE

All of the above suggests that obesity is a ‘polygenic’ disorder, or that there are a number of genetic components to obesity. Major excitement was aroused in scientific circles in late 1994 because of the identification of a gene apparently linked to ‘switching’ on and off hunger, called a satiety gene. The history of this discovery is fascinating and helps provide an understanding of the complexity of the problem.

It has been known for some time that substances must exist in the blood which signal the state of energy stores to the brain so that hunger can be turned on and off. In the early 1950s, a mechanism called an ‘appestat’ was hypothesised to operate like a thermostat in ‘switching off hunger after a certain level of food intake. This was further supported in the 1960s and 1970s by some ingenious research carried out by Dr Douglas Coleman at the Jackson Laboratory in Maine with two inbred strains of obese mice (called ‘db’ for diabetes and ‘ob’ for obese). Coleman joined these mice with normal lean mice (a process called ‘parabiosis’) so they both had the same circulatory system. In doing so, strange things happened.

When a normal mouse was joined with a ‘db’ strain mouse, the lean mouse actually starved to death—even in the presence of abundant food. This suggested that the ‘db’ strain had an over-supply of some substance in the blood to tell it to stop eating, but that this wasn’t working in the ‘db’ mouse. When an ‘ob’ and a ‘db’ mouse were joined, the ‘ob’ mouse died from starvation, but the ‘db’ mouse increased its weight by over-eating. Again, this suggests that the ‘db’ mouse was over-supplying a ‘switch off substance which was not working with it, but which worked excessively well with the ‘ob’ mouse. Finally, when a normal mouse was joined with an ‘ob’ mouse, the ‘ob’ mouse lost weight and became normal. All this suggested that normal mice have a normal amount of a substance which the ‘ob’ mouse does not have, and which the ‘db’ mouse has too much of, but which has no effect (i.e. does not reach a receptor) in the ‘db’ mouse.

Dr Jeremy Friedman and his team from Rockefeller University in New York then isolated a gene which codes for the production of a protein from fat cells, which tells the brain when satiation has been reached. The protein has since been identified, synthesised and injected into obese mice and found to reduce their body weight The substance has been called ‘leptin’ (after the Greek word ‘leptos’ meaning ‘thin’), and the race is now on to develop drugs which may be useful in human obesity. Most scientists, however, warn that the discovery is not likely to be as simple a remedy as some have claimed, and that much more work still needs to be done.

There are likely to be few, if any, human equivalents of the ob or db mice which have major single gene abnormalities. In humans, there may however, be gene variations which result in some people being less able than others to switch off their appetite. Genetic influences in human obesity are indicated by some simple factors such as:

• Presence of lifetime or long term obesity in one or both parents. Studies have shown that the chances of being obese are around 80 per cent if both parents are obese, 40 per cent if one parent is obese and only 7 per cent if neither parent is obese.

• Presence of obesity since childhood. Genetically influenced obesity is usually manifest early in life, particularly before or around adolescence. For this reason someone who has always had a problem, particularly if the problem is also in the immediate family, is more likely to be genetically influenced.

• Presence of type I obesity. Abdominal obesity, particularly in men, is generally regarded as being environmentally determined. Ovoid-shaped fatness, together with the factors mentioned above, may suggest genotypical influences.

Although the factors mentioned above provide no certainty about genetic influence, they may give some indications that fat loss is likely to be a more difficult proposition in an individual who is genetically predisposed to fatness and that efforts to prevent fat gain may need to be lifelong; therefore, this person needs long term goals which are realistic. Special attention may also need to be given to hunger and behavioural cues and to maintenance of body weight after slimming.

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PRODUCTION OF ADENOSINE TRIPHOSPHATE FROM FOOD SOURCES

Now we have outlined the source, storage depots and measurements of energy, the next step is to examine the production of the energy rich molecule adenosine triphosphate (ATP), the energy currency of the body. This is made up of adenosine with three phosphate groups attached. ATP is found in every cell. It is the common pathway for energy production for driving bodily functions. At the microscopic muscle filament level, the reduction of ATP to adenosine diphosphate (ADP) is the energy source used for contraction. That is, energy liberated from the reduction of ATP to ADP allows the basic protein filaments of muscle, actin and myosin, to slide across each other to cause muscular contraction.

Energy is derived through the cleaving-off of high energy phosphate bonds from the ATP molecule to form ADP+P.

The energy for the re-synthesis of ATP from ADP+P comes from nutrients as they get broken down in their catabolic pathways or from the small energy reserves in muscle called the creatine phosphate system The direct breakdown of nutrients only occurs by itself at very high temperatures. However, in the human body it must occur at normal body temperature (36.5 to 37.5°C), and this is done through a series of stepped chemical reactions, which are catalysed by many different enzymes. Enzymes are proteins that have the ability to promote specific chemical reactions without the need for high temperatures and without being changed or degraded themselves in the process. They can therefore be used over and over again.

Myth-information. Corset-like ‘sweat pants’ sold to reduce fat around the buttocks have only the superficial effect of tightening’ bulges. They cannot and do not reduce body fat.

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FEED YOUR BODY RIGHT: LENTEN PROMISE LED TO 20-POUND REWARD

If you’re having a hard time pinpointing the hidden calories in your diet, take a tip from Jim Gorman. The 33-year-old public relations supervisor from Hoboken, New Jersey, will tell you to look in the bottom of your empty glass. He knows from experience.

In 1995, Jim gave up all sugary beverages and alcohol for Lent, resolving to drink only water and club soda. By the time Easter rolled around, he was 20 pounds lighter. “I wasn’t really looking to lose weight,” he says. “But I have to admit that I was a bit bulkier than I wanted to be.”

Since then, Jim has kept his weight between 158 and 163 pounds, appropriate for his 5-foot-11-inch frame. He attributes his trim physique to his continued ban on sugary beverages. “Staying away from soda, lemonade, sweetened iced tea, and other flavored drinks has made all the difference on the scale,” he says.

While Jim sticks with water and club soda at home, he may order a beer or two when he’s socializing with friends. “I don’t

WINNING ACTION

Be wary of liquid calories. Alcohol and sugary beverages can contribute to weight gain—and they don’t do a thing to fill you up. A 12-ounce glass of beer supplies 146 calories; 12 ounces of soda, 150 calories; and 8 ounces of fruit juice, about 100 calories. If you’re having a tough time losing weight, take account of your liquid calories. Substitute water for your sugary beverages. You’ll be a lot happier eating a 300-calorie meal than quaffing a few colas. As for alcohol, save it for special occasions (like losing 10 more pounds), and stick to light beer or wine.

And remember to sip, not gulp.

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