Book 2 Listening (1108796), страница 24
Текст из файла (страница 24)
(From The Economist, April 10, 2010)Script 48. ObesityDoes light make you fat?When-not just what-mice eat affects how much weight they put onTHE blame for rising obesity rates has been pinned on many things, including a morecalorific diet, the spread of processed food, a lack of exercise and modern man's generallymore stressful lot. Something else may soon be included in the list: brighter nights.Light regulates the body's biological clock - priming an individual's metabolism forpredictable events such as meals illuminating the cause of obesity and slumber. Previousresearch has shown that, in mice at least, the genes responsible for this can be manipulatedso as to make the animals plumper and more susceptible to problems associated withobesity, including diabetes and heart disease.
It was not known, though, whether simplyaltering ambient light intensity might have similar effects.A team of researchers led by Laura Fanken of Ohio State University has cleared thematter up. As they report in the Proceedings of the National Academy of Sciences, theyexamined how nocturnal light affects weight, body fat and glucose intolerance (the underlyingcause of late-onset diabetes) in male mice. They found that persistent exposure to even alittle nighttime light leads to increases in all three.83To reach this conclusion Dr Fonken split her murine subjects into three groups.
Somewere kept in cages lit constantly, so as to resemble a never-ending overcast day. A secondgroup lived in conditions akin to their natural habitat, with 16 hours of overcast day-like light,followed by eight hours of darkness. The remaining rodents were also exposed to a cycle, butthe dark was replaced with a dim glow equivalent to the twilight at the first flickers of dawn.Over the eight-week period of the experiment the mice in the first and third groupsgained almost 50% more weight than those exposed to the natural light-dark cyde. They alsoput on more fat and exhibited reduced tolerance of glucose, despite eating comparableamounts of food and moving around just as much.
The only thing that seemed to differ waswhen the mice ate.In the wild, mice are nocturnal. Unsurprisingly, then, those in the quasi-naturalconditions consumed only about a third of their food in the "day" phase. For a mouseexposed to the twilight cycle, however, the figure was over 55%.In a follow-up experiment, Dr Fonken looked at whether the timing of food consumptionalone could explain the observed differences. It turned out that those forced to eat during the"day"-i.e., out of whack with their biological clock-did indeed gain about 10% more weightthan those fed at "night" (be it dark or just dim) or those with uninterrupted access to grub.How this might relate to people will require further investigation. Mice and humans arephysiologically alike, so a similar effect might be expected for people, but the fact that miceare nocturnal and humans diurnal is a serious complicating factor.
It is true, though, that thespread of electric lighting means many people eat their main meal when natural daylight islong gonethe obverse of a mouse eating during daylight hours. And that tendency to eat late,though it has never been tested properly, is believed by many nutritionists to be a factor inputting on weight.When the full explanation for the modern epidemic of obesity has emerged, it is unlikelythat the spiead of artificial lighting will be the whole of it But this work suggests it might be apart. When you eat could be as important as what you eat.
(From The Economist, October16, 2010)Script 49. The epigenetics of fatAltered statesEXERCISE is the closest thing medicine has to a panacea. Though hitting the treadmillis more effort than swallowing a pill, the benefits are worth it. Even modest amounts ofexercise protect against diseases ranging from diabetes and osteoporosis to heart attacksand senility.Exercise works its magic in many ways. It improves the power and efficiency of theheart; it boosts the release of certain neurotransmitters (the chemicals nerve cells use to talkto each other); and it stimulates cells' garbage-disposal machinery.
Now a group ofresearchers led by Charlotte Ling of Lund University, in Sweden, has discovered anothereffect of exercise. It alters the way genes work in the tissue that stores fat.In a paper published in the Public Library of Science, Dr Ling and her colleagues reportthe effects of six months of moderate exercise on 23 male couch-potatoes who were in their30s and 40s. The men were supposed to attend three workouts a week. In the event, theymanaged an average of 1.8.
Nevertheless, besides finding the usual effects-reduced heartrate, lowered blood pressure and a drop in cholesterol levels- the researchers also observedchanges in the men's adipose tissue, the place where fat is stored. Specifically, the way fatcells in this tissue expressed their genes had altered.This is epigenetics, a rapidly developing branch of biology that focuses not on the genesthemselves but rather on how particular genes behave in specific cells. Which genes areactive in a cell can be changed by making chemical alterations (known as epigeneticmarkers) to their DNA.
Such alterations let the body finetune its response to the environment,and modern gene-sequencing techniques can detect them without too much difficulty.Dr Ling, who is interested in adult-onset diabetes (often associated with too much bodyfat), knew that exercise stimulates epigenetic changes in muscle celts. These alter how84muscle processes sugar. When she and her colleagues looked for similar alterations in theircharges' adipose tissue, they found lots- t8,ooo markers distributed across 7,663 genes.
Thismatters, because adipose tissue is not just a passive store of energy, it is also an organ in itsown right, producing a range of biologically active chemicals that have all manner of effectson the rest of the body.What all these epigenetic markers are doing remains obscure. But among the alteredgenes were 18 known to be associated with obesity and another 21 linked with adult·onsetdiabetes. When Dr Ling's colleagues picked two such altered genes and silenced themcompletely in laboratory grown fat cells, the cells changed, becoming more efficient atprocessing and depositing fat.
That leads, Dr Ling notes, to the hypothesis that one reasonexercise is good for you is because it improves the ability of fatty tissue to do its job. Lipidsthus get stored in the right place instead of settling elsewhere in the body, where they doharm. As she observes, if you do have surplus fat it is better to have it stored in fatty tissuethan in the liver or the pancreas.This study is only a beginning.
Working out which epigenetic changes wrought byexercise are important, and which incidental, will take time. But, given worries about howoverweight people are becoming, and the incessant message from many governments thattheir citizens should take more exercise, studies like Dr Ling's should help by shining light onthe way exercise actually works its magic. (From The Economist, July 13, 2013)85.
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