Washington, Dec 5: A high-carb diet has always been considered as a factor behind piling on the pounds. Now, a study in mice conducted by researchers at the University of Wisconsin-Madison has found that the genetic basis as to why this happens.
The boffins have identified a gene in the liver, called SCD-1, is a key tissue in mediating weight gain induced by excess carbohydrates.
In the study, the research team, led by biochemistry and nutritional sciences professor James Ntambi, found that the gene is what caused mice to gain weight on a diet laden with carbohydrates. The gene encodes the enzyme SCD, whose job is to synthesize fatty acids that are a major component of fat.
When the researchers gave a starch- and sugar-rich diet to mice lacking SCD-1 in the liver, the extra carbohydrates were broken down rather than being converted into fat and stored - keeping the mice skinny. Meanwhile, control mice with normal gene activity grew plump on the same food.
"It looks like the SCD gene in the liver is responsible for causing weight gain in response to a high-carbohydrate diet, because when we take away the gene's activity the animals no longer gain the weight. These findings are telling us that the liver is a key tissue in mediating weight gain induced by excess carbohydrates," Ntambi said.
He explained that people gain weight in two ways, one of which is to eat extra fat, which then accumulates in adipose, or fat, tissue. However, the main cause of weight gain is excess carbohydrates, because they trigger the body to produce new fat.
Ntambi said that blocking SCD's action in the liver could therefore offer another means to help people lose weight, especially since obese people appear to have higher levels of the enzyme than do thin people.
"We think that obese individuals, in general, may have higher SCD activity in both the liver and in adipose tissue. So, they may have a higher capability of converting carbohydrate into fat," he said.
Ntambi's team demonstrated how carbohydrate diets act directly on a gene to boost fat synthesis and storage.
The current study has been built on previous work, in which the team created mice that lacked SCD-1 everywhere in the body, including the liver, muscle, brain, pancreas and adipose tissue. No matter how much they ate, the mice didn't gain weight on either a high fat or a high-carbohydrate diet. However, it was very difficult to make out which tissue was responsible for the effect.
To tease this out, the team subsequently bred mice that lacked SCD-1 in the liver only and placed them on either a high-fat diet or a high-carbohydrate, low-fat one. Surprisingly, the mice on the high-fat diet gained weight just as quickly as normal, control mice.
"This suggests that in weight gain induced by a high-fat diet, other tissues beyond the liver are involved," Ntambi said.
In contrast, the mice stayed thin when they feasted on food heavy in starch and table sugar, or sucrose. They were also protected from the condition known as fatty liver. Ntambi believes what's happening is that in the absence of SCD, the liver has no way to convert surplus carbohydrates into fat, causing the body to break them down instead.
He added that the results also highlight the central role of the enzyme and its main product, a fatty acid known as oleic acid, in overall carbohydrate metabolism. For example, mice lacking SCD could no longer make glucose - the sugar burned by cells for energy - leading to abnormally low blood sugar levels, or hypoglycemia. They also weren't able to make glycogen, a short-term storage form of glucose.
"It looks to us that if you don't have enough oleic acid - which the SCD enzyme makes - then the carbohydrate does not proceed through normal glucose metabolism," Ntambi said.
As further evidence of this, when the researchers supplemented the mouse diets with oleic acid, normal metabolism was restored.
In both mice and people, on the other hand, eating lots of carbohydrate appears to boost SCD activity, leading to a glut of oleic acid, increased fat storage - and, over time, obesity.
"Too much carbohydrate is not good. That's basically what we are saying." Ntambi said.
The new study is published in the December issue of Cell Metabolism. (ANI)