CARBONDALE, Ill. – Calling someone a fat pig is a huge insult, but being a fat pig might be worse.
“The goal in raising pigs is to make them as lean and efficient as possible while maintaining profitability for the farmer,” said Kolapo Ajuwon, animal scientist in Southern Illinois University Carbondale’s College of Agricultural Sciences.
“It’s cheaper for the farmer if the pigs make protein instead of fat because they use so much more energy in making fat. If you give them a pound of feed and half the weight they gain from it is fat, you’ve wasted money.” Ajuwon said.
“Whatever knowledge we gain with pigs applies almost directly to humans because they have so many physical similarities,” Ajuwon said.
Leptin. He began his master’s research, done with pigs as models, by looking at leptin.
“Leptin is what’s called a satiety hormone,” Ajuwon said.
“It’s produced in the fat cells, and when we eat, it goes to the brain and says we’ve had enough so we feel satisfied. We hypothesized that it would enhance the growth of pigs – that it would regulate their feed intake as it does in rodents and that it could act directly on the fat cell itself, reducing the amount of fat, or lipids, the cell could store.”
This proved to be true, and it was pioneering work.
“Leptin goes to the brain, to the organs, to the muscle, meaning that the fat cell contributes to the metabolism of the entire body – it doesn’t just store fat,” Ajuwon said.
Inflammation. In his doctoral research, still using pigs as a model, Ajuwon concentrated on the role that fat tissue plays in the development of diabetes.
This time, he zeroed in on a surprising target: inflammation.
Inflammation, which occurs when injury or infection activates the body’s defense mechanisms, is usually temporary.
But obesity can also induce inflammation, which in this case is chronic though low grade.
This chronic inflammation then interferes with the signals that are supposed to set off the body’s response to insulin, making the body insulin resistant.
Ajuwon figured if inflammation could be prevented, that might, in turn, prevent insulin resistance, so he took a closer look at what actually happens in fat cells when inflammation sets in.
“We found that a particular hormone called adiponectin, produced in the fat cell, makes cells respond better to insulin and also suppresses the inflammatory response,” he said.
“In obesity, production of that hormone is depressed. The fatter one is, the lower the level of adiponectin, and we think reduced adiponectin might compromise the ability to suppress the inflammatory response.”
Fatty acids. Ajuwon’s research also showed that the obese have a lot of lipids, or fats, circulating through their bodies.
“We found that fatty acids in the lipids from foods can directly initiate inflammation,” he said.
The next step lay in looking at the effect of diet on inflammation – an interest that brought Ajuwon to the university.
“This is a department that combines research in animal science with research in food and nutrition, and my work is relevant to both,” he said.
“The basic biology is the same. It’s just how you apply it.”
Soy relationship? He is particularly interested in the department’s work with dietary soy.
He plans to look at whether soy might prove useful in regulating inflammation in both humans and animals, an area in which he expects to break new ground.
Success could help in the fight against diabetes while at the same time aiding pork producers.
“In inflammation, the priority of the body shifts from growing to fighting off the inflammation,” he said. “If we can suppress inflammation, then the animals will grow better.”
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