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Baboons Give Clues to
Obesity, Diabetes in Humans

(HealthScoutNews) -- Research with wild baboons indicates that lack of exercise, not poor diet, causes obesity and diabetes in people who are predisposed to the conditions.

The finding comes in a study in the March issue of the Journal of Clinical Endocrinology and Metabolism.

Saint Louis University researchers also found that obese baboons were not the ones with the highest cholesterol levels. That suggests that obesity and cholesterol problems may be triggered by different mechanisms.

The researchers studied the diet and exercise behaviors of two wild baboon groups in East Africa. One group of baboons had to forage for their food, while the other group found a stash of food discarded by humans.

Both groups of baboons ate about the same amount of fat and calories. However, the stash of human food was close to where the second group of baboons lived, meaning they had to expend much less energy to eat.

More than a third of the baboons in that second group had indications of obesity, evidence of early diabetes caused by insulin resistance, and elevated cholesterol levels.

Their condition was similar to a condition in humans called metabolic Syndrome X, where everything breaks down at the same time as people develop diabetes, hyperlipedema, hypertension and obesity.

However, the study notes that 7 out of 11 baboons in the second group didn't develop the condition. That indicates that some primates are more sensitive than others to becoming obese and diabetic.

The baboons in the second group who didn't develop health problems had leptin levels similar to the baboons who had to forage in the wild for their food. Leptin is a protein produced by fat and an indicator of obesity.

The researchers found the baboons with highest cholesterol levels were those that ate the human food and had normal leptin levels. That indicates that high cholesterol and obesity may be controlled by different factors.

More information

Here's where you can learn more about diabetes.

Reference Source 101

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