Evolutionary factors may have led to increased diabetes susceptibility in humans

An evolutionary "wrong turn" may be responsible for humans' propensity to become obese and develop type 2 diabetes, according to a new study from researchers at the University of California, San Diego.

Humans are much more likely to become overweight than other mammals. While many factors may account for this, the findings, which were reported in the FASEB Journal, indicate that our genes may be a prime suspect.

All mammals have a gene called CMAH. However, humans are the only species with a mutation that renders this gene less functional. In other mammals, this gene encodes an enzyme that interacts with certain sugars that line the surfaces of cells.



The team showed that, lacking this function, humans are much more likely to become overweight and lose the function of the insulin-producing beta cells of the pancreas. For the study, the researchers genetically engineered one group of mice to have the same alteration of the CMAH gene as humans, then compared their development to a group of normal mice.



When fed a high-fat diet, both groups became overweight. However, the mice with the less active CMAH variation were the only ones that lost function in their beta cells. This led to low levels of insulin production and uncontrolled blood sugar levels.

"If this enzyme is unique to humans, it must also have given us a survival advantage over earlier species," said Gerald Weissmann, who led the study. "Now the challenge is to find the function of CMAH in defending us against microbes or environmental stress or both."

He added that a better understanding of the causes of type 2 diabetes may lead to improved treatments for the condition.
 
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