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The Mystery Of The Mutant Mice That Never Got Fat

The mystery of why some people get fat eating high-fat foods while others can stay skinny on a diet of burgers and chips is closer to being solved.

| May 6, 2013 | In the Lab

AsianScientist (May 6, 2013) – The mystery of why some people get fat eating high-fat foods while others can stay skinny on a diet of burgers and chips is closer to being solved.

A research team, led by Professor Merlin Crossley at the University of New South Wales and Dr. Kim Bell-Anderson of the University of Sydney, investigated a genetically modified strain of mice that unexpectedly remained thin on a high-fat diet.

The researchers already knew that a protein called KLF3 turns off genes involved in blood production, and were trying to work out the function of the protein KLF3 by making a mouse that didn’t have any KLF3. To their surprise, the mutant mice remained lean on a high-fat diet and also showed signs of improved glucose metabolism and insulin action.

“We knew KLF3 was important for turning off gene expression, but we didn’t know which genes it targeted, so we looked at the gene expression of about 20,000 genes to see which ones were abnormally expressed in our mutant mice,” said Bell-Anderson, the lead author of the paper.

The findings, published in the journal Diabetes, showed that the mutant mice encoded higher levels of a hormone called adipolin. Adipolin is a type of hormone, produced by fat cells, that enters the blood and modulates responses to food.

If mice have a lot of adipolin they can better maintain a stable blood glucose level and remain thin even on a high fat diet. If mice have less adipolin they can’t lower their blood glucose levels after a meal and are fatter.

“The amount of adipolin circulating in the blood of our mutant mice was more than doubled,” said Bell-Anderson. “The roles of KLF3 and adipolin in humans and their beneficial or harmful effects are yet to be determined, but therapies aimed at increasing adipolin levels may be a promising target for treatment of type 2 diabetes and obesity.”

The article can be found at: Bell-Anderson KS et al. (2013) Loss of Krüppel-like Factor 3 (KLF3/BKLF) leads to upregulation of the insulin-sensitizing factor adipolin (FAM132A/CTRP12/C1qdc2).

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Source: UNSW; Photo: P_Breen/Flickr/CC.
Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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