Swedish researchers have discovered new information as to how beta cells release insulin, and why smokers have an increased risk of type 2 diabetes.
In studies on mice and donated beta cells from humans, scientists at Lund University found that nicotine-sensitive receptors (known as nicotinic acetylcholine receptors) influence the way insulin is released.
Study author Isabella Artner explained: “The receptors in the beta cells that stimulate the release of insulin are normally activated by the signal substance acetylcholine, but they can also be activated by nicotine.”
Artner’s team studied a glucose-intolerant mouse model that was deficient in a gene called MafA (muscoloaponeurotic fibrosacoma oncogene family A). They demonstrated that MafA is found in beta cells and controls the number of nicotine-sensitive receptors. This then affects how signals are received from the central nervous system.
“Never before has the importance of nicotine-sensitive receptors been shown in terms of the function of beta cells,” said Artner. “Our research indicates that people who lack these receptors are at higher risk of developing type 2 diabetes.
“The effect that this single gene, MafA, alone has on insulin secretion was previously unknown, and nicotine receptors have never before been connected to type 2 diabetes.
“We know that smokers have an increased risk of developing type 2 diabetes, but the reason why has not been firmly established. Perhaps it has to do with the nicotine-sensitive receptors we describe. Our findings increase knowledge about the connection between smoking and type 2 diabetes.”
The study appears in the scientific journal Cell Reports.

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