Olga Göransson

Olga Göransson

Hjelt grant holder 2015, Lund university

Possible mechanisms behind insulin resistance to be mapped

During 2014, Olga Göransson’s group of researchers described the role of the hitherto unknown protein SIK2 in adipose cells from rats and mice. With the support of the Hjelt Foundation, they are now able to go further and investigate whether there is a link between SIK2 and the incidence of insulin resistance in humans.

Diabetes is an increasing among the population,health problem, which is partly due to insensitivity to the  blood-sugar lowering hormone insulin (insulinhjelt_projectreport resistance). The disease is very strongly linked to obesity. Insulin resistance means that the cells’ ability of cells to react to insulin is reduced. Consequently, the cells are unable to absorb energy from nutrients in the blood after a meal. Many overweight people develop insulin resistance, but the reason for this has not been established. Not Furthermore, not all overweight people develop type 2 diabetes either.  However, it is clear that disrupted adipose tissue function is an underlying cause of insulin resistance.

“To understand why obesity leads to insulin resistance in certain individuals, it is important to find out which mechanisms control the function of adipose cells and investigate the differences between sufferers and non-sufferers,” says Olga Göransson, who leads a group of researchers focusing on protein phosphorylation (a process that regulates cell activity).

Present in adipose tissue
SIK2 is a protein that primarily occurs in adipose tissue, the main function of which is primarily to store fat formed from fatty acids and sugar from the blood. Olga Göransson and her colleagues previously showed that SIK2 is required for an adipose cells to be able to absorb take up glucose, i.e. sugar, from the blood. By reducing the quantity of SIK2 in rats and mice, they showed that the level of a glucose transporter, GLUT4, was reduced.

“With our partners in Stockholm, we have also studied SIK2 in humans and our preliminary results show that the quantity of SIK2 is dramatically reduced in adipose tissue from insulin-resistant individuals.”

Investigating the link
The questions they are asking themselves now are: does SIK2 affect cells’ the sensitivity of cells to insulin? Can SIK2 itself be regulated by insulin? Can a change in the quantity of SIK2 lead to the biological response to insulin and thus the function of adipose cells being affected?

“We will test whether there is a causal connection between reduced SIK2 and the incidence of insulin resistance in human adipose cells, and thus reduced ability to store fat,” says Olga Göransson.

Sara Liedholm

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