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Early in the Sheffield years, Mark took the key decision to focus the lab on working with human beta-cells, rather than with rat or mouse cells, or with the cell lines he and others had earlier used to study KATP channels. Human islets were available from islet transplant programmes, though accessing them required establishing a lot of collaborations with clinicians around the UK, which Mark did with his usual energy and people skills. Over the next couple of years, Mark and his lab worked out the details of how to isolate and patch-clamp human betacells.
In the mid 90s, the human beta-cell work led to what was to become Mark’s primary research interest for the rest of his career, the rare but serious disease of congenital hyperinsulinism. Mark had forged a link with clinicians at Great Ormond Street treating children with severe forms of the disease. These children often required pancreatectomy to stop uncontrolled insulin secretion and severe hypoglycaemia, and Mark was able to obtain cells from the tissue to test. The striking result was that KATP channels, so prominent in normal beta-cells, could not be detected, leaving cells permanently depolarised. Mark’s lab collaborated with Lydia and Joe Aguilar-Bryan, who had earlier established the molecular identity of the KATP channel. A landmark case report in the New England Journal of Medicine, and other publications, showed that mutations in the sulphonylurea receptor led to non-functional KATP channels, and that this was the cause of at least some of the most severe cases of congenital hyperinsulinism.
In the mid 90s, the human beta-cell work led to what was to become Mark’s primary research interest for the rest of his career, the rare but serious disease of congenital hyperinsulinism. Mark had forged a link with clinicians at Great Ormond Street treating children with severe forms of the disease. These children often required pancreatectomy to stop uncontrolled insulin secretion and severe hypoglycaemia, and Mark was able to obtain cells from the tissue to test. The striking result was that KATP channels, so prominent in normal beta-cells, could not be detected, leaving cells permanently depolarised. Mark’s lab collaborated with Lydia and Joe Aguilar-Bryan, who had earlier established the molecular identity of the KATP channel. A landmark case report in the New England Journal of Medicine, and other publications, showed that mutations in the sulphonylurea receptor led to non-functional KATP channels, and that this was the cause of at least some of the most severe cases of congenital hyperinsulinism.
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