Glucokinase activity in diabetes: too much of a good thing?
Type 2 diabetes (T2D) is a global health problem characterised by chronic hyperglycaemia due to inadequate insulin secretion. Because glucose must be metabolised to stimulate insulin release it was initially argued that drugs that stimulate glucokinase (the first enzyme in glucose metabolism) would...
| Main Authors: | , , |
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| Format: | Journal article |
| Language: | English |
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Cell Press
2022
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| _version_ | 1824459321265618944 |
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| author | Ashcroft, FM Lloyd, M Haythorne, EA |
| author_facet | Ashcroft, FM Lloyd, M Haythorne, EA |
| author_sort | Ashcroft, FM |
| collection | OXFORD |
| description | Type 2 diabetes (T2D) is a global health problem characterised by chronic hyperglycaemia due to inadequate insulin secretion. Because glucose must be metabolised to stimulate insulin release it was initially argued that drugs that stimulate glucokinase (the first enzyme in glucose metabolism) would enhance insulin secretion in diabetes. However, in the long term, glucokinase activators have been largely disappointing. Recent studies show it is hyperactivation of glucose metabolism, not glucose itself, that underlies the progressive decline in beta-cell function in diabetes. This perspective discusses if glucokinase activators exacerbate this decline (by promoting glucose metabolism) and, counterintuitively, if glucokinase inhibitors might be a better therapeutic strategy for preserving beta-cell function in T2D. |
| first_indexed | 2025-02-19T04:39:56Z |
| format | Journal article |
| id | oxford-uuid:a5a411c0-5e96-45e8-95d2-8a6b0de3cf79 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2025-02-19T04:39:56Z |
| publishDate | 2022 |
| publisher | Cell Press |
| record_format | dspace |
| spelling | oxford-uuid:a5a411c0-5e96-45e8-95d2-8a6b0de3cf792025-02-18T12:46:59ZGlucokinase activity in diabetes: too much of a good thing?Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:a5a411c0-5e96-45e8-95d2-8a6b0de3cf79EnglishSymplectic ElementsCell Press2022Ashcroft, FMLloyd, MHaythorne, EAType 2 diabetes (T2D) is a global health problem characterised by chronic hyperglycaemia due to inadequate insulin secretion. Because glucose must be metabolised to stimulate insulin release it was initially argued that drugs that stimulate glucokinase (the first enzyme in glucose metabolism) would enhance insulin secretion in diabetes. However, in the long term, glucokinase activators have been largely disappointing. Recent studies show it is hyperactivation of glucose metabolism, not glucose itself, that underlies the progressive decline in beta-cell function in diabetes. This perspective discusses if glucokinase activators exacerbate this decline (by promoting glucose metabolism) and, counterintuitively, if glucokinase inhibitors might be a better therapeutic strategy for preserving beta-cell function in T2D. |
| spellingShingle | Ashcroft, FM Lloyd, M Haythorne, EA Glucokinase activity in diabetes: too much of a good thing? |
| title | Glucokinase activity in diabetes: too much of a good thing? |
| title_full | Glucokinase activity in diabetes: too much of a good thing? |
| title_fullStr | Glucokinase activity in diabetes: too much of a good thing? |
| title_full_unstemmed | Glucokinase activity in diabetes: too much of a good thing? |
| title_short | Glucokinase activity in diabetes: too much of a good thing? |
| title_sort | glucokinase activity in diabetes too much of a good thing |
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