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KMID : 1141520230380060782
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Endocrinology and Metabolism
2023 Volume.38 No. 6 p.782 ~ p.787
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Partial Deletion of Perk Improved High-Fat Diet-Induced Glucose Intolerance in Mice
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Lee Joo-Yeop
Kim Min-Joo
Moon Seo-Il
Lim Ji-Yoon
Park Kyong-Soo
Jung Hye-Seung
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Abstract
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Although pancreatic endoplasmic reticulum kinase (PERK) is indispensable to beta cells, low-dose PERK inhibitor improved glucose- stimulated insulin secretion (GSIS) and hyperglycemia in diabetic mice. Current study examined if partial deletion of Perk (Perk+/-) recapitulated the effects of PERK inhibitor, on the contrary to the complete deletion. Perk+/- mice and wild-type controls were fed with a high-fat diet (HFD) for 23 weeks. Glucose tolerance was evaluated along with serum insulin levels and islet morphology. Perk+/- mice on normal chow were comparable to wild-type mice in various metabolic features. HFD-induced obesity was not influenced by Perk reduction; however, HFD-induced glucose intolerance was significantly improved since 15-week HFD. HFD-induced compromises in GSIS were relieved by Perk reduction, accompanied by reductions in phosphorylated PERK and activating transcription factor 4 (ATF4) in the islets. Meanwhile, HFD-induced islet expansion was not significantly affected. In summary, partial deletion of Perk improved glucose tolerance and GSIS impaired by diet-induced obesity, without changes in body weights or islet mass.
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KEYWORD
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PERK, High-fat diet, Glucose intolerance, Insulin secretion
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