New classification and diagnostic criteria for insulin resistance syndrome
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- Ogawa Wataru
- Division of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan
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- Araki Eiichi
- Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Kumamoto 860-8556, Japan
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- Ishigaki Yasushi
- Division of Diabetes, Metabolism, and Endocrinology, Department of Internal Medicine, Iwate Medical University, Yahaba 028-3695, Japan
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- Hirota Yushi
- Division of Diabetes and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan
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- Maegawa Hiroshi
- Division of Diabetology, Endocrinology, and Nephrology, Department of Medicine, Shiga University of Medical Sciences, Otsu 520-2192, Japan
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- Yamauchi Toshimasa
- Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo 113-0003, Japan
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- Yorifuji Tohru
- Division of Pediatric Endocrinology and Metabolism, Children’s Medical Center, Osaka City General Hospital, Osaka 534-0021, Japan
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- Katagiri Hideki
- Department of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan
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抄録
<p>This report of a working group established by the Japan Diabetes Society proposes a new classification and diagnostic criteria for insulin resistance syndrome. Insulin resistance syndrome is defined as a condition characterized by severe attenuation of insulin action due to functional impairment of the insulin receptor or its downstream signaling molecules. This syndrome is classified into two types: genetic insulin resistance syndrome, caused by gene abnormalities, and type B insulin resistance syndrome, caused by autoantibodies to the insulin receptor. Genetic insulin resistance syndrome includes type A insulin resistance as well as Donohue and Rabson-Mendenhall syndromes, all of which are caused by abnormalities of the insulin receptor gene; conditions such as SHORT syndrome caused by abnormalities of PIK3R1, which encodes a regulatory subunit of phosphatidylinositol 3-kinase; conditions caused by abnormalities of AKT2, TBC1D4, or PRKCE; and conditions in which a causative gene has not yet been identified. Type B insulin resistance syndrome is characterized by severe impairment of insulin action due to the presence of insulin receptor autoantibodies. Cases in which hypoglycemia alone is induced by autoantibodies that stimulate insulin receptor were not included in Type B insulin resistance syndrome.</p>
収録刊行物
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- Endocrine Journal
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Endocrine Journal 69 (2), 107-113, 2022
一般社団法人 日本内分泌学会
