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糖尿病前期的新表型?

Novel phenotypes of prediabetes?

作者信息

Häring Hans-Ulrich

机构信息

Department of Internal Medicine IV, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, University of Tübingen, Otfried-Müller-Str. 10, 72076, Tübingen, Germany.

Institute of Diabetes Research and Metabolic Diseases (IDM), University of Tübingen, Tübingen, Germany.

出版信息

Diabetologia. 2016 Sep;59(9):1806-18. doi: 10.1007/s00125-016-4015-3. Epub 2016 Jun 25.

DOI:10.1007/s00125-016-4015-3
PMID:27344314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4969355/
Abstract

This article describes phenotypes observed in a prediabetic population (i.e. a population with increased risk for type 2 diabetes) from data collected at the University hospital of Tübingen. We discuss the impact of genetic variation on insulin secretion, in particular the effect on compensatory hypersecretion, and the incretin-resistant phenotype of carriers of the gene variant TCF7L2 is described. Imaging studies used to characterise subphenotypes of fat distribution, metabolically healthy obesity and metabolically unhealthy obesity are described. Also discussed are ectopic fat stores in liver and pancreas that determine the phenotype of metabolically healthy and unhealthy fatty liver and the recently recognised phenotype of fatty pancreas. The metabolic impact of perivascular adipose tissue and pancreatic fat is discussed. The role of hepatokines, particularly that of fetuin-A, in the crosstalk between these organs is described. Finally, the role of brain insulin resistance in the development of the different prediabetes phenotypes is discussed.

摘要

本文描述了从图宾根大学医院收集的数据中观察到的糖尿病前期人群(即2型糖尿病风险增加的人群)的表型。我们讨论了基因变异对胰岛素分泌的影响,特别是对代偿性高分泌的影响,并描述了基因变体TCF7L2携带者的肠促胰岛素抵抗表型。介绍了用于表征脂肪分布亚表型、代谢健康肥胖和代谢不健康肥胖的影像学研究。还讨论了肝脏和胰腺中的异位脂肪储存,它们决定了代谢健康和不健康脂肪肝的表型以及最近认识到的脂肪胰腺表型。探讨了血管周围脂肪组织和胰腺脂肪的代谢影响。描述了肝因子,特别是胎球蛋白-A,在这些器官之间相互作用中的作用。最后,讨论了脑胰岛素抵抗在不同糖尿病前期表型发展中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/1253b0f2b71a/125_2016_4015_Fig10_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/c7517da7cda9/125_2016_4015_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/1253b0f2b71a/125_2016_4015_Fig10_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/81ae792344be/125_2016_4015_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/039fcad62a2e/125_2016_4015_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/ac9a1816940a/125_2016_4015_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/c9c319b78f0e/125_2016_4015_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/77432c8cc193/125_2016_4015_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/ffcc1db25336/125_2016_4015_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/fbdc5bbc8b9d/125_2016_4015_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/c7517da7cda9/125_2016_4015_Fig9_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e7b4/4969355/1253b0f2b71a/125_2016_4015_Fig10_HTML.jpg

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Diabetes. 2016 Jun;65(6):1511-20. doi: 10.2337/db15-1552. Epub 2016 Feb 9.
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Exercise and diabetes: relevance and causes for response variability.运动与糖尿病:相关性及反应变异性的原因
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Gestational Diabetes Impairs Human Fetal Postprandial Brain Activity.妊娠期糖尿病会损害人类胎儿餐后大脑活动。
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Fatty Pancreas-Centered Metabolic Basis of Pancreatic Adenocarcinoma: From Obesity, Diabetes and Pancreatitis to Oncogenesis.以脂肪胰腺为中心的胰腺腺癌代谢基础:从肥胖、糖尿病和胰腺炎到肿瘤发生
Biomedicines. 2022 Mar 17;10(3):692. doi: 10.3390/biomedicines10030692.
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