Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes
Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is caused by insufficient insulin production due to excessive loss of pancreatic β cells (type I diabetes) or impaired insulin signaling due to peripheral insulin resistance (type II diabetes). Pancreatic β cell is the only...
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Wiley
2012-01-01
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| Series: | Biochemistry Research International |
| Online Access: | http://dx.doi.org/10.1155/2012/247275 |
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| author | Xuebao Zhang Kezhong Zhang |
| author_facet | Xuebao Zhang Kezhong Zhang |
| author_sort | Xuebao Zhang |
| collection | DOAJ |
| description | Diabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is caused by insufficient insulin production due to excessive loss of pancreatic β cells (type I diabetes) or impaired insulin signaling due to peripheral insulin resistance (type II diabetes). Pancreatic β cell is the only insulin-secreting cell type that has highly developed endoplasmic reticulum (ER) to cope with high demands of insulin synthesis and secretion. Therefore, ER homeostasis is crucial to the proper function of insulin signaling. Accumulating evidence suggests that deleterious ER stress and excessive intracellular lipids in nonadipose tissues, such as myocyte, cardiomyocyte, and hepatocyte, cause pancreatic β-cell dysfunction and peripheral insulin resistance, leading to type II diabetes. The excessive deposition of lipid droplets (LDs) in specialized cell types, such as adipocytes, hepatocytes, and macrophages, has been found as a hallmark in ER stress-associated metabolic diseases, including obesity, diabetes, fatty liver disease, and atherosclerosis. However, much work remains to be done in understanding the mechanism by which ER stress response regulates LD formation and the pathophysiologic role of ER stress-associated LD in metabolic disease. This paper briefly summarizes the recent advances in ER stress-associated LD formation and its involvement in type II diabetes. |
| format | Article |
| id | doaj-art-6eeed4c0cfa04eaf9e3bef995f8c447d |
| institution | Kabale University |
| issn | 2090-2247 2090-2255 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Biochemistry Research International |
| spelling | doaj-art-6eeed4c0cfa04eaf9e3bef995f8c447d2025-02-03T01:27:30ZengWileyBiochemistry Research International2090-22472090-22552012-01-01201210.1155/2012/247275247275Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II DiabetesXuebao Zhang0Kezhong Zhang1Center for Molecular Medicine and Genetics, The Wayne State University School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USACenter for Molecular Medicine and Genetics, The Wayne State University School of Medicine, 540 East Canfield Avenue, Detroit, MI 48201, USADiabetes mellitus (DM), a metabolic disorder characterized by hyperglycemia, is caused by insufficient insulin production due to excessive loss of pancreatic β cells (type I diabetes) or impaired insulin signaling due to peripheral insulin resistance (type II diabetes). Pancreatic β cell is the only insulin-secreting cell type that has highly developed endoplasmic reticulum (ER) to cope with high demands of insulin synthesis and secretion. Therefore, ER homeostasis is crucial to the proper function of insulin signaling. Accumulating evidence suggests that deleterious ER stress and excessive intracellular lipids in nonadipose tissues, such as myocyte, cardiomyocyte, and hepatocyte, cause pancreatic β-cell dysfunction and peripheral insulin resistance, leading to type II diabetes. The excessive deposition of lipid droplets (LDs) in specialized cell types, such as adipocytes, hepatocytes, and macrophages, has been found as a hallmark in ER stress-associated metabolic diseases, including obesity, diabetes, fatty liver disease, and atherosclerosis. However, much work remains to be done in understanding the mechanism by which ER stress response regulates LD formation and the pathophysiologic role of ER stress-associated LD in metabolic disease. This paper briefly summarizes the recent advances in ER stress-associated LD formation and its involvement in type II diabetes.http://dx.doi.org/10.1155/2012/247275 |
| spellingShingle | Xuebao Zhang Kezhong Zhang Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes Biochemistry Research International |
| title | Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes |
| title_full | Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes |
| title_fullStr | Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes |
| title_full_unstemmed | Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes |
| title_short | Endoplasmic Reticulum Stress-Associated Lipid Droplet Formation and Type II Diabetes |
| title_sort | endoplasmic reticulum stress associated lipid droplet formation and type ii diabetes |
| url | http://dx.doi.org/10.1155/2012/247275 |
| work_keys_str_mv | AT xuebaozhang endoplasmicreticulumstressassociatedlipiddropletformationandtypeiidiabetes AT kezhongzhang endoplasmicreticulumstressassociatedlipiddropletformationandtypeiidiabetes |