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4 results on '"Tang, Nie"'

1. Elovl6 Deficiency Improves Glycemic Control in Diabetic db / db Mice by Expanding β-Cell Mass and Increasing Insulin Secretory Capacity.

Author

Zhao H, Matsuzaka T, Nakano Y, Motomura K, Tang N, Yokoo T, Okajima Y, Han SI, Takeuchi Y, Aita Y, Iwasaki H, Yatoh S, Suzuki H, Sekiya M, Yahagi N, Nakagawa Y, Sone H, Yamada N, and Shimano H

Subjects
Acetyltransferases physiology, Animals, Apoptosis genetics, Blood Glucose metabolism, Diabetes Mellitus, Experimental metabolism, Diabetes Mellitus, Type 2 metabolism, Endoplasmic Reticulum Stress, Fatty Acid Elongases, Fatty Acids, Nonesterified metabolism, Female, Immunohistochemistry, In Vitro Techniques, Inflammation chemically induced, Inflammation genetics, Insulin Secretion, Insulin-Secreting Cells drug effects, Insulin-Secreting Cells pathology, Islets of Langerhans drug effects, Islets of Langerhans metabolism, Islets of Langerhans pathology, Lipid Metabolism genetics, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Oleic Acid pharmacology, Organ Size, Palmitates adverse effects, Real-Time Polymerase Chain Reaction, Receptors, Leptin genetics, Acetyltransferases deficiency, Acetyltransferases genetics, Diabetes Mellitus, Experimental genetics, Diabetes Mellitus, Type 2 genetics, Insulin metabolism, Insulin-Secreting Cells metabolism
Abstract

Dysfunctional fatty acid (FA) metabolism plays an important role in the pathogenesis of β-cell dysfunction and loss of β-cell mass in type 2 diabetes (T2D). Elovl6 is a microsomal enzyme that is responsible for converting C16 saturated and monounsaturated FAs into C18 species. We previously showed that Elovl6 played a critical role in the development of obesity-induced insulin resistance by modifying FA composition. To further define its role in T2D development, we assessed the effects of Elovl6 deletion in leptin receptor-deficient C57BL/KsJ db / db mice, a model of T2D. The db / db ; Elovl6 mice had a markedly increased β-cell mass with increased proliferation and decreased apoptosis, an adaptive increase in insulin, and improved glycemic control. -/- mice had a markedly increased β-cell mass with increased proliferation and decreased apoptosis, an adaptive increase in insulin, and improved glycemic control. db / db mice exhibited reduced susceptibility to palmitate-induced inflammation, endoplasmic reticulum stress, and β-cell apoptosis. In contrast, oleate-treated islets resulted in impaired glucose-stimulated insulin secretion with suppressed related genes irrespective of the Elovl6 gene. Taken together, Elovl6 is a fundamental factor linking dysregulated lipid metabolism to β-cell dysfunction, islet inflammation, and β-cell apoptosis in T2D, highlighting oleate as the potential culprit of β-cell lipotoxicity.Elovl6 -/- mice exhibited reduced susceptibility to palmitate-induced inflammation, endoplasmic reticulum stress, and β-cell apoptosis. In contrast, oleate-treated islets resulted in impaired glucose-stimulated insulin secretion with suppressed related genes irrespective of the Elovl6 gene. Taken together, Elovl6 is a fundamental factor linking dysregulated lipid metabolism to β-cell dysfunction, islet inflammation, and β-cell apoptosis in T2D, highlighting oleate as the potential culprit of β-cell lipotoxicity., (© 2017 by the American Diabetes Association.)

Published
2017
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2. Ablation of Elovl6 protects pancreatic islets from high-fat diet-induced impairment of insulin secretion.

Author

Tang N, Matsuzaka T, Suzuki M, Nakano Y, Zao H, Yokoo T, Suzuki-Kemuriyama N, Kuba M, Okajima Y, Takeuchi Y, Kobayashi K, Iwasaki H, Yatoh S, Takahashi A, Suzuki H, Sone H, Shimada M, Nakagawa Y, Yahagi N, Yamada N, and Shimano H

Subjects
Animals, Cells, Cultured, Fatty Acid Elongases, Female, Insulin Resistance, Insulin Secretion, Male, Mice, Mice, Knockout, Obesity etiology, Organ Specificity, Tissue Distribution, Acetyltransferases metabolism, Dietary Fats adverse effects, Insulin metabolism, Islets of Langerhans metabolism, Islets of Langerhans pathology, Obesity metabolism, Obesity pathology
Abstract

ELOVL family member 6, elongation of very long-chain fatty acids (Elovl6) is a microsomal enzyme that regulates the elongation of C12-16 saturated and monounsaturated fatty acids and is related to the development of obesity-induced insulin resistance via the modification of the fatty acid composition. In this study, we investigated the role of systemic Elovl6 in the pancreatic islet and β-cell function. Elovl6 is expressed in both islets and β-cell lines. In mice fed with chow, islets of the Elovl6(-/-) mice displayed normal architecture and β-cell mass compared with those of the wild-type mice. However, when fed a high-fat, high-sucrose (HFHS) diet, the islet hypertrophy in response to insulin resistance observed in normal mice was attenuated and glucose-stimulated insulin secretion (GSIS) increased in the islets of Elovl6(-/-) mice compared with those of the wild-type mice. Enhanced GSIS in the HFHS Elovl6(-/-) islets was associated with an increased ATP/ADP ratio and the suppression of ATF-3 expression. Our findings suggest that Elovl6 could be involved in insulin secretory capacity per β-cell and diabetes., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Published
2014
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3. Elovl6 promotes nonalcoholic steatohepatitis

Author

Takashi, Matsuzaka, Ayaka, Atsumi, Rie, Matsumori, Tang, Nie, Haruna, Shinozaki, Noriko, Suzuki-Kemuriyama, Motoko, Kuba, Yoshimi, Nakagawa, Kiyoaki, Ishii, Masako, Shimada, Kazuto, Kobayashi, Shigeru, Yatoh, Akimitsu, Takahashi, Kazuhiro, Takekoshi, Hirohito, Sone, Naoya, Yahagi, Hiroaki, Suzuki, Soichiro, Murata, Makoto, Nakamuta, Nobuhiro, Yamada, and Hitoshi, Shimano

Subjects
Blood Glucose, Male, Fatty Acid Elongases, Inflammasomes, Palmitic Acid, Mice, Transgenic, Diet, High-Fat, Severity of Illness Index, Mice, Acetyltransferases, Non-alcoholic Fatty Liver Disease, NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Humans, Insulin, RNA, Messenger, Triglycerides, Mice, Knockout, Analysis of Variance, Gene Expression Profiling, Fatty Acids, Fatty Liver, Mice, Inbred C57BL, Disease Models, Animal, Oxidative Stress, Cholesterol, Liver, Hepatocytes, Diet, Atherogenic, Insulin Resistance, Carrier Proteins, Transcription Factors
Abstract

Nonalcoholic steatohepatitis (NASH) is associated with obesity and type 2 diabetes, and an increased risk for liver cirrhosis and cancer. ELOVL family member 6, elongation of very long chain fatty acids (Elovl6), is a microsomal enzyme that regulates the elongation of C12-16 saturated and monounsaturated fatty acids (FAs). We have shown previously that Elovl6 is a major target for sterol regulatory element binding proteins in the liver and that it plays a critical role in the development of obesity-induced insulin resistance by modifying FA composition. To further investigate the role of Elovl6 in the development of NASH and its underlying mechanism, we used three independent mouse models with loss or gain of function of Elovl6, and human liver samples isolated from patients with NASH. Our results demonstrate that (1) Elovl6 is a critical modulator for atherogenic high-fat diet-induced inflammation, oxidative stress, and fibrosis in the liver; (2) Elovl6 expression is positively correlated with severity of hepatosteatosis and liver injury in NASH patients; and (3) deletion of Elovl6 reduces palmitate-induced activation of the NLR family pyrin domain-containing 3 inflammasome; this could be at least one of the underlying mechanisms by which Elovl6 modulates the progress of NASH.Hepatic long-chain fatty acid composition is a novel determinant in NASH development, and Elovl6 could be a potential therapeutic target for the prevention and treatment of NASH.

Published
2011

4. Elovl6 Deficiency Improves Glycemic Control in Diabetic / Mice by Expanding β-Cell Mass and Increasing Insulin Secretory Capacity.

Author

Zhao, Hui, Matsuzaka, Takashi, Nakano, Yuta, Motomura, Kaori, Tang, Nie, Yokoo, Tomotaka, Okajima, Yuka, Han, Song-Iee, Takeuchi, Yoshinori, Aita, Yuichi, Iwasaki, Hitoshi, Yatoh, Shigeru, Suzuki, Hiroaki, Sekiya, Motohiro, Yahagi, Naoya, Nakagawa, Yoshimi, Sone, Hirohito, Yamada, Nobuhiro, and Shimano, Hitoshi

Subjects
ACETYLTRANSFERASES, ANIMAL experimentation, ANTHROPOMETRY, APOPTOSIS, BLOOD sugar, CELL receptors, DIABETES, FATTY acids, GENETIC disorders, IMMUNOHISTOCHEMISTRY, INFLAMMATION, INSULIN, ISLANDS of Langerhans, LIPID metabolism disorders, MICE, TYPE 2 diabetes, POLYMERASE chain reaction, UNSATURATED fatty acids, IN vitro studies
Abstract

Dysfunctional fatty acid (FA) metabolism plays an important role in the pathogenesis of β-cell dysfunction and loss of β-cell mass in type 2 diabetes (T2D). Elovl6 is a microsomal enzyme that is responsible for converting C16 saturated and monounsaturated FAs into C18 species. We previously showed that Elovl6 played a critical role in the development of obesity-induced insulin resistance by modifying FA composition. To further define its role in T2D development, we assessed the effects of Elovl6 deletion in leptin receptor-deficient C57BL/KsJ db/db mice, a model of T2D. The db/db;Elovl6-/- mice had a markedly increased β-cell mass with increased proliferation and decreased apoptosis, an adaptive increase in insulin, and improved glycemic control. db/db islets were characterized by a prominent elevation of oleate (C18:1n-9), cell stress, and inflammation, which was completely suppressed by Elovl6 deletion. As a mechanistic ex vivo experiment, isolated islets from Elovl6-/- mice exhibited reduced susceptibility to palmitate-induced inflammation, endoplasmic reticulum stress, and β-cell apoptosis. In contrast, oleate-treated islets resulted in impaired glucose-stimulated insulin secretion with suppressed related genes irrespective of the Elovl6 gene. Taken together, Elovl6 is a fundamental factor linking dysregulated lipid metabolism to β-cell dysfunction, islet inflammation, and β-cell apoptosis in T2D, highlighting oleate as the potential culprit of β-cell lipotoxicity. [ABSTRACT FROM AUTHOR]

Published
2017
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