Adropin deficiency worsens HFD-induced metabolic defects

The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Ch...

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Published inCell death & disease Vol. 8; no. 8; p. e3008
Main Authors Chen, Shi, Zeng, Kai, Liu, Qi-cai, Guo, Zheng, Zhang, Sheng, Chen, Xiao-rong, Lin, Jian-hua, Wen, Jun-ping, Zhao, Cheng-fei, Lin, Xin-hua, Gao, Feng
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.08.2017
Springer Nature B.V
Nature Publishing Group
Subjects
38/23
631/208/2489/144
631/208/737
692/699/1503/1712
692/699/2743/137/773
Adipocytes
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Blood Proteins - deficiency
Cell Biology
Cell Culture
Diabetes
Diabetes mellitus
Diabetes Mellitus, Type 2 - pathology
Diabetes Mellitus, Type 2 - therapy
Diet, High-Fat - adverse effects
Fat metabolism
Female
Genetic diversity
Homeostasis
Humans
Immunology
Intercellular Signaling Peptides and Proteins
Life Sciences
Lymphocytes T
Metabolic disorders
Mice
Mice, Inbred C57BL
Middle Aged
Nitric oxide
Nitric-oxide synthase
Obesity - complications
Obesity - pathology
Original
original-article
Pancreas
Pancreas - pathology
Peptides - deficiency
Phosphorylation
Proteins
Online AccessGet full text

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Abstract The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho , serum adropin, and relative T reg amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative T reg amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin ( r =0.7220, P =0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho . In vivo , adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of T reg , and developed FP and T2DM. Adropin-deficiency contributed to loss of T reg and the development of FP disease and T2DM.
AbstractList The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho , serum adropin, and relative T reg amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative T reg amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin ( r =0.7220, P =0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho . In vivo , adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of T reg , and developed FP and T2DM. Adropin-deficiency contributed to loss of T reg and the development of FP disease and T2DM.
The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho, serum adropin, and relative Treg amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative Treg amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin (r=0.7220, P=0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho. In vivo, adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of Treg , and developed FP and T2DM. Adropin-deficiency contributed to loss of Treg and the development of FP disease and T2DM.
The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho, serum adropin, and relative Treg amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative Treg amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin (r=0.7220, P=0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho. In vivo, adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of Treg, and developed FP and T2DM. Adropin-deficiency contributed to loss of Treg and the development of FP disease and T2DM.The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho, serum adropin, and relative Treg amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative Treg amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin (r=0.7220, P=0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho. In vivo, adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of Treg, and developed FP and T2DM. Adropin-deficiency contributed to loss of Treg and the development of FP disease and T2DM.
The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how metabolic homeostasis is maintained, to improve treatment efficacy and identify novel treatment methods. We analyzed a three-generation family of Chinese origin with the common feature of T2DM attacks and fatty pancreas (FP), alongside 19 unrelated patients with FP and 58 cases with T2DM for genetic variations in Enho, serum adropin, and relative T amounts. Functional studies with adropin knockout (AdrKO) in C57BL/6J mice were also performed. It showed serum adropin levels were significantly lower in FP and T2DM patients than in healthy subjects; relative T amounts were also significantly decreased in FP and T2DM patients, and positively associated with adropin (r=0.7220, P=0.0001). Sequencing revealed that the patients shared a Cys56Trp mutation in Enho. In vivo, adropin-deficiency was associated with increased severity of glucose homeostasis impairment and fat metabolism disorder. AdrKO mice exhibited reduced endothelial nitric oxide synthase (eNOS) phosphorylation (Ser1177), impaired glycosphingolipid biosynthesis, adipocytes infiltrating, and loss of T , and developed FP and T2DM. Adropin-deficiency contributed to loss of T and the development of FP disease and T2DM.
Author Guo, Zheng
Chen, Xiao-rong
Wen, Jun-ping
Zhao, Cheng-fei
Zhang, Sheng
Lin, Xin-hua
Zeng, Kai
Chen, Shi
Gao, Feng
Lin, Jian-hua
Liu, Qi-cai
Author_xml – sequence: 1
  givenname: Shi
  surname: Chen
  fullname: Chen, Shi
  organization: Department of Hepatobiliary Surgery, Fujian Provincial Hospital, Fujian Medical University
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  surname: Zeng
  fullname: Zeng, Kai
  organization: Department of Anesthesiology, 1st Affiliated Hospital, Fujian Medical University
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  givenname: Qi-cai
  surname: Liu
  fullname: Liu, Qi-cai
  email: lqc673673673@163.com
  organization: Department of Laboratory Medicine, 1st Affiliated Hospital, Fujian Medical University
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  givenname: Zheng
  surname: Guo
  fullname: Guo, Zheng
  organization: Department of Bioinformatics, Fujian Medical University
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  givenname: Sheng
  surname: Zhang
  fullname: Zhang, Sheng
  organization: Department of Pathology, 1st Affiliated Hospital, Fujian Medical University
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  fullname: Chen, Xiao-rong
  organization: Department of Radiology, 1st Affiliated Hospital, Fujian Medical University
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  fullname: Lin, Jian-hua
  organization: Department of Central Laboratory, 1st Affiliated Hospital
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  surname: Wen
  fullname: Wen, Jun-ping
  organization: Department of Endocrinology, Fujian Provincial Hospital
– sequence: 9
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  surname: Zhao
  fullname: Zhao, Cheng-fei
  organization: Department of Pharmaceutical Analysis, Putian University
– sequence: 10
  givenname: Xin-hua
  surname: Lin
  fullname: Lin, Xin-hua
  organization: Department of Pharmaceutical Analysis, Fujian Medical University
– sequence: 11
  givenname: Feng
  surname: Gao
  fullname: Gao, Feng
  email: fengfang77777@163.com
  organization: Department of Pathology, 1st Affiliated Hospital, Fujian Medical University
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Snippet The limited efficacy of current treatment methods and increased type 2 diabetes mellitus (T2DM) incidence constitute an incentive for investigating how...
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proquest
pubmed
crossref
springer
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Publisher
StartPage e3008
SubjectTerms 38/23
631/208/2489/144
631/208/737
692/699/1503/1712
692/699/2743/137/773
Adipocytes
Animals
Antibodies
Biochemistry
Biomedical and Life Sciences
Blood Proteins - deficiency
Cell Biology
Cell Culture
Diabetes
Diabetes mellitus
Diabetes Mellitus, Type 2 - pathology
Diabetes Mellitus, Type 2 - therapy
Diet, High-Fat - adverse effects
Fat metabolism
Female
Genetic diversity
Homeostasis
Humans
Immunology
Intercellular Signaling Peptides and Proteins
Life Sciences
Lymphocytes T
Metabolic disorders
Mice
Mice, Inbred C57BL
Middle Aged
Nitric oxide
Nitric-oxide synthase
Obesity - complications
Obesity - pathology
Original
original-article
Pancreas
Pancreas - pathology
Peptides - deficiency
Phosphorylation
Proteins
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Title Adropin deficiency worsens HFD-induced metabolic defects
URI https://link.springer.com/article/10.1038/cddis.2017.362
https://www.ncbi.nlm.nih.gov/pubmed/28837146
https://www.proquest.com/docview/1931605347
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https://pubmed.ncbi.nlm.nih.gov/PMC5596552
Volume 8
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