Clues to quality of journals
Open Access Policy of Helmholtz Association 2016
CC Licencences
Publication Metrics
Home
Deutsch
New EVA Application
Advanced Search
Browse by ...
Publication overview
Statistics (last 5 years)
OA Publications
Submit Publication
Import publication from...
Report missing publication
Contact persons
Help
Text
Endnote (RIS)
BibTeX
Publ. Version/Full Text
Postprint
DOI
PMC
 |
Open Access Green |
as soon as is submitted to ZB.
A polygenic risk score of lipolysis-increasing alleles determines visceral fat mass and proinsulin conversion.
J. Clin. Endocrinol. Metab. 104, 1090-1098 (2019)
Context: Primary dysregulation of adipose tissue lipolysis caused by genetic variation and independent of insulin resistance could explain unhealthy body fat distribution and its metabolic consequences.Objective: To analyze common single nucleotide polymorphisms (SNPs) in 48 lipolysis-, but not insulin-signaling-related genes, to form polygenic risk scores of lipolysis-associated SNPs, and to investigate their effects on body fat distribution, glycemia, insulin sensitivity, insulin secretion, and proinsulin conversion.Study Design, Participants, and Methods: SNP array, anthropometric, and metabolic data were available from up to 2789 participants without diabetes of the Tubingen Family study of type 2 diabetes characterized by oral glucose tolerance tests. In a subgroup (n = 942), magnetic resonance measurements of body fat stores were available.Results: We identified insulin-sensitivity-independent nominal associations (P < 0.05) of SNPs in 10 genes with plasma free fatty acids (FFAs), in 7 genes with plasma glycerol and in 6 genes with both, plasma FFAs and glycerol. A score formed of the latter SNPs (in ADCY4, CIDEA, GNAS, PDE8B, PRKAA1, PRKAG2) was associated with plasma FFA and glycerol measurements (1.4*10(-9) <= P <= 1.2*10(-5)), visceral adipose tissue mass (P = 0.0326), and proinsulin conversion (P <= 0.0272). The more lipolysis-increasing alleles a subject had, the lower was the visceral fat mass and the lower the proinsulin conversion.Conclusions: We found evidence for a genetic basis of adipose tissue lipolysis resulting from common SNPs in CIDEA, AMP-activated protein kinase subunits, and cAMP signaling components. A genetic score of lipolysis-increasing alleles determined lower visceral fat mass and lower proinsulin conversion.
Impact Factor
Scopus SNIP
Web of Science
Times Cited
Times Cited
Scopus
Cited By
Cited By
Altmetric
5.605
1.879
2
4
Annotations
Special Publikation
Hide on homepage
Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Insulin Sensitivity; Acids; Homeostasis; Resistance; Glucose; Obesity
Language
english
Publication Year
2019
HGF-reported in Year
2019
ISSN (print) / ISBN
0021-972X
e-ISSN
1945-7197
Quellenangaben
Volume: 104,
Issue: 4,
Pages: 1090-1098
Publisher
Endocrine Society
Publishing Place
Bethesda, Md.
Reviewing status
Peer reviewed
Institute(s)
Institute of Diabetes Research and Metabolic Diseases (IDM)
Institute of Experimental Genetics (IEG)
Institute of Experimental Genetics (IEG)
POF-Topic(s)
90000 - German Center for Diabetes Research
30201 - Metabolic Health
30201 - Metabolic Health
Research field(s)
Helmholtz Diabetes Center
Genetics and Epidemiology
Genetics and Epidemiology
PSP Element(s)
G-502400-001
G-500600-001
G-500600-001
WOS ID
WOS:000469813500014
Scopus ID
85062080472
PubMed ID
30649496
Erfassungsdatum
2019-03-01