Genetic variation in adipokine genes and associations with adiponectin and leptin concentrations in plasma and breast tissue.
BACKGROUND
Circulating adipokines may be associated with breast cancer risk. Genetic variants governing adipokines and adipokine receptors may also predict risk, but their effect on breast adipokine concentrations is unknown.


METHODS
We conducted a cross-sectional analysis of functional SNPs in 5 adipokine genes [adiponectin, leptin (LEP), and their receptors] among 85 cancer-free women who were undergoing reduction mammoplasty.


RESULTS
In multivariable-adjusted regression models, compared with the common GG genotype, the AA genotype of the LEP A19G SNP was associated with 27% lower plasma adiponectin [ratio, 0.73; 95% confidence interval (CI), 0.54-0.98] and leptin (ratio, 0.73; 95% CI, 0.55-0.96). Women with the AG genotype of LEP A19G had 39% lower breast leptin (ratio, 0.61; 95% CI, 0.39-0.97) compared with those with the GG genotype. No associations were observed for SNPs in the remaining genes.


CONCLUSIONS
Genetic variation in LEP may alter endogenous adipokine concentrations in circulation and in breast tissues.


CONCLUSIONS
These preliminary findings may support the hypothesis that genetic variation in adipokine genes modifies circulating adipokine concentrations and possibly leptin concentrations in local breast tissues, which may be associated with breast cancer risk.
The Ohio State University Comprehensive Cancer Center; RBHS-School of Public Health and the Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Adana.Llanos@Rutgers.edu.
Adana A M
AA
Llanos
The Ohio State University Comprehensive Cancer Center; Division of Cancer Prevention and Control, College of Medicine, The Ohio State University, Columbus, Ohio;
Theodore M
TM
Brasky
Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC;
Jeena
J
Mathew
Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC;
Kepher H
KH
Makambi
The Ohio State University Comprehensive Cancer Center; Division of Cancer Prevention and Control, College of Medicine, The Ohio State University, Columbus, Ohio; University of Medicine and Pharmacy Timisoara, Timisoara, Romania; and.
Catalin
C
Marian
Saba University School of Medicine, Saba, Dutch Caribbean.
Ramona G
RG
Dumitrescu
Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, University at Buffalo, Buffalo, New York;
Jo L
JL
Freudenheim
The Ohio State University Comprehensive Cancer Center; Division of Cancer Prevention and Control, College of Medicine, The Ohio State University, Columbus, Ohio;
Peter G
PG
Shields
D054392:Adipokines / Q000097:blood / Q000235:genetics; D052242:Adiponectin / Q000097:blood / Q000235:genetics; D000328:Adult; D001943:Breast Neoplasms / Q000097:blood* / Q000235:genetics*; D003430:Cross-Sectional Studies; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D020738:Leptin / Q000097:blood* / Q000235:genetics*; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D020641:Polymorphism, Single Nucleotide; D054419:Receptors, Adiponectin / Q000097:blood / Q000235:genetics; D054411:Receptors, Leptin / Q000097:blood / Q000235:genetics
D054392:Adipokines; D052242:Adiponectin; D020738:Leptin; D054419:Receptors, Adiponectin; D054411:Receptors, Leptin