INSIG2 polymorphism is neither associated with BMI nor with phenotypes of lipoprotein metabolism.
OBJECTIVE
A previous epidemiological study showed an association of the insulin-induced gene 2 (INSIG2) gene with BMI. Additionally, experimental investigations in animals and cell culture provided evidence that this gene might be involved in lipoprotein and free fatty acid (FFA) metabolism. Therefore, the aim of this study was to examine the association between the rs7566605 variant near the INSIG2 gene and BMI and to extend it to other quantitative measures of obesity, as well as parameters of lipoprotein and FFA metabolism.


METHODS
We genotyped rs7566605 in a group of severely obese white patients (n = 1,026) with an average BMI of 46.0 kg/m(2) and a control group (n = 818) from Utah, as well as in the Salzburg Atherosclerosis Prevention Program in Subjects at High Individual Risk (SAPHIR) study from Austria, which is based on a healthy working population (n = 1,696).


RESULTS
We observed no difference in the genotype frequency of rs7566605 of INSIG2 between obese subjects and population-based controls from Utah. Furthermore, we did not find evidence of an association with measures of body composition (BMI, waist, waist-to-hip ratio, percentage body fat, amount of visceral and subcutaneous abdominal adipose fat) or lipoprotein metabolism (total cholesterol, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, triglycerides, and FFAs) in the Utah study population or in the independent SAPHIR study.


CONCLUSIONS
Our results do not support an association of the INSIG2 gene with the regulation of body weight or parameters related to lipoprotein metabolism.
Boes
Eva
E
Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Innsbruck Medical University, Innsbruck, Austria.
Kollerits
Barbara
B
Heid
Iris M
IM
Hunt
Steven C
SC
Pichler
Michaela
M
Paulweber
Bernhard
B
Coassin
Stefan
S
Adams
Ted D
TD
Hopkins
Paul N
PN
Lingenhel
Arno
A
Wagner
Stefanie A
SA
Kronenberg
Florian
F
D000328:Adult; D001317:Austria / Q000453:epidemiology; D001823:Body Composition / Q000235:genetics; D015992:Body Mass Index; D016022:Case-Control Studies; D019295:Computational Biology; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics*; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics*; D008875:Middle Aged; D009765:Obesity / Q000453:epidemiology / Q000235:genetics* / Q000378:metabolism*; D010641:Phenotype; D011110:Polymorphism, Genetic; D012307:Risk Factors; D014280:Triglycerides / Q000378:metabolism; D014589:Utah / Q000453:epidemiology
D005230:Fatty Acids, Nonesterified; C467727:INSIG2 protein, human; D047908:Intracellular Signaling Peptides and Proteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008565:Membrane Proteins; D014280:Triglycerides